Qbank Exam

Question 1

post epidural headache. what structure has been breached?
This patient presents with a severe headache after insertion of an epidural catheter. The most likely cause is

Answer 1

Must be Dura - an epidural is above the dura and not within the spinal chord proper. in an epidural- layers breached- suuptaspinus, interspinous, ligamentum flavum. Then in epidural space

POST DURAL HEADACHE

A spinal anaesthesia is within the CSF which lies in the sub arachnoid space- pierce the dura and arachnoid layer. suptaspinus, interspinous, ligamentum flavum. Then in epidural space - through dura and arachnoid. IN SUBARACHNOID SPACE- CSF back flash

The most likely cause is inadvertent puncture of the dura mater during the process of inserting the epidural needle and catheter. The intended target for an epidural catheter is the epidural space, a potential space that overlies the dura mater. If the dura mater is accidentally punctured during insertion of an epidural catheter, a post-dural headache can result. This can also sometimes occur following spinal anaesthesia (where the dura mater is intentionally pierced), however is much less common due to the smaller needles used.

Obstetric patients are at increased risk of post-dural puncture headache compared to non-obstetric patients receiving epidural analgesia.

The underlying pathophysiology is thought to involve leakage of cerebrospinal fluid (CSF) through the hole in the dura mater. If CSF leaks at a rate greater than that of fluid production, CSF pressure falls, particularly at the level of the brain when the patient is standing in the upright position.

This also explains why the headache is improved when lying flat. The headache is generally localised to the frontal or occipital region and can be accompanied by other symptoms including neck stiffness, nausea, vertigo, photophobia and tinnitus. Treatment is generally supportive and most dural puncture headaches will have resolved after one week, although symptoms can occasionally linger for months. Severe headaches that interfere with a patient’s activities can be treated with an epidural blood patch, a treatment that involves injection of the patient’s own blood into the epidural space, effectively “plugging” the dural puncture site.

During epidural catheterisation, the interspinous ligament and ligamentum flavum are always traversed by the needle and catheter. The reason for this is that they lie along the path the needle must take in order to reach the epidural space. Piercing these structures is not associated with a headache.

The arachnoid mater is pierced during spinal anaesthesia when local anaesthetic agents and/or opioids are injected into the CSF. As this is an epidural anaesthetic, it is most unlikely that the arachnoid mater has been penetrated.

Question 2

clear nasal discharge, hx trauma. no facial bruising. What to order?

Answer 2

• Beta-2-transferrin is a useful test in distinguishing the presence of cerebrospinal fluid in nasal discharge, which indicates a basal skull fracture.

ongoing nasal discharge following head trauma; it is important to rule out a base of skull fracture. Given his nasal discharge, the first-line test is to do a beta-2 transferrin analysis of the nasal discharge. This test provides a highly sensitive and selective, non-invasive test for the detection of cerebrospinal fluid (CSF) leakage in the case of head trauma. However, this test is not rapid and typically takes up to 24 hours to return a result. However, before that is done, with his increasing headache it would be prudent to admit the patient to hospital for clinical observation at least until the result returns. Likewise, if the patient had any neurological signs, or signs of infection, hospital admission would be wise.

Following this test, if it is positive, an imaging study such as a CT or MRI would be warranted to characterise the base of skull fracture.

Question 3

wernickes and broccas - aphasia

Answer 3

Aphasia is a disorder where you have problems speaking or understanding what other people say.

BP - B-proc Broccas is for production of speech- ( broken sounding language)

Wernickes - WUP understanding and processing ( would just produce strange words)

Question 4

to distinguish dementia from delerium what componene t of MMSE must be tested

Answer 4

Attention. In delirium attention is affected. In dementia attention is relatively well preserved

Deficits in attention are core to the diagnosis of delirium, whereas deficits in memory are more affected in dementia, both of these can be picked up in aspects of the MMSE

Attention: Test in MMSE- serial 7s and WORLD backward ( Look for ability to engage globally with attention)

Repitiion of no if and butts- language ( suspected Identifying objects such as a wristwatch is testing recognition and language. It could be affected if someone has visual agnosia, where someone is no longer able to recognise objects visually. This can be caused by insults/damage to the parietal lobe, such as in stroke.

Repeating after someone “no ifs, ands, or buts” is also used to test language impairment. The patient must be receptive to the sentence that you have stated and then repeat it back, testing language and repetition. This tests for impairments such as dysarthria or dysphagia, and requires the language areas of the brain, such as Broca’s, Wernicke’s and the arcuate fasciculus.

Getting a patient to write a sentence on a piece of paper is a good test of their basic writing skills. It can help to identify agraphia (loss of the ability to write), micrographia (small writing), which can be a sign of Parkinson’s disease and macrographia (large handwriting), which can be seen in patients with cerebellar disease and Huntington’s disease.

Question 5

When is an ICD indicated (Implantable Cardiac Defibrillators) - implantable cardioverter

Answer 5

Congestive heart failure is a common long term complication following myocardial infarction. CHFrEF<40%

Implantable cardiac defibrillators are indicated in persistently depressed left ventricular ejection fraction at least 40 days following a myocardial infarction.

<35% with a stemi

Implantable cardioverters detect aberrant life-threatening rhythms and deliver an automated shock in response. They are used in both primary and secondary prophylaxis against sudden cardiac death.

Indications for ICD include:

• ICD Indications ^[1]
  
  • Primary prophylaxis
    
    • Congestive heart failure with certain criteria
      • Left ventricular ejection fraction (LVEF) <35% due to prior MI, at least 40 days post MI
      • an ejection fraction <30% or
      • LVEF <35% with NYHA class II or III heart failure,
      • ejection fraction 30-40% >30 days after a STEMI in an asymptomatic patient.
    • Increased risk of life-threatening cardiac arrhythmias
      • Arrhythmogenic right ventricular cardiomyopathy
      • Hypertrophic obstructive cardiomyopathy
      • Brugada syndrome
      • Long QT syndrome
      • Structural heart disease with sustained VT
      • syncope of undetermined origin,
      • inducible VT or VF at electrophysiologic study (EPS)

Secondary prophylaxis:
history of sudden cardiac arrest, ventricular flutter, or ventricular fibrillation

An ICD is indicated if, despite maximal medical therapy, the patient has persistently depressed left ventricular ejection fraction at least 40 days following a myocardial infarction. This is due to risk of developing another episode of VT.

Question 6

trancutaneous pacing wire, pacemaker, LV assist device

Answer 6

Pacemakers are indicated where the heart’s conductivity is compromised, namely arrhythmias and heart block.

As the name implies, the temporary pacing wire is a temporary approach to pacing, used in situations such as the prevention and treatment of postoperative arrhythmias following coronary artery bypass.

a cardiac transplant or left ventricular assist device- classified as “end-stage” or NYHA Grade III-IV heart failure despite being symptomatic whilst on maximal medical therapy.

Question 7

brugda syndrome- st elevation mimic

Answer 7

• Brugda pattern
• Pseudo right bundle branch block

Pseudo-RBBB (rSR in V1)

An ECG pattern that resembles the findings of a right bundle branch block (rSr′ pattern) but is caused by a different etiology, such as an accessory electric pathway or an inherited arrhythmia (e.g., Brugada syndrome).

MX

• Pharmacological cardioversion with one of the following: ^[1][24][32]
  
  • Quinidine
  • Isoproterenol
• Avoid amiodarone, procainamide, calcium-channel blockers, β-blockers, and class IC antiarrhythmics. ^[33]
• Urgent referral for AICD

Question 8

Ventricular Tachy- wide complex

Mx of Torsde De Point, Polymorphic V-tach

Answer 8

Cannot give anything other than mag sulph TdP
VTach- procainamide/amioderone

Question 9

What does valsalva effect

Answer 9

Valsalva maneuver

• Definition: forceful exhalation against a closed airway
• Technique: four phases
  
  • Phase 1 (start strain) and phase 2 (continued strain): ↑ intrathoracic pressure → ↓ venous return/ventricular preload → ↓ cardiac output
  • Phase 3 (release of strain) & phase 4 (recovery phase): ↓ intrathoracic pressure → ↓ afterload → ↑ stroke volume → ↑ cardiac output
• Applications
  
  • Treatment of supraventricular tachycardia (e.g., AVNRT)
  • Evaluate conditions of the heart
    
    • Augments heart sounds on physical exam (e.g., earlier click in mitral valve prolapse and louder murmur in hypertrophic obstructive cardiomyopathy)
    • Decreases heart sounds intensity (most valve stenosis or regurgitation murmurs)
  • Test for hernia or varicocele (increased intraabdominal pressure → bulging)
  • Diagnosis of urinary stress incontinence (urine leakage during the maneuver)
  • Measure to normalize middle-ear pressure (e.g., in diving)
• Contraindications: include recent myocardial infarction, aortic stenosis, and glaucoma. ^[18]

Question 10

A 68-year-old man is admitted for work-up of a single episode of slurred speech, which resolved after five minutes. There was no weakness or visual changes. His medical history includes hypertension and high cholesterol, for which he takes perindopril and atorvastatin. He has a 20 pack-year history.

On physical examination, blood pressure is 150/100mmHg and the pulse is regular. Cardiorespiratory examination is unremarkable.

A CT scan is performed, which excludes intracranial haemorrhage. There are no features of early ischaemia and no masses are identified.

Which one of the following is the most appropriate next investigation?

CT angiography or Carotoid artery Ultrasound

Answer 10

• Anterior circulation symptoms in suspected TIA or stroke require carotid artery imaging.
• CTA (MRA if renal impairment) , not carotoid artery ultrasound

The stem describes a patient with an episode of slurred speech on a background of significant cardiovascular disease. This should raise suspicion for a transient ischaemic attack (TIA) or stroke affecting the brain’s language centre, most commonly the middle cerebral artery (MCA) or anterior cerebral artery (ACA).

When anterior circulation symptoms are present, carotid pathology should be investigated with CT angiography (CTA) from the aortic arch to circle of Willis. CTA can be used to evaluate intracranial vessels as well as carotid and vertebral arteries for stenosis or occlusion, allowing assessment of the patient’s stroke risk. Findings will determine whether the patient meets criteria for admission versus assessment in TIA clinic.

MRI is the most sensitive technique for identification of minor stroke but is not required in the setting of resolved neurological deficits. MRI may be used to exclude ischaemic stroke if there are atypical symptoms, or in the evaluation for extended window thrombolysis.

Carotid artery ultrasound is not required as the CT angiogram will provide a detailed assessment of these vessels. If CT angiography were not available, carotid artery ultrasound could be used to investigate for carotid artery stenosis.

Question 11

name the territory

right homonomous hemianopia with macula sparing and right sided sensory canges. whhere is the lession. what structures are affected

Answer 11

A posterior cerebral artery infarct (left-sided in this case) typically leads to the following clinical features:
– Contralateral sensory loss (due to lateral thalamic involvement)- right sided
– Contralateral homonymous hemianopsia with macular sparing (because the macula receives collateral vascular supply from the middle cerebral artery), rest of the occiptal lobe affetceted. Right homonomus hemianopia

Question 12

stroke patterns with territories

ACA

MCA

PCA

Answer 12

Question 13

migraine prophalaxis vs acute migraine treatment

Answer 13

acute migraine prophylaxis:

The following drugs can be used for migraine prophylaxis:

• Tricyclic antidepressants (amitriptyline, nortriptyline)
• Propranolol
• Sodium valproate
• Candesartan
• Verapamil
• Pizotifen
• Topiramate

In the case of the options provided, the most appropriate agent for migraine prophylaxis would be amitriptyline.

Propranolol is contraindicated as this woman suffers from asthma.

Sumatriptan and ibuprofen are not indicated for migraine prophylaxis, and rather can be used for the management of acute migraine.

Codeine is not indicated for migraine prophylaxis. In addition, sumatriptan and codeine are associated with medication-overuse headache with ongoing use. This can be a common exacerbating problem in patients with chronic headache syndromes.

Question 14

Mx and treatment of choice in eusimophillic oesophagitis

Answer 14

Non-pharmacological treatment can include a six food elimination diet, which involves excluding the 6 common allergen foods (wheat, egg, dairy, soy, nuts and seafood) to see if they experience improvement. This should ideally be done with the assistance of a dietician, and can prove to be extremely difficult and limiting for patients. The first line pharmacological therapy is a proton pump inhibitor (PPI) such as omeprazole for 4-6 weeks to see if symptoms improve with repeat endoscopy to determine true eosinophilic oesophagitis from PPI-responsive oesophageal eosinophilia. Once repeat endoscopy confirms the diagnosis then dietary elimination strategies and topical steroids such as a budesonide slurry can be given.

cenario describes a food bolus occurring secondary to a likely new diagnosis of eosinophilic oesophagitis. The endoscopy shows the characteristic concentric rings associated with this condition and in addition, there is some mucosal damage at the site where the food bolus was impacted. A food bolus can occur in anyone, but most commonly there is an underlying condition that pre-disposes them to getting the bolus stuck. Conditions that can predispose include peptic oesophageal stricture, eosinophilic oesophagitis and oesophageal cancer.

Eosinophilic oesophagitis is believed to be similar in pathophysiology to atopic conditions such as asthma and it can be triggered by common food allergens (wheat, egg, dairy, soy, nuts, seafood). The diagnosis is made through the characteristic oesophageal rings and linear furrows macroscopically on endoscopy along with a biopsy showing raised eosinophils (>15 per high power field).

Question 15

white out in right lower lobe

ddx for hilar enlargement

Answer 15

Right lower lobe collapse demonstrates a triangular opacity at the right lower zone, obstruction of right hemidiaphragm and inferior displacement of horizontal fissure. This is not seen on the chest x-ray above.

Hilar thickening describes enlargement of the hilum of the lung. This can be caused by tumour, sarcoidosis or infections causing enlarged hilar lymph nodes.

Question 16

bullae on CXR

Answer 16

Bulla is defined as an air-filled space within the lung of >1cm, which develops due to emphysematous damage to the lung. The two most common causes of bullous emphysema are smoking (the likely cause in this case) and alpha-1-antitrysin deficiency. Bullous emphysema can be asymptomatic, but when severe such as seen in this x-ray it may present with symptoms of shortness of breath and cough.

Learning Points
Bulla are air-filled spaces in the lung or >1cm due to emphysematous damage.
Bullous emphysema on x-ray shows septations within the bulla, which helps to differentiate on chest x-ray compared to pneumothorax where there are no lung markings.

Question 17

STEMI drugs

Answer 17

Options for initial MI treatment include “MONA-BASH”: Morphine, Oxygen, Nitroglycerin, Antiplatelet drugs (aspirin + ADP receptor inhibitor), Beta blockers, ACE inhibitors, Statins, and Heparin.

Statin- high dose Atorvastatin 80 mg PO every 24 hours

Aldosterone antagonists (when ACE cant be used)

• E.g., eplerenone ^[26]
• Consider in patients already receiving an ACE inhibitor and beta blocker with any of the following: ^[2]
  
  • LVEF ≤ 40%
  • Heart failure
  • Diabetes mellitus

Fibrinolytic therapy

• Indications (in STEMI and STEMI equivalents, if all of the following apply):
  
  • PCI cannot be performed ≤ 120 minutes after FMC.(first medical contact)
  • Symptom onset
    
    • ≤ 12 hours
    • OR 12–24 hours with clinical signs of ongoing ischemia (PCI is even more preferable in this context)
  • No contraindications to fibrinolysis present
• Timing: within < 30 minutes of patient arrival at the hospital
• Contraindications
  
  • If > 24 hours after symptom onset
  • See “Contraindications for fibrinolysis in STEMI and STEMI-equivalents.”
• Regimens (one of the following)
  
  • Tenecteplase
  • Alteplase
  • Reteplase
  • Streptokinase (cant be used in Ab/TSI)

Question 18

acute asthma Mx

acute asthma

Answer 18

severity- mild moderate severe

Mild/ModerateCan walk and speak whole sentences in one breath (Young children: can move about and speak in phrases)

JUST SALBUTAMOL PUFFS

• Give salbutamol (100 microg per actuation. Repeated every 20 minitus for first hour) via pMDI plus spacer (plus mask for younger children)
• 6 years and over: 4–12 puffs
• 1–5 years: 2–6 puffs

Severe

Any of: unable to speak in sentences, visibly breathless, increased work of breathing, oxygen saturation 90–94%

SALBUTAMOL,IPRATROPIUM,OXYGEN

• Salbutamol (100 microg per actuation) via pMDI plus spacer (plus mask for infants)
  
  • 6–11 years: 12 puffs
  • 1–5 years: 6 puffs
• Ipratropium (21 microg/actuation) via pMDI plus spacer (plus mask for infants)
  
  • 6–11 years: 8 puffs
  • 1–5 years: 4 puffs

Life-threatening

Any of: drowsy, collapsed, exhausted, cyanotic, poor respiratory effort, oxygen saturation less than 90%

• Salbutamol via continuous nebulisation driven by oxygen
  
  • 6–11 years: 2 x 5 mg nebules.
  • Add ipratropium 500 microg to nebulised solution.
  • 1–5 years: use 2 x 2.5 mg nebules.
  • Add ipratropium 250 microg to nebulised solution.
• Start oxygen Titrate to target oxygen saturation of at least 95%

all acute attacks get oral steroids within the first hour

Start oxygen (moderate/sever/life threatening) Titrate to target oxygen saturation of at least 95%

Initial treatment for severe asthma exacerbations involves oxygen therapy, inhaled salbutamol and ipratropium, and oral corticosteroids.

Spacers are non inferior to nebs- used when unable to use spacer ie life threatening

Question 19

SABA /LABA DRUGS

Answer 19

SABA medications:

• albuterol (Ventolin, Proair HFA, Proventil),
• bitolterol (Tornalate),
• levalbuterol (Xopenex),
• metaproterenol (Alupent),
• pirbuterol (Maxair),
• salbutamol (albuterol),
• and terbutaline (Brethaire).

Question 20

how to investigate short stature

Answer 20

Short stature (dwarfism) in children is defined as a height that is at least two standard deviations (SDs) below the mean for children of the same age and sex.

• In a normal distribution:
  
  • one standard deviation above and below the mean includes about 68% of the sample, (16% either side of SD)
  • 2 SDs include 95%, and (2.5% on either side)
  • 3 SDs 99.7%. (0.15 % on either side)

If child is 3rd percentile for height- lies between 1 and 2 SD.
If child is 2nd percentile for height- lies between 2 and 3SD.

There are a number of causes of short stature in children, both benign and pathological.

1. After a thorough history and examination, including
2. calculation of mid-parental height and growth velocity
3. a bone-age x-ray

can help in differentiating the cause of short stature based on the results.

Further diagnostic testing is indicated if a child’s growth is less than what might be expected given the average height of the parents.

An x-ray of the left hand and wrist are made to determine bone age (skeletal age), based on which the adult size of the child can be predicted.

In particular, it is useful for determining whether the short stature is due to familial short stature vs constitutional delay, both of which are normal benign variants in growth.

• Nonpathological variant short stature can be classified into three types: familial short stature (inherited short stature):
• children with familial short stature are short because they have short parents; the children have a normal bone age and are destined to be short like their parents
• constitutional delay of growth and puberty (an inherited pattern of short stature during childhood that is followed by a growth spurt during puberty ( late bloomers)
• The conventional definition of constitutional delay is a bone age at least 2 years less than chronologic age in combination with associated short stature, delayed puberty, or reaching final adult height later than peers

NOT GOING TO START AT SERUM GROWTH FACTOR AND IGF LEVELS

Question 21

a skin lesion on the back of his right hand. Noticed this lesion develop over the last year and reports no symptoms of pain or itchiness. He has not tried any treatments for it.

On examination he has Fitzpatrick skin type 2. There is a 5mm white/yellowish scaly plaque with surrounding skin erythema on the dorsal aspect of his right hand on a background of sun damaged skin.

HOW TO INVESTIGATE/TREAT

Answer 21

Pre cursor to SCC- solar keratosis (same name as actinic keratosis)
Rough, scally, normally elderly. can have erythema. CAn develope sally horns.

Rx is with cryotherapy ( liquid nitrogen) . Horns possibly shaved.

Most solar keratosis respond well to cryotherapy with liquid nitrogen and this should be used first line unless contraindicated or not tolerated. The fact that he has a single lesion on the back of his hand the most immediate and appropriate initial management is cryotherapy if he is happy to tolerate this procedure. This can be done on the spot in clinic and follow up organised for further cryotherapy until the lesion has resolved.

Second line options include fluorouracil 5% (Efudix) or imiquimod 5% (Aldara) cream. This should be considered if a person has multiple solar keratosis or cannot tolerate cryotherapy. Patients must be warned about the inflammation that these treatments cause and that they need to be used for a few weeks to be effective.

Question 22

When is each used

• Bolus of 1L normal saline
• Needle thoracostomy
• Large bore chest drain

Answer 22

• Bolus of 1L normal saline–unstable HD patient. If running fluid at 100ml per hour and not responsive. Need bolus!! ABCD first
• Needle thoracostomy–tension pnuemothorax
• Large bore chest drain- heamopneumotjorax

Question 23

immuno suppressed individual with pnuemonia unresponsive to ABs- atypical cases

Use X-ray to guide eatiology

Answer 23

Most likely in an immuno comp/suppressed- fungal

Fungi such as pneumocystis must be considered in immunosuppresed patients presenting with pneumonia that does not respond to initial antibiotic therapy.

CXR of pnumocystis- reticular
( mesh/lace pattern), upper lobes, patchy
Diffuse, bilateral, symmetrical, interstitial infiltrates that are patchy infiltrate, extending from the perihilar region (butterfly pattern) , can lead to consolidations. also pneumatoceles (cycts, smallish)

(legionaires) presents with bilateral , patchy infiltrate,and pleural effusions and consolidations.

(Staph Aurues)- cause empyema or cavitary lesions; however, these would not be isolated without the presence of surrounding lobar infiltrate.

influenza pneumonia is likely to present with widespread changes on chest X-ray; patchy areas of peribronchial ground-glass opacity and airspace consolidation and poorly defined nodules are characteristic of viral pneumonia.

Question 24

plural tap interpretation

Answer 24

Transudate is usually clear, has a decreased cell count, and has low levels of protein, albumin, and LDH.

Exudate typically appears cloudy, has an increased cell count, and has high levels of protein, albumin, and LDH.

MEAT has low glucose: Malignancy, Empyema, Arthritis (rheumatoid pleurisy), and Tuberculosis are causes of pulmonary effusion associated with low glucose levels.

Pleural fluid with a bloody appearance suggests a malignant etiology or hemothorax!

Question 25

What conditions are Nickolsy sign + in?

Answer 25

Nikolsky’s sign is pathognomic for pemphigus Valgaris, toxic epidermal necrolysis, and staphylococcal scalded skin syndrome (SSSS). T

his sign basically differentiates intraepidermal blisters from subepidermal blisters.

Nikolsky sign is present in pemphigus vulgaris , toxic epidermal necrolysis, staphylococcal scalded skin syndrome, scalding, bullous impetigo, and Stevens-Johnson syndrome
Not present in bullous pemphigoid

toxic epidermal necrolysis (TEN). About 90% of TENs cases are associated with a medication. Medications that are associated with TEN include allopurinol, antibiotics (e.g sulfonamide, penicillin, cephalosporin), antipsychotics/antiepileptics (e.g. carbamazepine, dilantin, lamotrigine), and NSAIDs (e.g piroxicam). If TEN is suspected, it is important to document an accurate medication timeline and cease all possible culprit drugs.

Staphylococcal scalded skin syndrome (SSSS) can appear similar clinically; however, mainly occurs in children and neonates caused by the release of Staphylococcus aureus epidermolytic toxins A and B. SSSS is an intradermal detachment pattern, as opposed to TEN which causes full-thickness epidermal (subepidermal) detachment (the positive Nikolsky sign).

The split is intradermal in the case of SSSS, while the split appears to be subepidermal in the case of TEN and SJS.

Question 26

bullous vesicles

A 60-year-old man comes to the physician because of tender blisters on his arm and flank, worsening over the last few months. His medical history includes hypertension and hyperlipidemia. He is taking atorvastatin and hydrochlorothiazide for these conditions. Physical examination shows blisters and flaccid bullae; a few have ruptured, leaving red, sore, denuded areas. Pathologic examination reveals acantholysis and few lymphocytes.

Which of the following findings is most likely in this patient?

A. Eosinophils within bullae.

B. IgA deposits in the dermal papillae.

C. IgG antibody against hemi-desmosomes.

D. Negative Nikolsky sign.

E. Oral mucosal lesions.

Answer 26

• A. Eosinophils within bullae. ( bullous pemphigoid)
  C. IgG antibody against hemi-desmosomes. ( bullous pemphigoid)
  D. Negative Nikolsky sign.
• B. IgA deposits in the dermal papillae. (dermatitis herpitiformis)
• E. Oral mucosal lesions. ( Pemphagoid valgaris: IgG antibodies to DG1 and DG3)

Choice A and C: An important condition on the differential diagnosis for autoimmune blistering conditions is bullous pemphigoid (BP). Histologically, prominent eosinophils within blisters would support bullous pemphigoid as the diagnosis. This condition presents with IgG autoantibodies against hemidesmosomes.

Hemidesmosomes anchor basal keratinocytes to the basement membrane. As a result, the epithelial layer lifts off the basement membrane producing a non-flaccid, tense sub-epidermal/sub-basal blister.

Unlike pemphigus vulgaris, bullous pemphigoid does not affect desmosome adhesion proteins. The associated antigens are: bullous pemphigoid antigen 1 and 2 (BPAG1, BPAG2). Patients with BP usually present with pruritus in the skin surrounding the blister rather than pain. Bullous pemphigoid can affect various areas of the skin but mucosal involvement is uncommon, unlike pemphigus. Pemphigoid also has a more favorable prognosis.

( bullous pemphigoid)

Question 27

Childhood exanthems

Childhood exanthems

Answer 27

Roseola infantum (sixth disease),

• caused by HHV-6 and HHV-7
• 3–5 day history of persistent high-grade fever (may present as febrile seizures) that rapidly subsides,
• followed by the development of a rose-pink, nonpruritic, blanching, maculopapular rash that begins on the trunk.
• conjunctivitis, upper respiratory tract symptoms, orbital edema, inflammation of the tympanic membranes, lymphadenopathy, and Nagayama spots (on uvula)

Rubella (German measles)

• should be considered in an unvaccinated child with fever and a generalized pruritic rash.
• rubella rash is
  
  • typically maculopapular (pink) and
  • begins on the face and moves downward
  • sparing the palms and soles.
• rubella is characterized by a prodromal phase in which patients usually present with post-auricular and/or suboccipital lymphadenopathy

Varicella (chickenpox) is caused by the varicella-zoster virus (HHV-3) and is characterized by

• should be considered in an unvaccinated child with fever and a generalized rash.
• fever AND a generalized pruritic rash
• rash in various stages of healing that
• typically begins on the trunk and spreads to the face and extremities.

Measles (rubeola) -5Cs move down

• caused by paramyxovirus
• should be considered in an unvaccinated child with fever and a generalized rash.
• the measles rash is typically confluent, nonpruritic (5th C)
• characteristically begins on the face and moves downward
• the rash is usually preceded by a constellation of symptoms (4Cs) including cough, coryza, conjunctivitis, and enanthem with Koplik spots.

Erythema infectiosum (fifth disease)

• which is caused by parvovirus B19, can manifest with fever and a generalized pruritic rash.
• rash is typically only mildly pruritic and initially appears on the cheeks (“slapped cheek” rash) before spreading to the trunk and extremities, where it has a lace-like, reticular appearance as it clears.

Question 28

oesophageal varices active intervention to prevent re-bleeding.

how to manage variceal bleeding - post acute phase

Answer 28

1. ACUTELY:
   Terlipressin- acute mx of variceal bleeding. Terlipressin is a synthetic analogue of vasopressin, utilised in the emergency setting to induce splanchnic vasoconstriction to reduce portal blood flow and variceal pressure in variceal hemorrhage, but it does not have a role in secondary prophylaxis.

Learning Points
Once oesophageal varices have bled, some form of active intervention is required to prevent re-bleeding.
2. 3. Post acute phase -

• risk of rebleeding from his oesophageal varices and requires secondary prophylaxis in the form of propanolol and endoscopic variceal ligation (EVL) as first-line therapy.
• Propanolol is a non-selective beta blocker that can reduce hepatic portal pressure through a reduction in cardiac output as well as splanchnic arterial blood flow, resulting in reduction of recurrent bleeding by 40% and mortality by 20%. It is usually titrated to patient’s heart rate, aiming for 55-60 beats per minute and continued indefinitely while monitoring for bradycardia or hypotension.
• Endoscopic variceal ligation is usually repeated every two weeks post-hospital discharge until varices is no longer visible endoscopically.

If there is failure of the gold standard (EVL and Propanaolo) , salvage
modalities like:

• transjugular intrahepatic portosystemic shunt (TIPS),
• percutaneous transhepatic embolization of varices (PTVE) or
• shunt surgery should be considered,
  with TIPS being preferred unless liver transplantation is being considered.

Compared to EVL, endoscopic injection sclerotherapy (EIS) has higher rates of recurrent varices and re-bleeding, oesophageal ulcerations and strictures and mortality. It may used in the acute setting to achieve haemostasis if EVL is technically challenging.

Question 29

A 58-year-old man presents to his general practitioner (GP) for review of his blood pressure control. The GP notes that his BP has been resistant to treatment thus far, with his current BP 168/110mmHg despite optimal medial management. On further review, he notes the patient has central adiposity and purple striae over his abdomen, with bruising noted in the periumbilical region. He also has pronounced dorsal fat pad. The GP takes a further history and elicits that the patient has had difficulty in climbing stairs and standing up from chairs in the past few months. He also reports weight gain of approximately 10kg in the past few months, with no notable changes to his diet or exercise regimen. A random BGL is 9.8mmol/L, with all other vitals being in the normal range. He has no significant medical history and does not take any regular medications.

When considering the most likely diagnosis, which one of the following investigations would be most appropriate to perform first?

Answer 29

The patient is clinically cushingoid, which helps explain his hypertension, hyperglycaemia, easy bruising, recent weight gain and central fat distribution. In the absence of any exogenous steroids, it is presumed he has an endogenous cause for his Cushing’s syndrome.

The diagnosis of Cushing’s syndrome begins with screening tests, including 24-hour urinary free cortisol levels, midnight serum/salivary cortisol levels and low-dose dexamethasone overnight tests [1]. ? 2 tests

The only option which reflects a screening test is the 24-hour urinary free cortisol level.

If any of the screening tests are positive, the patient requires further workup to consider whether the syndrome is ACTH-independent (i.e. originating from the adrenals) or ACTH-dependent (i.e. released from the pituitary gland or an ectopic tumour, commonly in the lungs) [1].
To elucidate this, the most valuable investigation will be performing a high-dose dexamethasone overnight test. High doses of dexamethasone should physiologically inhibit release of ACTH from the pituitary gland, with only very small functioning pituitary cells required [1]. Therefore, in ACTH-dependent Cushing’s syndrome, cortisol levels will be suppressed, whilst in ACTH-independent Cushing’s syndrome(i.e. originating from the adrenals) , cortisol levels remain elevated [1]. Following this, further investigations like CT adrenal glands, brain and chest can be performed based on the likely underlying diagnosis.

A Cosyntropin test is performed in suspected cases of adrenal insufficiency, including Addison’s disease, in which the patient is given synthetic ACTH (cosyntropin) and their subsequent serum cortisol levels: in cases of adrenal insufficiency, cortisol levels will remain low [2].

Learning Points
If hypertension is treatment-resistant, look for underlying causes.
Cushing’s disease refers to a pituitary cause for Cushing’s syndrome.
Perform screening tests before undertaking diagnostic tests in the work-up of Cushing’s syndrome.

Question 30

Cholestrol tests

values for LDL HDL TC trigd

Answer 30

HDL-cholesterol is 0.8 mmol/L (0.9-2.0), and his LDL-cholesterol is 3.5 mmol/L (<3.7), and his total cholesterol is 5.1 mmol/L (<5.5).

• HDL- more than 1
• LDL: <3.7
• TC <5.5
• triglicerides: <1.7

statin therapy in a young male without diabetes should only be instigated in patients with an LDL-cholesterol greater than 4.9mmol/L.

HDL-

LDL- mainly treated with Statins. High dose in severe moderate ASCVD
expect 50% reduction
Atorvastatin 40–80 mg PO once daily
Rosuvastatin, 20–40 mg PO once daily

If LDL not sufficiently reduced by statin- add ezetimide (Reduces LDL by 13–20%) or nicin (nicotinic acid)

Triglicerides- fibrates (not monotherapy) (and HDL is high)
Gemfibrozil 600 mg PO twice daily, 30 minutes before morning and evening mealsFibrates (e.g., fenofibrate) can cause a 30–50% decrease in the levels of triglycerides but can only cause a mild reduction in LDL. wont be used as an alternative for statins

Fibrates are contraindicated in renal insufficiency because they are excreted by the kidneys. There is a risk of drug accumulation, which can further increase the risk of side effects.

Nicotinic acid- Niacin, Vitamin B₃

A water-soluble vitamin that is synthesized from tryptophan. It is used to synthesize NAD, which is used in redox reaction. Niacin can be used as a lipid-lowering agent because it decreases hepatic VLDL synthesis and inhibits the activity of hormone-sensitive lipase in adipose tissue. Deficiency of niacin causes pellagra (diarrhea, dermatitis, dementia), while niacin toxicity causes podagra (hyperuricemia), flushing, and hyperglycemia.

Niacin upregulates prostaglandin synthesis in the skin by activating a G-protein coupled receptor in keratinocytes and dermal Langerhans cells. These prostaglandins cause cutaneous flushing, which is sometimes accompanied by paresthesias such as tingling or itching. The flushing typically begins within an hour of niacin intake. NSAIDs (e.g., aspirin, ibuprofen) taken 30–60 minutes before niacin can prevent flushing by inhibiting prostaglandin synthesis. Alternatively, the use of an extended-release niacin formulation, which is associated with less flushing, can be considered. Niacin-induced flushing often subsides over the course of a few weeks as a result of tachyphylaxis.

Question 31

lung functions

Pulmonary function testing is arranged to assess: Forced Expiratory Volume in 1 second (FEV1)/Forced Vital Capacity (FVC), Total Lung Capacity (TLC) and Diffusing Capacity of carbon monoxide (DLco).

in thoracic wall movement limitation

Answer 31

The ratio of forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) is used to determine whether the defect is obstructive or restrictive. Obstructive defects will have an FEV1/FVC <80% of predicted, while restrictive defects will be >80% of predicted.

FEV1 alone can be used to determine severity, with 60-80% representing a mild defect, 40-60% representing a moderate defect and <40% representing a severe defect, as outlined in the COPD-X guidelines.

Total lung capacity (TLC) is used to measure the total lung volume, in a restrictive defect, this will be reduced, while in an obstructive defect, with gas trapping or carbon dioxide retention, the TLC will be increased.

The diffusion capacity of carbon monoxide (DLCO) determines the pulmonary diffusion capacity. A reduced DLCO suggests impaired diffusion, which may be seen in emphysema, interstitial lung disease or pulmonary vascular diseases.

extra-thoracic cause of restrictive lung disease. Therefore, her FEV1/FVC ratio must be >80%, while her TLC will be reduced due to impaired ventilation. The DLCO will likely be normal as the restriction is extra-thoracic and not affecting diffusion.

Question 32

mass below the inguinal ligament and lateral to the pubic tubercle

Answer 32

The anatomical site and lesion description is consistent with a femoral hernia. Due to the narrow neck of the femoral canal, femoral hernias are at high risk of incarceration and always require surgical management.

An inguinal hernia would be found above and medial to the pubic tubercle.

A saphena varix is an enlarged vein, which could certainly occur at the location described. However, this would soft and compressible on palpation.

Femoral hernias occur below the inguinal ligament and lateral to the pubic tubercle

Question 33

Temporal lobe epilepsy s

Answer 33

should always be considered for psychotic like symptoms

however it generally presents with hallucinations, stereotyped motor behaviours and sympathetic stimulation.

Question 34

The patient’s primary complaint is about her general practitioner, stating he gave her 10x the correct anti-epileptic dose in her 20’s (no record of this) which subsequently lead to her developing breast and bowel cancer which she states were surgically managed.

On review of her past notes as well as a physical exam for surgical scars, you can find no evidence of colectomy or mastectomy. Attempts to gain other history are met with suspicion and she frequently returns to issue of her GP, and is difficult to redirect from this topic. On attempts to explain she has not had these procedures she does not understand and flatly denies your opinion. She is avoidant of doctors because of this and is frequently suspicious of staff she does not know.

Answer 34

The predominant symptom in this case is a fixed delusion regarding mistreatment by her GP in her 20’s leading to beliefs about cancer diagnosis. This opinion is unwavering despite evidence in the contrary making it a delusion rather than an overvalued idea. She denies any hallucinations and is not grossly thought disordered at this time. A diagnosis of schizophrenia or serious psychoses requires delusions as well as hallucinations or a thought disorder, which is not present in this case, making a delusional disorder more likely. A delusional disorder is when a patient has one or more fixed, false beliefs that others know to be false and is incongruent with cultural norms. Frequently, there is coexistent mood component and rarely there are hallucinations associated.

She denies any hallucinations.

Question 35

Stem in a patient with COPD

Answer 35

Initial management of a STEMI would include morphine, oxygen, nitrates, and aspirin. However given he has COPD/CO2 retains it would not be advisable to give oxygen unless he is below 88% oxygen saturation as this would diminish his respiratory drive, causing hypercapnic respiratory failure. He would also require revascularisation therapy given he is having a STEMI. However, given there are no PCI facilities available and the closest major hospital is over 90mins away, he would require fibrinolytic therapy at the rural location.

After fibrinolytic therapy is given, transfer to a tertiary centre for angiography, and PCI if indicated, within 24 hours is recommended. This has been shown to reduced the rates of secondary ischaemic events. For those who do not have a satisfactory response to fibrinolytic therapy, or those who remain haemodynamically unstable, immediate transfer for rescue angioplasty has shown to significantly reduces the rates of re-infarction.

Dual antiplatelet therapy should also be commenced prior to transfer.

Question 36

AWS

delerium tremens- name clinical signs of altered mental status, autonomic instability, nuerological

Answer 36

Alcohol withdrawal delirium (delirium tremens) ^[2][3]

• Definition: persistent alteration of consciousness and sympathetic hyperactivity due to alcohol withdrawal
• Onset: usually 72–96 hours after cessation of or reduction in alcohol consumption
• Clinical features
  
  • Symptoms of altered mental status
    
    • Impaired consciousness and disorientation
    • Visual and tactile hallucinations (usually small moving objects, e.g., mice, crawling insects), oneirism (a condition characterized by visual hallucinations, typically experienced during a waking state, that are dreamlike and rich in detail)
    • Increased suggestibility
  • Worsening symptoms of autonomic instability
    
    • Tachycardia
    • Hypertension
    • Anxiety
    • Nausea
    • Sweating
  • Worsening symptoms of neurological impairment
    
    • Psychomotor agitation (e.g., fidgeting, restlessness, tearfulness)
    • Alcohol withdrawal seizures can occur during this phase.
    • Insomnia
    • Rest and intention tremor (first high frequency, then low frequency)
• Duration: usually 2–3 days; may be lethal
• *First-line**: benzodiazepines
  
  • Shorter or intermediate-acting (e.g., oxazepam, lorazepam): Consider in patients with a slow metabolism (e.g., the elderly, those with liver failure). ^[9]
  • Longer acting (e.g., chlordiazepoxide, diazepam): preferred in all other patients
• Lorazepam, Oxazepam, and Temazepam are preferred in those who drink a LOT because they have fewer active metabolites after hepatic metabolism; therefore they are safer for use in patients with alcoholic liver disease.
• Remember ATOM for benzodiazepines with a short half-life: Alprazolam, Triazolam, Oxazepam, and Midazolam.

Wernicke encephalopathy

An acute neurological syndrome caused by thiamine deficiency that is characterized by a triad of confusion, ophthalmoplegia, and ataxia. Requires emergency treatment with thiamine repletion

1. Oculomotor dysfunction
   
   • Gaze-induced horizontal/vertical nystagmus (most common)
   • Diplopia
   • Conjugate gaze palsy

Thiamine

1. 200–500 mg IV every 8 hours for 2–7 days;
2. followed by 250 mg IV/IM once daily for 3–5 days (or until clinical improvement);
3. followed by 30–100 mg PO every 8–12 hours for 1–2 weeks;
4. followed by 100 mg PO daily

• *Wernicke’s COAT:** Confusion, Oculomotor dysfunction, Ataxia, and Thiamine administration (see Treatment section)
• *Korsakoff’s CART:** Confabulation, Anterograde and Retrograde amnesia, and altered Temper

*

Question 37

midazolom (iv/im) / DIAZAPAM (iv) is DOC in seizures in kids

DO NOT GIVE IM DIAZEPAM

management of seizures is accounting for medications received (i.e., benzodiazepine doses) before admission to the hospital by either a parent or paramedic. In the stem above, the child was given an oral medication by the paramedics. This was most likely oral benzodiazepine (buccal midazolam), which is part of the management algorithm

Answer 37

iF iV ACAILABLE, USE iV

As part of status epileptics management, if seizure activity continues for an additional 5 minutes after the first dose a repeat dose of benzodiazepines is indicated. In the above instance, a repeat dose of benzodiazepines is indicated; midazolam is a good choice. This can be given by IV or IM but as an IV line has been obtained it is the most appropriate route.

Intravenous phenytoin or levetiracetam infusion: These options are both inappropriate at this point in the management of her seizure. Phenytoin and levetiracetam can be given after 15 minutes of seizure activity when resolution of seizure is not achieved with repeat benzodiazepine dosing. Phenytoin is administered via IV infusion over 20 minutes whereas levetiracetam can be administered over 5 minutes making it a more useful second-line agent while a phenytoin infusion is being set up.

• If IV access is available, administer:
  
  • IV lorazepam ^[30][38]
  • OR IV diazepam ^[30][33]
• If IV access is unavailable, administer one of the following:
  
  • Preferred: IM midazolam ^[37]
  • Alternatives
    
    • Intranasal midazolam ^[33][37]
    • OR buccal midazolam ^[33][37]
    • OR rectal diazepam

Question 38

TTP

WHAT DO SCHISTOCYTES MEAN ON SMEAR

Answer 38

Microangiopathic hemolytic anemia

A type of hemolytic anemia that is the result of mechanical damage to erythrocytes by microthrombi in small blood vessels. Characterized by schistocytes on the peripheral blood smear. Common causes include thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, disseminated intravascular coagulation, and HELLP syndrome.

TTP vs other conditions ( image )

TTP: Thrombocytopenia is generally severe, with a median platelet count of 10,000–17,000/mm³

Normochromic, normocytic anemia with Hb < 8 g/dL

Coombs neg: In contrast to autoimmune hemolytic anemia

Coagulation studies: Significant elevations should raise concern for other disorders such as disseminated intravascular coagulation.

Indirect bilirubin may be elevated in hemolytic anemia. Elevated transaminases can also indicate other underlying causes of TTP (e.g., HELLP syndrome).

Impaired renal function, including anuria or oliguria, is uncommon but, if present, may be seen in older patients. Severe dysfunction may indicate another cause (e.g., hemolytic uremic syndrome).

Question 39

which thrombotic microangiopathies -TTP and HUS- uses mnneumonic FART’N for presentation

Answer 39

• Thrombotic thrombocytopaenic purpura is a life-threatening condition characterised by the pentad of
  
  • fever, anaemia, renal impairment, thrombocytopaenia, and neurological problems.
• Plasma exchange is the mainstay of treatment for thrombotic thrombocytopaenic purpura.
• Platelet transfusion will aggravate the condition - not routinely indicated in TTP despite the thrombocytopaenia unless there is life-threatening bleeding. Due to the underlying pathology of TTP involving abnormal platelet aggregation and consumption

TTP occurs primarily in adults and is typically due to acquired autoantibodies against a proteolytic enzyme (ADAMTS13) that cleaves von Willebrand factor (vWF).

Other supporting features include the purpuric rash described, easy bleeding, schistocytosis, and blood results consistent with haemolysis. This is a life-threatening condition which requires urgent plasma exchange. Clopidogrel is an uncommon but documented cause in susceptible individuals, however most cases are idiopathic and associated with severe ADAMTS13 dysfunction.

– Hemolytic uremic syndrome

A condition in which microthrombi occlude the arterioles and capillaries, which results in microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. Predominantly affects children and most commonly occurs following dysentery due to Shiga toxin-producing enterohemorrhagic Escherichia coli (EHEC), typically serotype O157:H7.

Question 40

upper right homonyomous quadrantopia

Where is the lession of upper right homonyomous quadrantopia

Answer 40

left temporal lobe in the inferior optic radiation

Several visual field defects may occur from lesions along the optic pathway (from the retina to the visual cortex). Some of these defects include:

1. Central scotoma is a feature of optic neuritis affecting the optic disc or intraorbital optic nerve. It may also manifest as a result of macular degeneration. The patient may complain of being unable to see a person’s face, but the rest of the visual fields would be unaffected. To distinguish between macular and intraorbital optic nerve etiology of the central scotoma, pay attention to the color desaturation. Patients with intraorbital optic nerve damage leading to a central scotoma will complain of red desaturation (i.e. red objects appear pink, pale or orange) much sooner than those with a macular problem. Also, patients with optic nerve damage do not experience visual distortion.
2. Monocular visual field loss refers to complete transection of the optic nerve prior to the optic chiasm.
3. Bitemporal hemianopia is loss of the temporal fields of both eyes. It is usually a consequence of a pituitary adenoma compressing the central fibers of the chiasma. Note that patients may begin to experience red desaturation in the central visual fields prior to loss of peripheral visual fields.
4. Nasal hemianopia would arise from a lesion of the lateral perichiasmal fibers of the optic nerve. Calcification of the internal carotid artery is a likely preceding event.
5. A complete lesion of one optic tract will result in a contralateral homonymous hemianopia. Patients with lesions of the geniculocalcarine tract are often unaware of the visual field loss.
6. Discontinuity of the inferior optic radiations (known as Meyer’s loop) can result in a contralateral upper homonymous quadrantanopia. This is in-keeping with temporal lobe involvement.
7. Similarly, a lesion of the upper fibers of the optic radiation causes a contralateral lower homonymous quadrantanopia. This is in-keeping with parietal lobe involvement.
8. Another cause of a homonymous hemianopia is a complete lesion of the optic radiation.
9. A lesion of the posterior cerebral artery resulting in ischemia of the visual cortex will result in a homonymous hemianopia. However, the macular will be spared.

Question 41

26-year-old man presents with changes in vision in the left eye since this morning. The previous evening he was hit in the forehead by a cricket ball, he was able to carry on playing but noticed several floaters and occasional flashes of light in his left eye. When he woke up this morning, he noticed his left eye vision had deteriorated significantly. His visual acuity is 6/6 corrected in the right eye and 6/120 corrected in the left. Intraocular pressures are 17mmHg in right eye and 16mmHg in the left eye. There was marked periorbital bruising, eye movements were full and examination of the anterior chamber was unremarkable.

Which one of the following is the most likely diagnosis?

• Corneal abrasion
• Hyphaema
• Commotio Retinae
• Retinal detachment
• Retrobulbar haematoma

Answer 41

Trauma to the globe can cause any of the above complications, however their presentations are different.

A retinal detachment is a potential complication of blunt trauma. Trauma causes transient change in the antero-posterior diameter of the eye and may result in a retinal tear which precipitates a retinal detachment. Patients will initially complain of flashes and floaters in their vision as the retinal tear occurs. As the retinal detachment progresses, the flashes continue and the patients may notice a curtain in their vision inversely correlating to the location of the detachment. Visual acuity remains preserved until the macula is affected by the detachment, which causes significant reduction in vision as seen in this case.

A corneal abrasion will present with symptoms of pain worse with blinking, foreign body sensation and will be highlighted with fluorescein dye on the cornea. A hyphaema will be evident on inspection of the eye as blood within the anterior chamber. Commotio Retinae will not cause floaters or flashes but can cause a patch of decreased or altered vision.

Retrobulbar haematoma will occur acutely presenting with orbital signs including raised intraocular pressure, painful and tense exophthalmos and potential optic nerve compression causing visual acuity deterioration, visual field defect and a relative afferent pupillary defect. A retrobulbar haematoma with optic nerve compression is an ophthalmic emergency as it can cause irreversible vision loss within hours.

Learning Points
A traumatic retinal detachment can result from blunt trauma to the eye.
Think of retinal detachment as a differential diagnosis when a patient presents with any of the 4Fs: Flashes, Floaters, Falling Curtains, Failing Vision

Question 42

two-day history of absolute constipation on a background of increasing constipation over the last two months. He reports weight loss during this period. He does not take any medications. On examination, his blood pressure is 130/90 mmHg, pulse 100/min, and temperature 37.2C.

His abdomen is distended with guarding in the right iliac fossa. No rebound tenderness is seen. Digital rectal examination shows an empty rectum. A plain abdominal X-ray shows a grossly distended caecum, with distension of the rest of the large bowel down to a cut-off point in the sigmoid colon. Intravenous fluids are started.

Which one of the following is the most appropriate next step in management?
Choose the single best answer.

CT scan chest and abdomen
Rigid sigmoidoscopy
Flexible sigmoidoscopy
Gastrograffin enema
Laparotomy

Answer 42

This patient with a progressive history of constipation, eventually presenting with obstipation, and typical imaging findings has a large bowel obstruction - possibly due to malignancy (eg, stenosing carcinoma of the sigmoid colon). He is tender over the caecum - suggesting a local inflammatory process. The radiological finding of gross distension of the caecum puts this patient at high risk of perforation. The caecum is at high risk of rupture due to a thin bowel wall. Such high-risk patients should immediately undergo surgical exploration and decompression to prevent serious complications.

Whilst a CT scan might be some comfort to the less experienced clinicians, the priority of management must be urgent laparotomy with a view to preventing rupture of the caecum and consequent peritonitis.

• *Lower endoscopy** (eg, sigmoidoscopy, colonoscopy) has little utility in patients presenting with acute obstruction. It may be used in the diagnosis of patients with chronic obstruction.
• *Sigmoidoscopy** may be of therapeutic use in patients with sigmoid volvulus which appears as an inverted U-shaped loop (“coffee bean” sign) on plain radiography.

Gastrograffin enema may be used in patients with adhesive small bowel obstruction. It is contraindicated in patients with complicated obstruction (eg, complete obstruction, perforation, necrosis, closed-loop obstruction).

Learning Points
Patients presenting with acute complicated obstruction are at high risk of perforation and need to undergo urgent surgical exploration.

Question 43

immigrant patient from a TB-endemic country has a 2cm lymphadenopathy for six weeks along with constitutional symptoms (eg, low-grade fever, weight loss, lassitude). His clinical features are consistent with the diagnosis of cervical tuberculous lymphadenitis (CTL).

Answer 43

• Cervical tuberculous lymphadenitis (CTL) is the most common extrapulmonary finding seen in patients with disseminated TB.
• CTL is the most common extrapulmonary finding seen in patients with disseminated TB. It is caused by either haematogenous or local spread of tuberculosis to the lymph nodes. Patients typically present with constitutional symptoms and lymphadenopathy. Commonly involved lymph nodes are cervical, axillary, and inguinal lymph nodes. Patients suspected of CTL should undergo needle aspiration as the initial test since it is a highly sensitive test and will enable tissue samples to be collected for histology, cytology, smear and culture. It may show caseous granulomatous necrosis. The aspirate is submitted for an acid-fast bacillus smear test, culture, and nucleic acid amplification test.

Question 44

istory of a recent puncture wound to the palm of his hand whilst using a sharp instrument at his workbench. He has been otherwise well and reports no medical history.

On examination, there is fusiform swelling of the digits of the left hand and the fingers are held in slight flexion. Any attempt to passively move his fingers is limited by pain.

Answer 44

This patient has infectious flexor tenosynovitis secondary to the penetration of the tendon sheath and introduction of infection. Infectious flexor tenosynovitis is characterised by tenderness along the flexor sheath, digits held in slight flexion, pain on passive extension, and swelling of the digits. Incision and drainage of the tendon sheath is essential and urgent. Infectious flexor tenosynovitis is a clinical diagnosis; no further investigations are required.

Question 45

choice of imaging in a head injury

10-month-old child is brought into the Emergency Department by her mother, who saw her daughter fall off her chair and appeared to hit her head on the floor. The child immediately screamed and there was no loss of consciousness. It was easy to placate the child and she promptly resumed her normal behaviour. Out of concern the mother has brought her daughter to be checked.

On examination the child is fully alert and moving around in a normal manner. She has a small bruise on her forehead, but no evidence of injuries elsewhere.

• CT scan is indicated in selected cases in children with head trauma.
• PECARN (Paediatric Emergency Care Applied Research Network) clinical decision criteria help to decide the need for CT imaging.
• CT imaging in children carries a definite risk for malignancy later.

Answer 45

The inclusion criteria for the PECARN clinical decision rule are as follows:

• Age <18 years
• GCS 14 or 15
• Presentation within 24h

If the GCS is <14, then CT is immediately indicated. Exclusion criteria for PECARN decision rule include past medical history of brain tumour, bleeding disorder or pre-existing neurological disorders, as well as trivial injury mechanisms or penetrating trauma. (In these situations, CT imaging is recommended in any head injury.)

As per PECARN, a CT is recommended if there were any of the following:

• Altered mental status
• Abnormal behaviour
• Signs of basilar skull fracture (such as Racoon’s eyes sign)
• Scalp haematoma in the temporal, occipital and parietal regions.
• A period of loss of consciousness of 5 sec or more
• Severe mechanism of injury (which include:)
  
  • Fall from a height more than one metre
  • Head strike by high impact object
  • Motor vehicle accident
  • Pedestrian or cyclist struck by motor vehicle when not wearing a helmet

In any head trauma, the concern is the risk of missing an intracranial bleed and the lucid interval could last several hours. Thus it would be pertinent to observe the child in the emergency department for some six hours after the time of the injury and then allow the child home. Clear instructions should be given to the parents with regards to warning signs - such as altered mental status, lethargy or vomiting.

Whilst a CT scan might be considered if there was cause for concern, an MRI would be inappropriate as this procedure takes longer than a CT and (for infants) would require some form of sedation.

Question 46

proximal weakness and unable to stand from squat

Learning Points

• *Anticholinesterase inhibitors** are the first line treatment for patients with acetylcholine receptor (Ach-R) positive MuSK- negative Myasthenia Gravis (MG), however a low or high-dose corticosteroid can be given to ocular MG or moderate- severe generalised MG respectively.
• *Plasma Exchange and IVIG** therapies can be used as bridging therapies in MG crises, however these therapies are short acting.
• *Rituximab is a monoclonal antibody** that has shown good responses in MuSK MG patients and should be considered as an early therapeutic option. PLEX should also be considered.

Answer 46

This patient has clinical features consistent with myasthenia gravis (MG). Her progressive proximal muscle weakness (worst on exertion and relieved by rest) is characteristic (her proximal muscles are affected as she cannot climb stairs or squat and has weak shoulder abduction).
The weakness of MG is classically fatiguable. It can involve the eyes and cause ptosis (ocular MG).
MG can be mild, moderate or severe (as well as ocular or generalised). This patient has no eye involvement (therefore has generalised MG) and has no oropharyngeal or respiratory muscle weakness, signifying mild disease.
MG can be associated with Acetylcholine Receptor (Ach-R) Autoantibodies. It can also be associated with Muscle-specific Tyrosine Kinase (MuSK) Autoantibodies.

Acetylcholinesterase inhibitors (e.g. Pyridostigmine) are the first line treatment for Ach-R-positive MuSK-negative mild generalised MG
If her symptoms worsened or if pyridostigmine was ineffective then a high dose corticosteroid and a corticosteroid-sparing drug could be added.

Acetylcholinesterase inhibitors and low dose corticosteroids, as well as a corticosteroid- sparing drug, are a treatment option for patients with ocular MG (only if the patient’s response to an acetylcholinesterase inhibitor is incomplete or if symptoms are moderate to severe)

Acetylcholinesterase inhibitors and high dose corticosteroids, as well as a corticosteroid- sparing drug, are a treatment option for patients with moderate to severe generalised MG (3). This patient has no oropharyngeal or respiratory muscle weakness, signifying a mild form of her generalised MG.

If this patient were presenting with respiratory failure, severe swallowing difficulty, or speech dysfunction, then she would be experiencing myasthenia gravis crisis (MGC) which has a 3-8% mortality rate.
Plasma exchange (PLEX) and intravenous immunoglobulin (IVIG) are two equally effective short-term MGC stabilising therapies.
PLEX allows the removal of the Ach-R autoantibodies from circulation while IVIG’s mechanism of action remains uncertain. Both methods effects are only typically seen for up to a week, however they both allow the control of a MGC event.

Anti-muscle-specific kianse (MuSK) autoantibodies are associated with a more rare but severe form of MG (MuSK MG) which typically produces respiratory, neck and bulbar muscle weakness earlier than Ach-R MG.
MuSK MG patients typically respond poorly to anticholinesterase agents and tymectomy, Administration of Rituximab should be considered as an early therapeutic option as it is a monoclonal antibody against CD20 antigens on B cells, which allows a reduction in autoimmune B antibodies. PLEX has also shown good responses in MuSK MG patients.

Answer 47

The diagnosis of hepatitis B is determined through serological testing.

• HBsAg (hepatitis B surface antigen)
  
  • indicates active infection
  • Active infection can be acute or chronic
• If HBsAg is negative then the infection is resolved
• Anti-HBs (hepatitis B surface antibody) - indicates immunity gained
  
  • Immunity can be gained through vaccination or resolved prior infection
• If Anti-HBs is negative then immunity has not been gained
• Anti-HBc (hepatitis B core antibody) - indicates status of infection
  
  • Status of infection can be resolved or current
    
    • Current infection can be acute or chronic
  • Antibody can be IgM (current acute) or IgG (past or current chronic)
• The presence of a positive HBsAg and IgM Anti-HBc antibodies suggests a current acute active infection of hepatitis B.

If he was susceptible to hepatitis B, all serological testing would be negative.

If he had a past resolved HBV infection:

• HBsAg = negative (no active infection, infection is resolved)
• Anti-HBs = positive (immunity has been gained through resolved prior infection)
  
  • these antibodies would be IgG
• Anti-HBc = positive (status of infection = resolved infection)
  these antibodies would be IgG

If he was vaccinated:

• HBsAg = negative (no active infection, infection never existed)
• Anti-HBs = positive (immunity has been gained through vaccination)
  
  • these antibodies would be IgG
• Anti-HBc = negative (status of infection = never infected)

If he had a current chronic active HBV infection:

HBsAg = positive (has active infection)
Anti-HBs = negative (immunity has not been gained)
Anti-HBc = positive (status of infection = current chronic infection)
these antibodies would be IgG

Learning Points
Positive HBsAg, along with the presence of core IgM antibodies indicates acute infection with hepatitis B.

Question 48

NF1 and tuberous sclerosis

Kid with siezures and small hypo-pigmented lesions across his body and an erythematous rash across his cheeks comprised of small red nodules.

Answer 48

• Tuberous sclerosis is a genetic condition that commonly affects the skin, brain, eye, kidneys and heart.
• Neurofibromatosis type 1 has cafe-au-lait spots (hyperpigmented) and skin neurofibromas, where as
• neurofibromatosis type 2 may present with bilateral acoustic neuromas (hearing loss) without skin signs
• An afebrile seizure in a child requires a work-up for the cause

The most common brain tumour in children is a pilocytic astrocytoma. Hence, this could explain his presentation. However, the presence of a seizure along with hypo-pigmented spots and a facial rash suggests a diagnosis of tuberous sclerosis.
Tuberous sclerosis is a genetic condition affecting a range of organ systems through abnormalities in cell differentiation and proliferation that cause hamartomas. Spontaneous genetic mutations occur in 65% of the cases, so the family history is not always indicative. The common organs affected are skin, brain, eye, kidney and heart. Therefore, common presentations of the condition include skin lesions, seizures and developmental delay. Some of skin lesions of tuberous sclerosis are described in the case such as hypomelanotic macules (hypo-pigmented patches of skin, also known as ash-leaf spots) and facial angiofibroma (red rash across the cheeks in a butterfly distribution comprised of small red rodules). Therefore, the presentation of seizure along with the distinct skin lesions suggests a diagnosis of tuberous sclerosis is the most likely out of these options.

Neurofibromatosis is also a genetic disorder that affects bone, soft tissue, skin and nervous system. Neurofibromatosis type 1 (NFT1) has features of 6 or more café-au-lait macules (light brown skin macules), freckling in skin folds, lisch nodules in the iris and neurofibromas (benign nerve tumour that forms soft bumps on/under the skin). This patient has hypo-pigmented skin lesions rather than pigmented café-au-lait macules and there is no mention of skin neurofibromas present.

Neurofibromatosis type 2 (NFT2) is characterised by multiple tumours/neurofibromas of the brain and spinal cord. It does not have skin signs such as NFT1, but often presents with hearing loss due to bilateral acoustic neuromas. There is no mention of impaired hearing in the stem.

Both of these conditions can present with seizures due to the presence of tumours in the brain. But, with the presence of other physical signs suggestive of tuberous sclerosis, it makes NF a less likely cause in this case.

Question 49

rash, hepititis, immune deposits in wall of vessels

petechial rash on the anterior surface of both lower legs. He has a known history of Child’s C liver cirrhosis, alcohol abuse, and hepatitis C. A biopsy of the skin lesions demonstrates small vessel inflammation with immune deposits in the vascular walls.

Answer 49

Learning Points
Thrombocytopaenia and hypocomplimentaemia are expected findings in chronic liver disease

extra-hepatic manifestations of hepatitis C infection, a common accompaniement to the disease.

The presence of a petechial rash and biopsy demonstrating inflammatory vascular changes is suggestive of cryoglobulinemia manifesting with leucocytoclastic vasculitis.
It is a lymphoproliferative disorder that leads to deposition of circulating immune complexes in small to medium size blood vessels. More than 90 percent of patients with essential mixed cryoglobulinemia are HCV infected. Other manifestations of this condition include arthralgia, renal disease, neurologic disease, and hypocomplementemia. Peripheral neuropathies may also result, often in an asymmetric pattern. Antiviral treatment should be considered in patients with symptoms related to cryoglobulinemia.

Neutrophilia would also be unexpected in the setting of chronic hepatitis C infection, as this disease is usually associated with neutropaenia.

Question 50

GBS

a recent conscious collapse-he reports onset of double vision followed by his legs suddenly “giving way”
he has experienced a tingling sensation in his feet.
viral upper respiratory tract infection two weeks ago, from which he has fully recovered. At that time, he experienced several days of nausea and vomiting, sore throat,
his observations are within normal ranges. There is loss of the right nasolabial fold and he is unable to lift his right eyebrow. There is patchy numbness in both lower limbs to the level of the knees. His reflexes are absent at knees and ankles.

DX?

Answer 50

very suggestive of Guillain-Barré syndrome (GBS), characterised by bilateral symmetrical progressive ascending limb weakness,
sensory loss and areflexia in the weak limbs, and cranial nn palsies on the background of a recent infection.

Cranial nerve palsies are also common, with facial nerve palsies accounting for about half. GBS is usually preceded by some form of infection or another immune stimulus that sets off an abnormal autoimmune response. This response usually focuses on peripheral nerves and the associated spinal roots. Some cases are associated with a preceding diarrhoeal illness, where Campylobacter jejuni infection appears to be a significant trigger.

A lumbar puncture may reveal albuminocytologic dissociation, with a proportion of patients demonstrating oligoclonal bands. MRI and CT imaging is used to exclude a spinal lesion. Nerve conduction studies may be helpful in classifying the variant of GBS, but are not necessary for diagnosis.

The duration of the illness is usually less than four weeks, with symptoms usually being maximal within two weeks of onset. Up to 30% of patients will develop respiratory complications and some may need ventilatory support in an intensive care unit.

Question 51

Answer 51

Question 52

HB

Answer 52

Question 53

Learning Points
Seborrheic keratoses are benign skin tumours that have a typical raised, wart-like surface and stuck-on appearance.

Answer 53

These are most likely seborrhoeic keratoses, with a typical raised, wart-like surface and stuck-on appearance. Though benign, they may be removed with cryotherapy, shave or excision biopsy for cosmetic reasons.

Occasionally melanoma can develop within a seborrhoeic keratosis; however, this is far less likely the case in this patient, given the lesion does not have multiple colours, is not rapidly changing, bleeding, itchy, and is not irregularly bordered.

Lentigo maligna is also known as Hutchinson’s melanocytic freckle, which presents as a single slowly changing patch of discoloured skin. At first, this often resembles a freckle, but over a long period of time grows in size to be >6mm, and develops an irregular shape with variable pigmentation.

Solar keratosis (or actinic keratosis) are rough scaly patches of skin that present on areas that have been exposed to the sun (such as the forehead or face). They are thick scaly growths which develop in varying sizes, often with a scaly yellow-white crust at the top.

Dysplastic naevi are moles that are irregular in shape and larger than the average mole. They also have several colours on the mole, with an irregular surface. Despite these characteristics, dysplastic naevi rarely progress to malignant melanoma. Patients with a large number of naevi (50-100) are at increased risk (5 to 17 times) of one developing into a melanoma.

Question 54

suspecected child abuse

Answer 54

Discussion with the senior consultant is vital, and this case will likely entail notification of protective services, via the Child Abuse Report Line or the police if there is concern of imminent harm. As there is no concern for imminent harm at this point, it would be more appropriate to contact the Child Abuse Report Line. Healthcare professionals are personally responsible for mandatory reporting; it is not necessary to arrange a social work review for a report to be made [3]. However, in cases of uncertainty, healthcare practitioners can contact a paediatrician or the department of child protection for advice.

Question 55

SIADH

Px with nausea, confusion and headache. epilepsy controlled on carbamazepine. prior urinary frequency, and was prescribed trimethoprim

blood tests which show her sodium concentration is 126 mmol/L (135-145) and her serum osmolality is 265 mmol/kg (normal ~285). Her urine osmolality is 1100 mOsm/kg (500-800) and has a urine sodium concentration of 35 mmol/L (high). Her other electrolytes are normal. On clinical examination she appears euvolaemic.

Which of the following is the most likely cause of his hyponatraemia?

Answer 55

Na (low -s, high -u) ; H20 (osmolality proxy) (low-s; high -u)

SIADH does cause a hypo-osmolar hyponatraemia that is commonly euvolaemic; with high urine osmolality and elevated urine sodium concentration. SIADH works via several unknown mechanisms that lead to increased ADH release, however, there are many known precipitants including: major surgery, ectopic production (e.g. small cell lung carcinoma), medications (anti-depressants, anti-convulsants, anaesthetic agents, some antibiotics - trimethoprim), CNS disorders (trauma, tumour, meningitis), and pulmonary disorder (pneumonia, TB etc.).

The increased ADH inserted aquaporin V2 channels in the collecting ducts of renal nephrons, absorbing more water irrespective of sodium. This results in very concentrated urine = high osmolarity and urine sodium. The increased retention of water activates stretch baroreceptors as well as natriuretic peptides to promote salt excretion, as this normally should increase water excretion also. In minimally symptomatic patients, fluid restriction can be effective management. This patient is suffering neurological symptoms and thus may require hypertonic (3%) saline boluses and ICU admission.

Nephrotic Syndrome does cause a hypo-osmolar hyponatraemia but in the presence of hypervolaemia (secondary to third spacing of fluids) and a low urine sodium concentration - which is appropriate.

Adrenal insufficiency (low cortisol) results in subsequent increase in CRH which also increases ADH release –> leading to hypo-osmolar hyponatraemia. Also, there is often low aldosterone which decreases sodium and increases potassium concentrations. The potassium is normal in this case making adrenal insufficiency less likely.

Low sodium intake does cause a hypo-osmolar hyponatraemia in the presence euvolaemia but will also have a low urine sodium concentration and reduced urine osmolality (in attempt to retain as much sodium as possible).

Chronic Kidney Disease does cause a hypo-osmolar hyponatraemia with an elevated urine sodium concentration but in the presence of hypervolaemia.

Answer 56

Wernicke’s COAT: Confusion, Oculomotor dysfunction, Ataxia, and Thiamine administration (see Treatment section)

Question 57

His right arm is adducted and internally rotated, the forearm is extended and pronated, and the wrist is flexed. Moro reflex is asymmetrical, and the grasp reflex is present bilaterally.

Which one of the following is the likely site of the underlying pathology?
Choose the single best answer.

C5 - T1 nerve roots
Radial nerve
C8 - T1 nerve roots
C5 - C6 nerve roots
Clavicle

Answer 57

This deformity (known as the “waiter’s tip”) is characteristic of Erb’s palsy; damage to C5 and C6 (upper trunk) of the brachial plexus resulting in paralysis of the deltoid, biceps brachii, and brachialis. Lower plexus injury, referred to as “Klumpke palsy”, is a rare neonatal plexus injury and would result in wrist extension with loss of the grasp reflex. Total brachial plexus palsy results in an absent Moro and grasp reflex with complete arm flaccid paralysis, often with Horner’s syndrome. Radial nerve palsy is associated with loss of elbow extension and no change to shoulder positioning. Clavicular fractures present with decreased movement of the affected side however are not associated with this pattern of arm positioning. The only statistically significant risk factor for neonatal brachial plexus injury is shoulder dystocia [1], however macrosomia, as seen in this case, and operative vaginal delivery have also been reported as risk factors.

Question 58

worsening chest pain on exertion over the last 3 months. S

following skin lesion (shown below) located on her right antecubital fossa. On further questioning, she says that it has been present since her early 20s, and has not changed since then. Angioid streaks were found on fundoscopy.

Answer 58

Pseudoxanthoma elasticum is a genetic disorder that leads to degeneration of elastic tissue and premature atherosclerosis. The changes are often manifest in the skin first, where yellow, thickened areas occur. Often starts on the lateral neck first before progressing to flexural folds of limbs (‘plucked chicken skin’ appearance). The changes to blood vessels can lead to early atherosclerotic changes (angina, claudication), cardiomyopathy, chronic gastrointestinal blood loss and retinal haemorrhage (characterised by progressive visual loss, angioid streaks on fundoscopy).

Ehlers-Danlos syndrome is a group of inherited disorders that involve a genetic defect in collagen or connective tissue synthesis and structure. This results in varying degrees of hyper-extensive skin, joint hypermobility, and tissue fragility (including that of vasculature). Retinal involvement can include angioid streaks.

Question 59

multiple episodes of staring motionlessly into space and unresponsiveness when spoken to. These episodes last anywhere from 30 seconds to a minute, and afterwards she appears confused and lethargic. She also reports episodes of hearing voices and strong feelings of having experienced certain situations before.

Answer 59

This woman is experiencing focal seizures with impaired awareness (previously termed complex partial seizures) most consistent with temporal lobe epilepsy. Her auditory hallucinations and déjà vu are also characteristic of the dyscognitive aura that can manifest in temporal lobe seizures. Her post-ictal confusion is not consistent with absence seizures. Carbamazepine is generally considered the first line treatment for focal (partial) seizures in Australia, supported by high quality evidence, and is thus the correct answer. Levetiracetam is second line and whilst it is usually well tolerated, this drug does have side effects that include irritability, moodiness and emotional lability.

In pregnancy???
Compared to AEDs such as lamotrigine and levetiracetam, exposure to AEDs such as valproate, phenobarbital, and topiramate is associated with a significantly increased risk of congenital malformations (e.g., neural tube defects, hypospadias, cardiac defects)

Question 60

diagnosis of cushings

Cushings syndrome biochemistry

Answer 60

Biochemical diagnosis of Cushing’s syndrome typically requires at least two cross-confirmatory results among three commonly-used tests:

• low-dose dexamethasone suppression test,
• 24-hour urinary free cortisol (ideally 3 separate collections),
• and/or midnight salivary cortisol. (Midnight plasma cortisol may also be used in circumstances where midnight venepuncture is feasible, e.g. hospital inpatients.)

Once hypercortisolism has been demonstrated by at least two tests,hypercortisolism has been adequately demonstrated and a diagnosis of Cushing syndrome can be made.

A plasma ACTH level is the next step to determine ACTH dependence (i.e. whether the hypercortisolism is driven by endogenous ACTH over-production or direct cortisol over-production), which helps distinguish between pituitary / ectopic ACTH-secreting tissue (in which case the ACTH level will be normal or high) versus adrenal pathologies (in which case the ACTH level will be suppressed due to negative feedback within the hypothalamic-pituitary-adrenal axis).

A pituitary MRI, corticotropin-releasing hormone test (CRH test), and/or high-dose dexamethasone suppression test help to localise ACTH-dependent disease to the pituitary gland.
CT adrenal glands is performed to characterise ACTH-independent disease, which typically reflects either adrenal hyperplasia or a unilateral adrenal mass.

Learning Points
Once Cushing’s syndrome is diagnosed, a serum ACTH level is the first step to localise the underlying pathology.

• The low-dose dexamethasone suppression test is a reliable investigation for Cushing syndrome. Especially in GP setting
• Midnight salivary cortisol is less useful in the presence of disrupted circadian rhythm- is shift worker. Better 24 hour cortisol level then.

Question 61

HAP drugs

HAP drugs

Answer 61

In all cases of hospital-acquired pneumonia, the risk of multidrug-resistant (MDR) organisms must be assessed. As this man was in a high-risk ward (ICU/HDU) for a relatively short time (<5 days) and has not recently been on antibiotic therapy, he is unlikely to have a MDR infection.
Based on his clinical picture, this would likely be categorised as low-moderate severity HAP, due to the absence of hypotension, signs of sepsis, need for intubation and rapid deterioration. Thus, empirical therapy would aim to target Streptococcus pneumoniae and aerobic Gram-negative bacilli. Where tolerated, oral therapy is typically preferred over enteral (e.g. via nasogastric tube) or parenteral (i.e. intravenous) administration. Therefore, oral amoxicillin (aminopenicillin) and clavulanate (β-lactamase inhibitor) would be the most appropriate treatment for this patient as it offers broad coverage of all relevant organisms.

Piperacillin-tazobactam is reserved for high-severity HAP or those with high risk of MDR organisms.

Benzylpenicillin and doxycycline is the typical treatment for moderate community acquired pneumonia (CAP).

Metronidazole covers anaerobic infections which are unlikely in this case where aspiration has not occurred.

Vancomycin is used to treat methicillin-resistant Staphylococcus aureus.

Question 62

• *Adrenal insufficiency:**
• *fatigue**, abdominal pain, hypoglycaemia and postural hypotension.

–

Cushing’s disease is due to a pituitary adenoma causing hypercortisolism, and leads to symptoms of weight gain, skin thinning, and also headaches or visual changes.

“CUSHINGOID” is the acronym for side effects of corticosteroids: Cataracts, Ulcers, Striae/Skin thinning, Hypertension/Hirsutism/Hyperglycemia, Infections, Necrosis (of the femoral head), Glucose elevation, Osteoporosis/Obesity, Immunosuppression, Depression/Diabetes.

Patients with secondary hypercortisolism due to ectopic ACTH production may present with rapid onset of hypertension and hypokalemia without other typical features of Cushing syndrome.

Consider a diagnosis of hypercortisolism in patients who present with proximal muscle weakness, central obesity, thinning skin, weight gain, sleep disturbance, and/or depression.

Answer 62

Long-term glucocorticoid use (in this case, long term steroids to control ulcerative colitis flare) can lead to suppression of the hypothalamic pituitary adrenal axis that normally regulates adrenal gland function. Due to her recent job change, the patient has inadvertently and rapidly tapered off her steroid dose causing secondary adrenal insufficiency. Symptoms of adrenal insufficiency include fatigue, abdominal pain, hypoglycaemia and postural hypotension.

Primary adrenal insufficiency (Addison disease)

Damage to the adrenal gland leads to the deficiency in all three hormones produced by the adrenal cortex: androgen, cortisol, and aldosterone.

• Hypoandrogenism
  
  • Loss of libido
  • Impaired spermatogenesis (in men)
• Hypocortisolism leads to:
  
  • ↑ ACTH → ↑ production of POMC (in order to increase ACTH production) → ↑ melanocyte-stimulating hormone (MSH) → hyperpigmentation of the skin (bronze skin) ^[11]
  • ↑ ADH level → retention of free water → dilutional hyponatremia
  • ↓ Expression of enzymes involved in gluconeogenesis → ↓ rate of gluconeogenesis → hypoglycemia
  • Lack of potentiation of catecholamines action → hypotension
• Hypoaldosteronism → hypotension (hypotonic hyponatremia and volume contraction), hyperkalemia, metabolic acidosis

Secondary adrenal insufficiency

• ↓ ACTH → hypoandrogenism and hypocortisolism
• Aldosterone synthesis is not affected (mineralocorticoid production is controlled by RAAS and angiotensin II, not by ACTH).

Tertiary adrenal insufficiency

• ↓ CRH → ↓ ACTH → hypoandrogenism and hypocortisolism
• Aldosterone synthesis is not affected.

Question 63

let down

Let-down reflex is what makes breastmilk flow. When baby sucks at the breast, tiny nerves are stimulated. This causes two hormones – prolactin and oxytocin – to be released into your bloodstream.

Prolactin helps make the milk (anterior pit), while oxytocin (post pit) causes the breast to push out the milk.

Answer 63

The two main physical functions of oxytocin are to stimulate uterine contractions in labor and childbirth and to stimulate contractions of breast tissue to aid in lactation after childbirth.

Prolactin is necessary for the secretion of milk by the cells of the alveoli.

Question 64

posterior pituitary hormone (ADH, or vasopressin)

posterior pituitary is to store and releases two hormones: oxytocin and antidiuretic hormone (ADH, or vasopressin)

Question 65

compression # in older man.. causes

stem mentions gynacomastia

Answer 65

Pathological fractures are bone fractures caused by diseases that lead to weakness in bone structures. The most common underlying process is osteoporosis, and in men up to 50% of patients with osteoporosis have an underlying cause, known as secondary osteoporosis.

Hypogonadism is a common cause and is supported by the presence of gynaecomastia, making it the most likley cause. This can be either primary - that originating in the testes, or secondary - originating in the feedback pathways of the hypothalamus or pituitary.

• • • Primary hyperparathyroidism: high bone turnover from increased bone resorption, caused by increased PTH secretion
• Hypogonadism: low androgen levels reduce osteoblast proliferation and results in less inhibitory effect on osteoclasts
• Grave’s disease: high bone turnover from increased bone resorption, caused by increased circulating T3 / T4
• Long-term corticosteroid use: mechanism is not completely understood, however the inhibitory effect of corticosteroids on osteoblasts is likely the main mechanism
• Multiple myeloma: high bone resorption and low bone formation from pro- inflammatory cytokines released from local bone lesions

Question 66

noticing he has trouble breathing and his face flushes red when he lays flat. This began about two weeks ago.

On examination his vital signs are within normal range. He has no nail changes or tremor. He has a neck mass that is palpable, it has many multi-nodular components to it and the lower pole is not palpable with his neck hyper-extended. Percussion across his chest is dull

Pemberton’s sign is positive when a patient lifts their arms above their head and they demonstrate trouble breathing, facial flushing and stridor
Pemberton’s sign suggests there is a mass obstructing the thoracic inlet (often a large restrosternal goitre)

Answer 66

Pemberton’s sign is positive when a patient lifts their arms above their head and they demonstrate trouble breathing, facial flushing and stridor
Pemberton’s sign suggests there is a mass obstructing the thoracic inlet (often a large restrosternal goitre)

A positive Pemberton’s sign occurs when there is a temporary superior vena cava obstruction and the process of raising the arms above the head obstructs the thoracic inlet. This is represented with the triad of trouble breathing, stridor and facial flushing. Additional symptoms can include conjunctival injection and dilated neck veins.

All the above options can cause a superior vena cava obstruction and hence a positive Pemberton’s sign. However, due to his other symptoms such as a neck lump and it’s consistency, suggest a goitre as a cause.

Traditionally, Pemberton’s sign is done during a thyroid examination as retrosternal goitres can cause a positive result. The most common type of goitre that leads to this is a multinodular goitre that has grown slowly over many years. These types of goitres are large and can produce symptoms such as problems breathing, wheezing, cough, hoarse voice, stridor or dysphagia. They can also cause similar symptoms with changes in position such as lying flat or with neck movements. A CT scan should be ordered to show how far it extends and to guide management, which most often involves surgery.

A hilar lung cancer is another pathology that can cause of a positive Pemberton’s sign. If large enough compression of the thoracic inlet could occur. Again, this patient does not report any other findings consistent with this such as weight loss, cough and haemoptysis.

An extremely large thoracic aortic aneurysm could cause a positive Pemberton’s sign if it compressed the thoracic inlet. However, if it were large enough to do this the patient may display symptoms such as chest/back pain, and in the case of rupture the patient can become haemodynamically unstable. This would not explain the neck lump and this patient does not mention symptoms of chest/back pain.

A mediastinal tumour is rare type of tumour. They can be benign or malignant, one cause is lymphoma. The lump in his neck could be consistent with a mediastinal tumour, however he does not display features of weight loss, night sweats, loss of appetite or fatigue that can be present in lymphoma.

Question 67

Corticotropin-releasing hormone (CRH)-secreting tumour (ectopic)

Pituitary corticotroph adenoma

High dose dexamethasone supp test demonstrates a reduction in plasma cortisol

Answer 67

If reduction is more than 50 %