Up To Fate


Home

Links

This Week

Topics

Study Fast Facts

Study Planner

Exam Questions

 

Clinical Exam

References

 

2004 FRACP paper two

Questions

1 | 2 | 3 | 4 | 5 | 6 | 7 | 8 | 9 | 10 | 11 | 12 | 13 | 14 | 15 | 16 | 17 | 18 | 19 | 20 | 21 | 22 | 23 | 24 | 25 | 26 | 27 | 28 | 29 | 30 | 31 | 32 | 33 | 34 | 35 | 36 | 37 | 38 | 39 | 40 | 41 | 42 | 43 | 44 | 45 | 46 | 47 | 48 | 49 | 50 | 51 | 52 | 53 | 54 | 55 | 56 | 57 | 58 | 59 | 60 | 61 | 62 | 63 | 64 | 65 | 66 | 67 | 68 | 69 | 70 | 71 | 72 | 73 | 74 | 75 | 76 | 78 | 79 | 80 | 81 | 82 | 83 | 84 | 85 | 86 | 87 | 88 | 89 | 90 | 91 | 92 | 93 | 94 | 95 | 96 | 97 | 98 | 99 | 100

Question 1 top

Question 2 top Download PDF

A 42yo man with acromegaly undergoes transphenoidal pituitary surgery for a growth hormone-secreting macroadenoma. Six months post-op he has an elevated insulin-like growth factor type I (IGF-I) concentration. A repeat MRI scan reveals a residual and inoperable tumour confined to the right cavernous sinus only.

Which of the following is the most appropriate mamangement?

A. Expectant management
B. B. Radiotherapy
C. Bromocriptine
D. Octreotide
E. Cabergoline

Answer D. Octreotide


GROWTH HORMONE


Reference: http://www.colorado.edu/kines/Class/IPHY3430-200/17endo1.html

Growth hormone:

  • mobilises fatty acids from adipose tissue
  • opposes action of insulin on glucose metabolism
  • increases muscle growth

IGF-I:

  • produced in liver
  • promote DNA synthesis and cell multiplication

 

ACROMEGALY

  • Almost always caused by somatotroph adenoma
  • Associated with increased morbidity and mortality
  • Almost all patients should be treated

Features:

  • Overgrowth of cartilage and collagen-containing tissues
    • Frontal bossing
    • Deeply furrowed creases on face
    • Growth of lower jaw and laryngeal cartilage
    • Broad, thick hands
    • Thickened heel pads
    • Skin tags
    • Shiny, sweaty skin
  • Symptoms
    • Headache
    • Sweating
    • Poor bite
    • Arthritis
    • Carpal tunnel
    • Symptoms of hypopituitarism
  • Can develop
    • Cardiovascular disease, cardiomyopathy, hypertension
    • Respiratory disease, sleep apnoea
    • Arthropathy
    • Neuropathy
    • Malignancy, colonic polyps
    • Glucose intolerance or diabetes

Autonomous secretion of GH is demonstrated by lack of suppression by glucose

Treatment:

  • Aim is to lower serum IGF-1 concentration to within the reference range for pt’s age and gender and to lower serum GH concentration to < 1ng/mL (1mcg/L) as measure after glucose load
  • If IGF-1 level normalised then life expectancy is close to normal
  • Also aim to rid pt of symptoms without causing hypopituitarism
  • GH cannot often be returned to completely normal
  • Metabolic symptoms (s/a diabetes mellitus) often improve
  • Bone and joint symptoms usually persist

Trassphenoidal Surgery

  • Treatment of choice in pts with somatotrophs that are
    • Small
    • Large but still resectable
    • Large and causing visual impairment
  • GH falls to normal in about 80 – 90% of pts with microadenomas
  • Lower in pts with macroadenomas (ie. 50%) and/or higher pre-op GH concentrations
  • GH concentrations usually fall to normal in 1-2 hrs
  • IGF-1 levels can be normal in 7-10 days but can remain high for months
  • Headaches and vision impairment should improve in days
  • Soft tissue swelling and hyperglycaemia diminish in few days

Recurrence is 3-10%, can be several yrs later. Higher risk if nadir GH concentration after oral glucose load is even slightly high.

Peri-op mortality <1% in pts w large invasive adenomas, negligible in pts w microadenomas. Hormone deficiencies in 0-2% of pts.

Other major complications in ~8% of pts: central diabetes insipidus (2%), CSF rhinorrhoea (2%), meningitis (2%). Less likely with experienced surgeons.

Medical Therapy

Used when surgery alone has not reduced GH and IGF-1 to normal.

  1. Somatostatin analogs - 1st line
    • Octreotide, lanreotide
    • Analogs of growth-hormone-inhibitory hormone (somatostatin)
    • Inhibit GH secretion
    • Octreotide binds to specific receptors for somatostatin and its analogs
    • Octreotide has long acting forms (monthly IM injection) and short acting forms (tds s/c injection)
    • Both can be increased if initial response inadequate
    • Should lead to normalisation of IGF-1 and GH and reduced adenoma size and reduced soft tissue swelling and improved insulin sensitivity, LV function improves, sleep apnoea improves
    • Normalisation of bloods occurs in 40 to 75% of pts
    • Can consider combination with cabergoline if not effective alone
    • Side effects: nausea, abdo discomfort, bliating, diarrhoea, fat malabsorption – tends to resolve in few weeks
    • Octreotide reduces postprandial GB contractility and delays GB emptying so 25% of pts get asymptomatic cholesterol gallstones or sludge in 1st 18/12 of Rx
  2. Dopamide angonists
    • Cabergoline (better than bromocriptine)
    • Inhibit GH secretion
    • Not as good as somatostatin analogues
    • Oral form
    • Reduced GH and IGF-1 to near normal in ~40% of pts
    • Not very effective at reducing adenoma size
  3. GH receptor antagonist
    • Pegvisomant
    • Used if no response to other treatments
    • Blocks native GH from binding
    • Cannot use serum GH to monitor effectiveness of Rx
    • Normalises IGF-1 in 97% of pts
    • Potentially increases adenoma size due to increase GH concentration
    • Side effects: elevated liver enzymes, avoid in pts w abnormal LFTs
    • Combination w somatostatin analogue is good
  4. XRT
    • Used for pts who have failed surgical and medical Mx
    • Stops adenoma growth
    • Slow decline in GH secretion, slow clinical improvement
    • Hormone deficiencies relatively common
    • Other complications: cranial nerve palsies, loss of vision, memory deficits (all rare), increased incidence of other intracranial tumours

Long-term Monitoring

  1. 3-4/12 GH and IGF-1 after glucose
  2. Other pituitary hormones yearly
  3. Adenoma size on MRI – yearly at first
  4. Visual field assessments if close to chiasm
  5. Colonoscopy every 3-4 yrs in pts > 50 (increased risk of polyps)
  6. Regular cardiovascular check-up

Topic

Endrocrinology - acromegaly

 

Question 3 top Download PDF

A 65 yo man presents to outpatients complaining of breathlessness on exercise, which has been progressive over the last four years. He has a 40 pack-year smoking history and has had daily cough with clear sputum production over the past 10 years.

Lung function testing shows:

FEV1 0.70L (30% predicted)
FVC 3.77L (90% predicted)
PaO2 61mmHg [75-90]

Which of the following interventions is most likely to improve his survival?

A. Inhaled anticholinergics
B. Long-term oxygen therapy
C. Inhaled corticosteroids
D. Smoking cessation
E. Lung volume reduction surgery


Severity of COPD

FEV1/FVC less than 0.7 = airflow limitation

Factor
Mild
Moderate
Severe
Spirometry findings – postbronchodilator FEV1% 60 – 80% predicted 40 - 59% predicted Less than 40% predicted
Functional assessment (Activities of daily living) Few symptoms
No effect on daily activities
Breathless on moderate exertion Increasing dyspnoea

Breathless on the flat
Increasing limitation of daily activities Dyspnoea on minimal exertion
Daily activities severely curtailed

Complications No Exclude complications; consider sleep apnoea if there is pulmonary hypertension Severe hyponxaemia (PaO2 ,60mmHg)
Hypercapnia (PaCO2 >45mmHg)
Pulmonary HT
Heart failure
Polycythaemia

TREATMENT OF COPD

Optimise Function
Summary
Evidence Level
Inhaled bronchodilators provide symptom relief and may increase exercise capacity A

Long-acting bronchodilators provide sustained relief of symptoms in moderate to severe COPD
A
Long term use of systemic glucocorticoids is not recommended A
Inhaled glucocorticoids should be condiered in pts with documented response or those who have severe COPD with frequent exacerbations B

Identify and treat hypoxaemia and pulmonary HT
A
Pulmonary rehab reduces dyspnoea, anxiety and depression, improves exercise capacity and quality of life and may reduce hospitalisation A
In selected patients, a surgical approach may be considered for symptom relief C
Prevent or treat osteoporosis A
Inhaled bronchodilators
  • Provide symptom relief and may increase exercise capacity
  • Changes in FEV1, FVC not closely correlated with symptomatic improvement
  • Nebulisers not recommended for routine use in stable pts
  • All bronchodilators (beta -2 agonists and anticholinergics) have similar effects on quality of life
  • Combination of the two may be more effective and better tolerated than higher doses of one alone
Severity
FEV1
Suggested treatment
Mild COPD 60 - 80% Intermittent bronchodilator - salbutamol 200mcg or ipratropium bromide 40mcg as needed before exercise
Moderate COPD 40 - 59% Intermittent or regular bronchodilator - salbutamol 200 - 400mcg QID or ipratropium 40mcg daily. Combination may be considered
Severe COPD less than 40% Regular combination bronchodilator - salbutamol 200 - 400mcg QID and ipratropium 40 - 80mcg daily

Long-acting Bronchodilators

  • Long-acting beta-agonists are not currently subsidised by PBS for COPD
  • Improve exercise endurance, quality of life and reduce exacerbation rate and number of hospitalisations
  • More effective and convenient than short-acting bronchodilators but more expensive
  • Salmeterol 50mcg bd
  • Higher dose does not significantly improve response
  • Tiotropium 18mcg daily is approved by PBS for COPD
  • Reduces dyspnoea and improved health status compared to placebo or ipratropium
  • Reduces exacerbations and hospitalisations
  • Improves exercise endurance by reducing hyperinflation
Theophyllines
  • Modest effect on FEV1 and FVC
  • Slightly improves ABGs in moderate to severe COPD
  • Narrow therapeutic range and potential side effects so rarely used
Oral Glucocorticoids
  • Long-term use not recommended (limited efficacy and potential toxicity)
  • Short-course (2 weeks) can be tried
  • Some patients with stable COPD show a significant response (on spirometry and functional assessment)
Inhaled Glucocorticoids
  • Does not influence rate of decline in FEV1
  • Patients with clinically significant acute bronchodilator reversibility may benefit from long-term inhaled glucocorticoid therapy
  • Also indicated in pts who have frequent exacerbations
  • RCT showed pts with severe non-reversible COPD had reduced exacerbations and a slower decline in quality of life with fluticasone 1000mcg daily
  • No effect on overall decline in lung function
Combination Inhaled Glucocorticoid and Long-acting Bronchodilator
  • Improves quality of life, symptoms and exacerbations
  • But some conflicting results so more studies are necessary
Surgery
  • No survival advantage
  • Bullectomy
  • Lung volume reduction surgery (experimental/palliative)
  • Lung transplantation
Identify and Treat Aggravating Factors
  • Sleep apnoea, hypoventilation and hypoxaemia (overlap syndrome = COPD plus OSA)
  • GORD
  • Aspiration
  • Alcohol and sedatives
  • Hypoxaemia and pulmonary HT
Other Treatment
  • Supplemental oxygen
    • long-term O2 therapy (> 15hrs/day) prolongs life in hypoxaemic patients (PaO2 < 55mmHg)
  • Ventilatory support (CPAP or NIPPV for pts with OSA or hypoventilation)
  • Diuretics – may reduce RV filling pressure and oedema
  • Pulmonary rehabilitation
  • Exercise training
  • Patient education
  • Psychosocial support
  • Chest physio
  • Weight reduction/nutrition
  • STOP SMOKING
    • Reduces the rate of decline in lung function
    • Smoking cessation remains the only effective means to affect the decline in lung function
  • Vaccinations (influenza, pneumococcal)


A. Inhaled anticholinergics may improve quality of life but do not influence survival.

B. Long-term oxygen therapy prolongs life in hypoxaemic patients only (PaO2 < 55mmHg) – this patient does not meet this criteria.

C. Inhaled corticosteroids may reduce exacerbations and reduce decline in quality of life but no effect on survival.

D. Smoking cessation is the only effective means to reduce decline in lung function and thus prolong survival.

E. Lung volume reduction surgery may be appropriate in certain patients, results vary among patient groups. This patient is 65 which is considered to be the upper limit when considering surgery for COPD. He has not been trialed on other therapies and we don’t know anything about his health otherwise so we can’t make a judgement on surgery. There is not clear evidence to say it would improve survival in any case.

Topic

Respiratory - Smoking-related chronic lung disease

 

Question 4 top Download PDF

A 35yo married indigenous woman presents with a 4 day history of fever, mild headache and severe polyarthritis involving the wrists, elbows and knees. Joint pain has been only slightly relieved by naproxen 250mg twice daily and paracetamol 1-2g daily. Prior to the onset of arthritis, she had a sore throat for several days but denies rash, vaginal discharge or history of sexually transmitted diseases.
On examination, she appears unwell with a temperature of 39 degrees, an erythematous throat with tonsillar enlargement and a few small tender cervical lymph nodes. There is tenderness and soft tissue swelling of the wrists and knees. Cardiovascular examination is normal.
Which of the following investigations is most likely to identify the diagnosis?

  1. Blood cultures for Staphylococcus aureus
  2. A high vaginal swab for Neisseria gonorrhoea
  3. A throat swab for Stretococcus species
  4. A stool culture for Yersinia enterocolitica
  5. A synovial fluid culture for Neisseria meningitidis

 

The symptoms described clinically fit with acute rheumatic fever:

        1. Sore throat in past 1-5 weeks
        2. Arthritis typically involving the large joints such as elbows, wrists and knees, classically migratory

    SYMPTOMS OF ACUTE RHEUMATIC FEVER

        1. Sore throat (2/3 patients recall sore throat in past 1-5 weeks)
        2. Polyarthritis (75%, more common in adults)
          • Typically migratory involving mainly the large joints such as the knees, ankles, elbows and wrists
          • Usually subsides within 4 weeks
        3. Carditis (40-50%, more common in younger children)
          • Can cause clinical picture of CCF
        4. Sydenham chorea (15%)
        5. Erythema marginatum (10%)
          • Non-pruritic, non-painful erythematous eruption on trunk
          • Can persist intermittently for weeks to months
        6. Other symptoms that can occur
          • Fever
          • Abdominal pain
          • Epistaxis
          • Arthralgia

 

SIGNS

 

      • Polyarthritis
        1. Typical symptoms of inflammatory arthritis can occur
        2. Small joints of hands and spine rarely involved
        3. Classically migratory
      • Carditis
        1. Usually pancarditis
        2. New murmur (MS common, isolated aortic disease rare)
        3. Features of CCF
        4. Pericarditis with rub or effusion
      • Subcutaneous nodules
        1. Associated with severe carditis
        2. Usually appear several weeks after onset
        3. Over bony prominences and tendons
        4. Commonly at elbows, knees, wrists, ankles and over Achilles tendon, occiput or spinous processes of vertebrae
        5. Usually persist for 1-2 weeks
      • Erythema marginatum
        1. Evanescent
        2. Tendency to advance at the margins while clearing in the centre
        3. Can disappear in minutes to hours
        4. On trunk and proximal extremities
      • Sydenham chorea

       

      • Rapid and uncoordinated involuntary purposeless movements
      • Emotional lability
      • Muscle weakness
      • Disappear during sleep
      • Can involve face, hands and feet

      Untreated attacks last approximately 3 months.
      Chronic rheumatic fever (> 6 months) occurs in < 5%.

       

      CAUSES

      Group A betahaemolytic strep (but not all serotypes)

          1. Thought to be due to an abnormal immune response to streptococcal components
          2. Resulting antibodies cross react with host antigens cause immunologic damage leading to the clinical manifestations
          3. Genetic differences in susceptibility

       

      INVESTIGATIONS

          1. No single specific laboratory test can confirm the diagnosis
          2. Throat culture is the standard test to confirm the presence of group A streptococcus
          3. Rapid antigen detection tests have high specificity but low sensitivity so high number of false negatives
          4. Throat swab more sensitive
          5. ASOT, anitstreptococcal DNAse B titre, antihyaluronidase titre
          6. Need to demonstrate a rise in the titre between acute and convalescent sera (3-6 weeks for ASOT, 6-8 weeks for DNAse B)
          7. Blood cultures to rule out IE, bacteraemia, gonococcal infection

       

      DIAGNOSTIC CRITERIA

      Major Criteria

      1. Carditis
      2. Polyarthritis
      3. Chorea
      4. Erythema marginatum
      5. Subcutaneous nodules

       

      Minor Criteria

      1. Arthralgia
      2. Fever
      3. Elevated acute phase reactants
      4. Prolonged PR interval

       

      Evidence of preceding streptococcal infection

      1. Positive throat culture for group A beta-haemolytic streptococci or positive rapid streptococcal antigen test
      2. Elevated or rising streptococcal antibody titre

       

      Criteria met if:

          1. Evidence of preceding group A streptococcal infection plus 2 major criteria or one major and two minor criteria

       

      COMPLICATIONS

          1. Rheumatic heart disease occurs usually 10 to 20 years after original attack
          2. Mitral valve most commonly involved (classically mitral stenosis)

       

      TREATMENT

      Aim is to:

          1. Symptomatic relief
          2. Eradication of group A beta-haemolytic strep
          3. Prophylaxis against future infection to prevent recurrent cardiac disease

       

       

      Symptomatic Relief:

          1. For arthritis use anti-inflammatories (aspirin 4-8g/day in 4 divided doses or naproxen (5-7.5mg/kg bd)
          2. Paracetamol +/- codeine
          3. For carditis, treat the same as for cardiac failure of any cause

      If treatment for chorea is required can use carbamazepine or valproate

      Eradication:

          1. Phenoxymethylpenicillin (500mg orally bd) for at least 10 days

      OR

          1. Benzathine penicillin G as single dose (900mg IM)

      For patients with penicillin allergy:

          1. Erythromycin 800mg (500mg) orally bd for 10 days

       

      Antibiotic Prophylaxis:

          1. Recurrence rates decline with increasing age
          2. Monthly benzathine penicillin (900mg IM)
          3. If IM route not possible, use phenoxymethylpenicillin 250mg orally bd
          4. For patients with penicillin allergy, erythromycin 400mg (250mg) orally bd
          5. Treatment recommended for minimum 10 years after last episode of acute rheumatic fever or until age 21 (whichever is longer)
          6. If residual heart disease of more than mild severity exists then continue until age 35
          7. If severe valve disease or surgery involved continue until age 40 at least
          8. Guidelines recently published by AHA regarding antibiotic prophylaxis for dental procedures etc (see below)
          9. Do not recommend any prophylaxis for RHD which is different to the previous guidelines (as published in therapeutic guidelines)

       

      References: UTD, e-medicine, Circulation April 19 2007 (circ.ahajournals.org)

       

      GONOCOCCAL ARTHRITIS

          1. Most common cause in young adults (while staph aureus most common overall)
          2. Caused by gram-negative diplococcus Neisseria gonorrhoeae
          3. Due to disseminated gonococcal infection which can manifest as arthritis-dermatitis syndrome (60%) or localised septic arthritis (40%)

       

      Arthritis-Dermatitis Syndrome:

          1. Symptoms usually for 3-5 days before diagnosis
          2. Classic triad of migratory polyarthritis, tenosynovitis and dermatitis
          3. Migratory arthralgias most common presenting symptom
          4. Typically asymmetrical, polyarticular and involve upper extremities more than lower extremities
          5. Wrists, elbows, ankles and knees most commonly affected
          6. Tenosynovitis can occur, usually over dorsum of wrist and hand
          7. Painless, non-pruritic rash, typically on extremities – small papules, pustules or vesicles
          8. Non-specific constitutional symptoms (fever, myalgia, malaise)

       

      Septic Arthritis Form:

          1. Usually 3-6 days after onset of illness
          2. Pain, redness and swelling in one or sometimes multiple joints

       

      Diagnosis:

          1. Blood cultures
          2. Joint aspirate (although often negative)
          3. Culture from primary mucosal infection (positive in 90% of cervical samples, 50-75% of male urethral samples, 20% of pharyngeal samples and 15% of rectal samples)
          4. Urine culture
          5. Proven disseminated gonogoccal infection = positive blood cultures, synovial fluid cultures or other site sources
          6. Probable DGI = positive swab from primary mucosal surface
          7. Possible DGI = clinical syndrome and treatment responsive

       

      Treatment:

          1. Same for both forms
          2. Joint washout rarely required
          3. Ceftriaxone 1g IV daily OR cefotaxime 1g IV tds

       

      Clinical picture does not fit with staph aureus (polyarthritis not a common feature), yersinia (not history of GIT symptoms) or meningococcal infections (headache not prominent, arthritis not a common feature).

      While both B and C could be correct, there are more features that suggest acute rheumatic fever rather than disseminated gonococcal infection:

          1. Symmetrical polyarthritis
          2. No rash
          3. No vaginal discharge or history of STDs
          4. Sore throat and cervical lymphadenopathy

       

      In addition, the criteria for acute rheumatic fever will be met if there is evidence of preceding strep infection (pt has polyarthritis, arthralgia, fever).

      So the answer is C – throat swab for streptococcus

       

      just to be aware of….

      TABLE 3. Cardiac Conditions Associated With the Highest Risk of Adverse Outcome From Endocarditis for Which Prophylaxis With Dental Procedures Is Recommended

          1. Prosthetic cardiac valve
          2. Previous IE
          3. Congenital heart disease (CHD)*
            1. Unrepaired cyanotic CHD, including palliative shunts and conduits
            2. Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure†
            3. Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
          4. Cardiac transplantation recipients who develop cardiac valvulopathy

       

      *Except for the conditions listed above, antibiotic prophylaxis is no longer
      recommended for any other form of CHD.
      †Prophylaxis is recommended because endothelialization of prosthetic
      material occurs within 6 months after the procedure.

      TABLE 4. Dental Procedures for Which Endocarditis Prophylaxis Is Recommended for Patients in Table 3

          1. All dental procedures that involve manipulation of gingival tissue or the

      periapical region of teeth or perforation of the oral mucosa*

      *The following procedures and events do not need prophylaxis: routine anesthetic
      injections through noninfected tissue, taking dental radiographs, placement of removable
      prosthodontic or orthodontic appliances, adjustment of orthodontic appliances, placement
      of orthodontic brackets, shedding of deciduous teeth, and bleeding from trauma to the lips.

      TABLE 5. Regimens for a Dental Procedure

      Amoxicillin/Ampicillin 2g orally/IM/IV 30 to 60 mins prior to procedure

      If allergic to penicillin

      Cephalexin 2g orally or clindamycin 600mg orally 30 to 60 mins prior to procedure

      *Or other first- or second-generation oral cephalosporin in equivalent adult or pediatric dosage.
      †Cephalosporins should not be used in an individual with a history of anaphylaxis, angioedema, or urticaria with penicillins or
      ampicillin.

      TABLE 6. Summary of Major Changes in Updated Document

      We concluded that bacteremia resulting from daily activities is much more likely to cause IE than bacteremia associated with a dental procedure.
      We concluded that only an extremely small number of cases of IE might be prevented by antibiotic prophylaxis even if prophylaxis is 100% effective.
      Antibiotic prophylaxis is not recommended based solely on an increased lifetime risk of acquisition of IE.
      Limit recommendations for IE prophylaxis only to those conditions listed in Table 3.
      Antibiotic prophylaxis is no longer recommended for any other form of CHD, except for the conditions listed in Table 3.
      Antibiotic prophylaxis is recommended for all dental procedures that involve manipulation of gingival tissues or periapical region of teeth or perforation of oral mucosa only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from IE (Table 3).
      Antibiotic prophylaxis is recommended for procedures on respiratory tract or infected skin, skin structures, or musculoskeletal tissue only for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from IE (Table 3).
      Antibiotic prophylaxis solely to prevent IE is not recommended for GU or GI tract procedures.
      The writing group reaffirms the procedures noted in the 1997 prophylaxis guidelines for which endocarditis prophylaxis is not recommended and extends this to other common procedures, including ear and body piercing, tattooing, and vaginal delivery and hysterectomy.
      Previous guidelines (from antibiotic guidelines) suggest prophylaxis for medium to high risk groups.
      Prevention of endocarditis: cardiac conditions that have a risk for infective endocarditis with dental and other procedures (Table 2.11)


High-risk conditions

Medium-risk conditions

Low-risk conditions

prosthetic cardiac valves
bioprosthetic
homograft
previous infective endocarditis
complex cyanotic congenital heart disease (transposition, tetralogy of Fallot)
surgically constructed systemic-pulmonary shunts, or conduits
mitral valve prolapse with clinically significant regurgitation
acquired valvular dysfunction (eg rheumatic heart disease) in Indigenous patients

acquired valvular dysfunction (eg rheumatic heart disease) in non-Indigenous patients
congenital cardiac malformations other than those defined as high- or low-risk
hypertrophic cardiomyopathy
significant valvular/haemodynamic dysfunction associated with septal defects

isolated secundum atrial septal defects
surgical repair of septal defects
previous coronary artery bypass grafts or stents
mitral valve prolapse without regurgitation
physiological, functional or innocent murmur
previous Kawasaki disease without valvular dysfunction
cardiac pacemakers
pulmonary stenosis
heart-lung transplants

High-risk procedures

Medium-risk procedures

Low-risk procedures

extraction
periodontal procedures including surgery and root planing
replanting avulsed teeth
other surgical procedures (eg implant placement, apicoectomy)

periodontal probing
intraligamentary and intraosseous local anaesthetic injection
supragingival calculus removal/cleaning
rubber dam placement with clamps (where risk of damaging gingiva)
restorative matrix band/strip placement
endodontics beyond the apical foramen
placement of orthodontic bands
placement of interdental wedges
subgingival placement of retraction cords, antibiotic fibres or antibiotic strips

oral examination
infiltration and block local anaesthetic injection
restorative dentistry
supragingival rubber dam clamping and placement of rubber dam
intracanal endodontic procedures
removal of sutures
impressions and construction of dentures
orthodontic bracket placement and adjustment of fixed appliances
application of gels
intraoral radiographs
supragingival plaque removal

Topic

Infectious Diseases Recognition and management of common community-acquired infection

Question 5 top

Question 6 top

Question 7 top Download PDF

A 57yo man with a long history of poorly controlled hypertension and smoking presents with sudden onset of right-sided sensory change and mild change of speech. On examination his speech is slurred but content and comprehension are normal. He has a mild right hemisensory change to pin-prick, with normal power and symmetrical reflexes.

His MRI scans are shown below (T2 weighted axial image (A) and diffusion weighted image (B)).

The most likely cause of the stroke syndrome is:

A. Left middle cerebral artery thrombosis

B. Left basal ganglia haemorrhage

C. Amyloid angiopathy

D. Left middle cerebral penetrating artery occlusion

E. Acute demyelination

 

This question is very similar to one of I-Lynn’s (2005 paper one question 66)– answer is D.

MRI

  1. T1: Fat and subacute haemorrhage have high signal intensity, water has low signal intensity
  2. T2: Water has high signal intensity
  3. CSF and oedema therefore appear white-ish on T2 and dark on T1
  4. Grey matter has more water than white matter so it also has higher intensity on T2 and lower on T1
  5. T2 images better for oedema, demyelination, infarction and chronic haemorrhage
  6. T1 images better for subacute haemorrhage and fat-containing structures
  7. FLAIR is a T2 image but with the normally high signal of the CSF suppressed – allows better visualisation of lesions adjacent to CSF
  8. Diffusion weighted images are the best to detect acute infarct (<7 days) which show up as high signal lesions; also good for encephalitis and abscesses
  9. Gadolinium is the form of IV contrast used for MRIs – seen as high signal on T1 and low signal on T2
  10. Gadolinium does not cross an intact BBB but with enhance lesions lacking a BBB – good for seeing tumours
  11. MRI less sensitive than CT for acute bleeds

 

MCA STROKES

  1. Contralateral hemiplegia
  2. Hemianaesthesia
  3. Homonymous hemianopia
  4. 1-2 days of gaze preference to ipsilateral side
  5. Dysarthria common due to facial weakness
  6. If dominant hemisphere involved:
    1. Global aphasia
  7. If non-dominant hemisphere involved:
    1. Anosognosia
    2. Construction apraxia
    3. Neglect

 

Partial Syndromes:

  1. Various combinations of face +/- hand +/- arm +/- leg weakness +/- expressive or receptive aphasia +/- sensory loss +/- neglect or quadrantanopia
  2. Due to emboli occluding branches of MCA

 

MCA Lacunar Infarcts:

  1. Lenticulostriate vessel occlusion - pure motor or pure sensory stroke contralateral to lesion
  2. Ischaemia of internal capsule causes primarily facial weakness followed by arm and then leg weakness
  3. Lacunar infarcts of globus pallidus and putamen often have few clinical signs

 

ACA STROKES

  1. Divided into 2 segments:
    1. Precommunal (A1) circle of Willis which connects internal carotid to anterior communicating artery
    2. Postcommunal (A2) segment distal to the anterior communicating artery
  2. Occlusion of proximal ACA usually well tolerated due to collateral flow through anterior communicating artery, MCA and PCA
  3. Occlusion of A2 leads to:
    1. Contralateral paralysis of foot and leg
    2. Lesser degree of paresis of contralateral arm
    3. Sensory loss over toes, foot and leg
    4. Urinary incontinence
    5. Gait apraxia
    6. Slowness

 

ANTERIOR CHOROIDAL ARTERY STROKES

  1. This artery arises from the internal carotid artery and supplies the posterior limb of the internal capsule
  2. Compete syndrome:
    1. Contralateral hemiplegia
    2. Hemianaesthesia
    3. Homonymous hemianopia
  3. However, this area is supplied by other vessels also so minimal deficits may occur

 

PCA STROKES

  1. Supplies the cerebellum, medulla, pons, midbrain, thalamus, hippocampus, medial temporal and occipital lobes
  2. 2 clinical syndromes:
    1. P1 – midbrain, subthalamic and thalamic signs due to proximal disease
      1. 3rd nerve palsy WITH
      2. Contralateral ataxia (Claude’s syndrome) OR
      3. Contralateral hemiplegia (Weber’s syndrome)
    2. P2 – cortical temporal and occipital lobes due to distal disease
      1. Contralateral homonymous hemianopia with macula sparing
      2. Memory disturbance
  3. Bilateral infarcts of distal PCA can cause cortical blindness – pt often unaware

 

VERTEBRAL AND CEREBELLAR ARTERIES

  1. PICA is a branch of the 4th segment of the vertebral artery
  2. Posterior inferior cerebellar artery supplies the lateral medulla and the inferior cerebellum
  3. Lateral medullary syndrome:
    1. Vertigo
    2. Numbness of ipsilateral face
    3. Numbness of contralateral body
    4. Diplopia
    5. Hoarseness
    6. Dysarthria
    7. Dysphagia
    8. Ipsilateral Horner’s syndrome
    9. Caused by occlusion of vertebral or PICA
  4. Rarely medial medullary syndrome can occur with contralateral hemiparesis of arm and leg but sparing the face; can involve hypoglossal nerve and medial lemniscus (causing contralateral loss of joint position sense)
  5. Atherothrombotic lesions of single vertebral artery usually compensated by collaterals from the other vertebral artery
  6. If both arteries involved, collateral flow may be insufficient leading to low-flow TIAs – syncope, vertigo and alternating hemiplegia

 

BASILAR ARTERY

  1. Branches supply the pons and superior cerebellum
  2. Complete occlusion:
    1. Bilateral sensory and motor deficits
    2. Cranial nerve signs
    3. Cerebellar dysfunction
    4. “Locked-in” state
  3. TIAs may cause dizziness, diplopia, dysarthria, facial or circumoral numbness and hemisensory symptoms (pending basilar occlusion – important to recognise) – usually last 5 to 30 mins and occur multiple times in a day
  4. Occlusion of a branch of the basilar artery usually causes unilateral sensory, motor and CN signs

 

Acute stroke syndromes


Artery involved

Syndrome

Pathophysiology

Anterior cerebral artery

Motor and/or sensory deficit (foot >> face, arm)
Grasp, sucking reflexes
Abulia, paratonic rigidity, gait apraxia

Embolic > atherothrombotic

Middle cerebral artery

Dominant hemisphere: aphasia, motor and sensory deficit (face, arm >leg >foot), may be complete hemiplegia if internal capsule involved, homonymous hemianopia.
Non-dominant hemisphere: neglect, anosognosia, motor and sensory deficit (face, arm > leg>foot), homonymous hemianopia.

Embolic > atherothrombotic

Posterior cerebral artery

Homonymous hemianopia; alexia without agraphia (dominant hemisphere); visual hallucinations, visual perseverations (calcarine cortex); sensory loss, choreoathetosis, spontaneous pain (thalamus); III nerve palsy, paresis of vertical eye movement, motor deficit (cerebral peduncle, midbrain).

Embolic > atherothrombotic

Penetrating vessels

Pure motor hemiparesis (classic lacunar syndromes)
Pure sensory deficit
Pure sensory-motor deficit
Hemiparesis, homolateral ataxia
Dysarthria/clumsy hand

Small artery (lacunar) infarct

Vertebrobasilar

Cranial nerve palsies
Crossed sensory deficits
Diplopia, dizziness, nausea, vomiting, dysarthria, dysphagia, hiccup
Limp and gait ataxia
Motory deficit
Coma
Bilateral signs suggest basilar artery disease.

Embolic = atherothrombotic

Internal carotid artery

Progressive or stuttering onset of MCA syndrome, occasionally ACA syndrome as well if insufficient collateral flow.

Atherothrombotic > embolic

 


Eligibility criteria for the treatment of acute ischemic stroke with recombinant tissue plasminogen activator (rt-PA)


Inclusion criteria

Clinical diagnosis of ischemic stroke, with the onset of symptoms within three hours of the initiation of treatment (if the exact time of stroke onset is not known, it is defined as the last time the patient was known to be normal), and with a measurable neurologic deficit

Exclusion criteria

Historical

Stroke or head trauma within the prior 3 months

Any prior history of intracranial hemorrhage

Major surgery within 14 days

Gastrointestinal or gentitourinary bleeding within the previous 21 days

Myocardial infarction in the prior 3 months

Arterial puncture at a noncompressible site within 7 days

Lumbar puncture within 7 days

Clinical

Rapidly improving stroke symptoms

Only minor and isolated neurologic signs

Seizure at the onset of stroke with postictal residual neurologic impairments

Symptoms suggestive of subarachnoid hemorrhage, even if the CT is normal

Clinical presentation consistent with acute MI or post-MI pericarditis

Persistent systolic BP>185, diastolic BP>110 mmHg, or requiring aggressive therapy to control BP

Pregnancy or lactation

Active bleeding or acute trauma (fracture)

Laboratory

Platelets <100,000/mm3

Serum glucose <50 mg/dL (2.8 mmol/L) or >400 mg/dL (22.2 mmol/L)

INR >1.7 if on warfarin

Elevated partial thromboplastin time if on heparin

Head CT scan

Evidence of hemorrhage

Evidence major early infarct signs, such as diffuse swelling of the affected hemisphere, parenchymal hypodensity, and/or effacement of >33 percent of the middle cerebral artery territory

Adapted from Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 1996; 47:835 and Adams, HP, Adams, RJ, Brott, T, et al. Stroke 2003; 34:1056.

Topic

Neurology: Stroke

Question 8 top Download PDF

QUESTION 8

Which of the following is the most appropriate medication to maintain remission in ileo-colonic Crohn’s disease?

A. Nicotine

B. Azathioprine

C. Mesalazine

D. Budesonide

E. Cyclosporin

 

CROHN’S DISEASE

  1. Inflammatory condition
  2. Unknown cause (genetic and environmental factors important)
  3. Can affect any part of GIT
  4. Transmural, focal inflammation
  5. Relapsing and remitting course
  6. Aim of treatment is to induce remission and prevent relapse

 

MILD TO MODERATE ACTIVE DISEASE

  1. Oral or parenteral corticosteroids are most effective
  2. Response rates 60-70% at 12-16 weeks
  3. Prednisone 25 to 60mg orally weaning to zero over 8 to 12 weeks after a clinical response
  4. In ileocaecal disease, budesonide controlled-ileal release formulation is also an option, especially in pts with adverse reactions to corticosteroids in past, but expensive and not on PBS
  5. Budesonide 9mg orally daily reducing to zero over 8-12 weeks after clinical response
  6. Benefit of aminosalicylates are limited and of doubtful clinical significance
  7. Metronidazole has a limited effect as a single agent – 20mg/kg orally in divided doses daily
  8. No evidence for adding antibiotics to steroids

 

SEVERE ACTIVE DISEASE

  1. Initially parenteral therapy
  2. Methylprednisolone 60-80mg IV daily in divided doses or hydrocortisone 100mg IV QID
  3. Broad spectrum antibiotics often also used though no actual evidence for this
  4. Change to oral corticosteroids when disease activity has subsided

 

REFRACTORY ACTIVE DISEASE

  1. Infliximab has 60-70% response rates
  2. Response to single infusion lasts 6-8 weeks
  3. If response, maintenance therapy every 8 weeks is used
  4. Serious adverse effects can occur and it is expensive
  5. If still refractory, surgery may be necessary

 

CHRONIC ACTIVE DISEASE

  1. Consider AZA or 6-MP or MTX (plus folic acid) in pts who do not respond to corticosteroids or those who require prolong steroid therapy
  2. Onset of action may be delay – should be continue for at least 3-6 months (or 2-3 months for MTX)
  3. Infliximab also effective
  4. Consider surgery

 

MAINTENANCE THERAPY

  1. AZA, 6-MP have good evidence
  2. Azathioprine 2 to 2.5mg/kg daily
  3. Mercaptopurine 1 to 1.5mg/kg daily
  4. If not tolerated or ineffective, consider MTX 25mg IM weekly (plus folica acid)
  5. Requires monthly monitoring of FBE and LFTs
  6. Infliximab also shown to be effective
  7. Should not use corticosteroids long-term

 

ILEAL MALABSORPTION

  1. Extensive ileal disease or resection can lead to bile salt malabsorption à bile salt diarrhoea or steatorrhoea
  2. Can occur in absence of active inflammation
  3. Treatment = cholestyramine 4-8g daily to tds
  4. Can also use loperamide

 

BACTERIAL OVERGROWTH

  1. Causes diarrhoea and malabsorption
  2. Augmentin DF or metronidazole or norfloxacin for 1-2 weeks

 

PERIANAL DISEASE

  1. Fissures, fistulas and abscesses are common
  2. Surgery often required
  3. Metronidazole usually used 400mg tds – may be needed for weeks to months +/- ciprofloxacin
  4. Refractory perianal disease may respond to AZA
  5. Infliximab is effective in pts with fistulas unresponsive to other treatment

 

OTHER TREATMENTS

  1. Quit smoking à fewer relapses
  2. Diet important to maintain nutrition, TPN may be required
  3. Risk of Fe, zinc, B12, calcium, mg, folic acid and vitamin D deficiency – replace as required

 

Answer: B

 

ULCERATIVE COLITIS

  1. Mucosal disease
  2. Confined to colon
  3. Continuous inflammatory changes extending from rectum

 

ACTIVE PROCTITIS OR DISTAL COLITIS

  1. Rectal and oral 5-ASA therapy more effective than either alone
  2. Rectal corticosteroids are added if 5-ASA ineffective
  3. Continue rectal therapy until symptoms resolve then wean over several weeks
  4. Consider rectally administered maintenance in pts with repeated relapses
  5. If no response, add oral prednisolone

 

EXTENSIVE UC – MILD TO MODERATE

  1. Rectal therapy alone is ineffective for pts with colitis proximal to splenic flexure
  2. Use 5-ASA +/- prednisolone

 

EXTENSIVE UC – SEVERE

  1. > 8 bloody stools/day plus at least one of:
    1. T>37
    2. HR>100
    3. Hb<100
    4. Albumin<35
  2. Hospital admission, early surgical consultation
  3. Methylprednisolone or hydrocortisone for 5-7 days then oral weaning dose
  4. Deterioration or failure to respond over 3-7 days requires consideration of colectomy
  5. Can use IV cyclosporine or infliximab in specialist centres
  6. Avoid loperamide or other antidiarrhoeal and anticholinergic agents and opioids in severe disease as they can precipitate toxic megacolon

 

CHRONICALLY ACTIVE DISEASE

  1. AZA, 6-MP or infliximab
  2. Consider surgery

 

MAINTENANCE THERAPY

  1. 5-ASA is first line
  2. AZA or 6-MP second line
  3. Can consider infliximab if poor response or surgery

 

5-ASA

  1. Exact mechanism of action not known but exerts anti-inflammatory action in bowel wall
  2. Side effects more common at higher doses – nausea, rash, headache, diarrhoea common
  3. Interstitial nephritis infrequent
  4. Blood dyscrasias, pancreatitis and hepatitis rare
  5. Mesalazine, balsalazide, olsalazine and sulfasalazine
  6. Higher risk of adverse effects with sulfasalazine

 

 

 

 

Crohn’s Disease

 

Ulcerative Colitis

 

Mild-Moderate Active Disease

 

Prednisolone
Consider budesonide for ileal disease only

 

1st line: 5-ASA
2nd line: 5-ASA plus prednisolone
Use rectal for distal disease

 

Severe Active Disease

 

1st line: IV steroids
2nd line: infliximab

 

1st line: IV steroids
2nd line: surgery or cyclosporin or infliximab

 

Chronic Active Disease

 

1st line: AZA, 6-MP, MTX
2nd line: infliximab

 

1st line: AZA, 6-MP
2nd line: infliximab or surgery

 

Maintenance Therapy

 

1st line: AZA or 6-MP
2nd line: infliximab

 

1st line: 5-ASA
2nd line: AZA, 6-MP

Topic

Gastroenterology: Chron's Disease

Clinical Pharmacology

Question 9 top

Question 10 top Download PDF

An 80yo woman with long-standing AF and HT is referred for a 2nd opinion on further management. She has been on metoprolol and started warfarin a month ago. She is asymptomatic.

On examination, she has an apex rate of 60/minute and BP of 136/84. She has no signs of cardiac failure. An ECG confirms AF. A CXR shows cardiomegaly with a cardiothoracic ration of 14.5/28 but clear lung fields. Echocardiography demonstrates left ventricular hypertrophy and diastolic dysfunction. Systolic function is preserved with fractional shortening of 28%. Atrial dimensions are normal.

Which of the following long-term management strategies is most appropriate?

  Attempt DC cardioversion Thromboprophylaxis Anti-arrhythmic therapy
a yes continue wafarin Beta blocker
b yes change to aspirin Beta blocker
c yes change to aspirin Amiodarone
d no continue wafarin Beta blocker
e no continue wafarin Amiodarone

Answer D


Rate control vs Rhythm control in AF

  • Two big trials (RACE and AFFIRM) both show that there is not difference in thromboembolic events between rate control methods and rhythm control methods.
  • It is recommended that all patients with AF be on warfarin unless there is a contraindication
  • This includes patients who have been successfully reverted with either DCR or medications
  • Most likely these patients will still have episodes of AF and can be completely asymptomatic
  • So, the 1st thing is to continue warfarin
  • Rate control or rhythm control are both acceptable approaches
  • In most patients rate control is employed:
    • There is a trend toward reduced mortality with rate control
    • Multiple potential side effects to anti-arrhythmic drugs
    • Recurrent AF is common after reversion (DCR or medication)
  • Rhythm control should be considered for patients who:
    • have persistent symptoms despite rate control
    • cannot be adequately rate controlled
    • have a preference for reversion
  • In addition there is a tendency to attempt rhythm control in young patients with a first presentation of AF (with DCR)
  • So, in this 80yo woman rate control is going to be the best option, especially if it has been working so far
  • Having said this there is a theoretical advantage to rhythm control in patients with heart failure as the failure would be easier to control and in diastolic failure the heart relies on the atrial contraction to push that last bit of blood through to the ventricle
  • There have been to trials on this though, and this patient is not symptomatic with her failure so don’t really need to worry about this
  • Therefore answer is d: continue warfarin, continue Bblocker, not for DCR

Just for some additional info, risk factors for thromboembolic event in AF:

  • age > 65
  • female
  • Hx of TIA/stroke
  • HT
  • DM
  • CCF

Topic

Cardiology - Arrhythmias