investigation Flashcards
When interpreting an arterial blood gas, a high serum anion gap is consistent with:
a) lithium toxicity
b) Salicylate toxiticy
c) Hypercholeraemia
d) Hypoalbuminaemia
e) Hypercalcaemia
b) Salicylate toxicity
Salicylate toxicity can cause an elevated serum anion gap due to the production of organic acids (salicylic acid and its metabolites) that are not measured by the standard anion gap calculation. This leads to an increased anion gap metabolic acidosis.
HAGMA results from accumulation of organic acids or impaired H+ excretion
Causes (LTKR)
Lactate
Toxins
Ketones
Renal
Causes (CATMUDPILES)
CO, CN
Alcoholic ketoacidosis and starvation ketoacidosis
Toluene
Metformin, Methanol
Uremia
DKA
Pyroglutamic acidosis, paracetamol, phenformin, propylene glycol, paraladehyde
Iron, Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates
NAGMA results from loss of HCO3- from ECF
Causes (CAGE)
Chloride excess
Acetazolamide/Addisons
GI causes – diarrhea/vomiting, fistulae (pancreatic, ureters, billary, small bowel, ileostomy)
Extra – RTA
Causes (ABCD)
Addisons (adrenal insufficiency)
Bicarbonate loss (GI or Renal)
Chloride excess
Diuretics (Acetazolamide)
LITFL
A drug which is unlikely to interfere with skin testing is oral:
a) Diphenhydramine
b) Amitriptyline
c) Prednisolone
d) Risperidone
e) Ranitidine
MAYANK Risperidone
Avoid antihistamines and steroids
TCAs known to interfere
Mayo clinic website
See allergy.org.au - risp mentioned in appendix b as a med that may need held
A drug which is unlikely to interfere with skin testing is oral:
a) Diphenhydramine
b) Amitriptyline
c) Prednisolone
d) Risperidone
e) Ranitidine
MAYANK Risperidone
Avoid antihistamines and steroids
TCAs known to interfere
Mayo clinic website
See allergy.org.au - risp mentioned in appendix b as a med that may need held
Steph In a patient presenting with an Addisonian crisis, the electrolyte disturbances MOST LIKELY to be seen are:
a) Low BSL, hyperkalaemia, hyponatraemia
b) High BSL, hyperkalaemia, hyponatraemia
c) Hypocalcaemia, hyperkalaemia, hyponatraemia
d) Hypercalcaemia, hyperkalaemia, hyponatraemia
a) Low BSL, hyperkaelamia, hypernatraemia
Adrenal crisis is a medical emergency and should be considered in any patient presenting with one or more of the following symptoms:
* altered consciousness
* circulatory collapse
* hypoglycaemia
* hyponatraemia
* hyperkalaemia
* seizures
* history of steroid use/withdrawal
* any clinical features of Addison disease
Adrenal crisis may be precipitated by stress, sepsis, dehydration or trauma; clinical features may be modified accordingly. In patients with known adrenal insufficiency, nonadherence with therapy, inappropriate cortisol dose reduction or lack of stress related cortisol dose adjustment can cause adrenal crisis.
Aus Family Physician - RACGP
Re chat below - incorrect recall, have updated
A
Why A? All three should be seen - glucocorticoid deficiency causes low Na and glucose while simultaneous mineralocorticoid deficiency low K.
Crisis typically presents with hypotension abdo pain, nausea, vomiting and confusion. No one electrolyte/lab value can tie all those together.
In pulmonary function testing the presence of airflow limitation is defined by a post- bronchodilator FEV1/FVC ratio less than:
a) 0.5
b) 0.6
c) 0.7
d) 0.8
c) 0.7
A 70-year-old patient booked for a revision total hip replacement is reviewed in preadmission clinic ten days before surgery. The following blood test results are
noted:
haemoglobin 110 g/L
ferritin 51 mcg/L
CRP (c-reactive protein) 10 mg/L
The most appropriate management for this patient should be to:
a) Proceed
b) Give PO iron and delay 6 weeks
c) Give IV iron
d) Blood transfusion pre-op
Victoria
Screenshot sent to JJ
B
Kate A bleeding patient has ROTEM results including: [table attached]. The most
appropriate treatment is:
a) Fibrinolysis
LINDON
22.2 Regarding cardiopulmonary exercise testing before major surgery, oxygen pulse is the
a. Arterial oxygen content at peak HR
b. Arterial oxygen saturation at mean HR?
c. Arterial oxygen saturation at peak HR
d. PaO2 at peak HR
e. Oxygen consumption/min divided by HR
e. Oxygen consumption/min divided by HR
VO2/HR: oxygen consumption divided by HR, known as the ‘oxygen pulse’ (ml beat–1)
https://www.bjaed.org/article/S2058-5349(19)30021-6/fulltext
The objective of CPET is to determine functional capacity in an individual.
Deficiencies in CPET-derived variables—specifically:
1. ventilatory anaerobic threshold (AT)
2. peak O2 consumption (VO2peak)
3. ventilatory efficiency for carbon dioxide (VE/VCO2)
—are associated with poor postoperative outcomes (mortality, morbidity, admission to intensive care, and length of hospital stay) after intra-abdominal surgery.
- Does the oxygen pulse increase with exercise?
The oxygen pulse is the VO2 divided by HR, and represents the product of the stroke volume and the arterial-venous oxygen difference. It can be seen in panel 2 and can be viewed as a surrogate for stroke volume, and as such should increase at the start of exercise before slowly reaching a plateau at its highest predicted value.
An awake patient in the post-anaesthesia care unit complains of breathlessness. The FiO2 through the patient’s rebreather mask is 40%. An arterial blood gas taken at the time shows (ABG shown). The alveolar-arterial gradient (in mmHg) is approximately
Blood gas shows:
PaO2 135
PaCO2 48
SpO2 100%
The A-a gradient is:
A. 5
B. 30
C. 60
D. 90
E. 110
D 90
A-a = PAO2 - PaO2
Alveolar air equation gives PAO2
PAO2 = PiO2 - PaCO2 / R
PAO2 = 0.4 x (760 - 47) - 48 / 0.8
so, as PaO2 given as 135
A-a = 228 - 135 = 93
21.2 The image below on the left shows a normal central venous pressure (CVP) trace. The CVP
trace in the image below on the right is most consistent with
a) AF
b) MR
c) AR
d) TR
e) Pericardial constriction
TR
19.2 An 80-year-old woman is admitted to hospital with respiratory failure. Her arterial blood gas on oxygen 4 litres per minute via a Hudson mask is as follows: (ABG shown) Which of the following most accurately describes this blood gas result?
pH 7.2, pO2 91, pCO2 84, BE 16, HCO3- 43, Na 145
a) Metabolic alkalosis, acute resp acidosis + normal AG
b) Metabolic alkalosis resp acidaemia + abnormal AG
c) Mixed acidaemia
d) Respiratory Acidosis with incomplete compensation
e) Compensated Respiratory acidosis
d) Respiratory Acidosis with incomplete compensation
Uncertain of this answer, not enough info to calculate anion gap
pH 7.2 = acidaemia
pCO2 84 = respiratory acidosis
HCO3 43 = metabolic alkalosis as compensation
BE 16 = metabolic alkalosis
Boston rules:
Chronic fully compensated Respiratory acidosis
Expected compensation is 3-4 mmol/L rise for every 10mmHg rise in PCO2.
Expected metabolic compensation therefore is
HCO3 = 24 + 4 x ((84-40)/10)
= 24 + 4x (44/10)
= 24 + 4 x (4.4)
= 24 + 17.6
= 41.6
Metabolic acidosis
PaCO2 should be 1.5 x HCO3 + 8
= 72.5
Rules (from K.Brandis Acid-base rules anaesthesia mcq):
- 1 for 10 (acute resp acidosis), 4 for 10 (chronic resp acidosis)
- 2 for 10 (acute resp alkalosis), 5 for 10 (chronic resp alkalosis)
- 1.5xHCO + 8 = expected pCO2 in a metabolic acidosis
- 0.7xHCO3 + 22 = expected pCO2 in a metabolic alkalosis
https://www.anaesthesiamcq.com/AcidBaseBook/ab9_3.php
22.1 A 68-year-old woman presents with a loud systolic murmur in the anaesthesia room before total
hip joint arthroplasty. A transthoracic echocardiogram is performed (image provided) and shows
a. AS
b. LVOT
c. MR
MR
22.1 A 57-year-old female smoker presents for a laparotomy with the following pulmonary function tests
(normal FEV1 FVC, low RV and FRC only, normal DLCO)
They are consistent with a diagnosis of
a. Obesity
b. PE
c. Pulmonary fibrosis
d. COPD
a. Obesity
Obesity and pulmonary function testing
https://www.jacionline.org/article/S0091-6749(05)00164-8/fulltext
- Full pulmonary function tests are often necessary to better characterize the spirometric abnormalities seen in the obese patient
- The most sensitive indicator of obesity is a low expiratory reserve volume (ERV) and functional residual capacity
- Restriction is seen in more severe obesity, with reductions in TLC and FVC.
- However, residual volume is often preserved because of the relative high closing volume in relation to ERV.
23.1 The following is a chest X-ray from a patient complaining of dyspnoea after thoracic surgery. The diagnosis is
(not the image from the exam)
A. Dextracardia
B. Cardiac hernation
C. LLL collapse
D. Tension Pneumohorax
B. Cardiac hernation
https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.109.896829
20.2 A patient presents with a serum sodium of 110mmol/L. A feature NOT consistent with a diagnosis of syndrome of inappropriate antidiuretic hormone (SIADH) is
a. urinary sodium >40
b. Euvolemia
c. Increased cortisol
d. Urine osmolarity <100
e. Serum Na <145
d. Urine osmolarity <100
DIAGNOSTIC CRITERIA
>hypotonic hyponatraemia
>urine osmolality > plasma osmolality (<275mOsm/kg) (i.e. concentrated urine despite hypotonic blood)
>urinary Na+ > 20mmol/L
>normal renal, hepatic, cardiac, pituitary, adrenal and thyroid function
>euvolaemia (absence of hypotension, hypovolaemia, and oedema)
correction by water restriction
CAUSES (MAD CHOP)
Major Surgery
>abdominal
>thoracic
>transsphenoidal pituitary surgery (6-7 days post op)
ADH production by tumours (Ectopic)
>small cell bronchogenic carcinoma
>adenocarcinoma of pancreas/duodenum
>leukaemia
>lymphoma
>thymoma
Drugs
>antidepressants (e.g. SSRI, TCAs, MAOIs)
>psychotropics (e.g. haloperidol, chlorpromazine), carbamazepine, Na+ valproate)
>anaesthetic drugs (barbiturates, inhalational agents, oxytocin, opioids)
>ADH analogues (vasopressin, DDAVP)
>chemotherapy (e.g.Vinca alkaloids, Melphalan, Methotrexate and cyclophosphamide)
>others (e.g. NSAIDs, amiodarone, ciprofloxacin, morphine, MDMA, proton pump inhibitors)
CNS Disorders
>cerebral trauma
>brain tumour (primary or metastases)
>meningitis/encephalitis
>brain abscess
>SAH
>acute intermittent porphyria
>SLE
Hormone deficiency
>hypothyroidism
>adrenal insufficiency
Others
>Guillain-Barre Syndrome
>HIV infection (early symptomatic or AIDS)
>hereditary SIADH
>giant cell arteritis
>idiopathic (occult small cell or olfactory neuroblastoma)
Pulmonary Disorders
>pneumonia (viral, fungal, bacterial)
>TB
>lung abscess
MANAGEMENT
1. see hyponatraemia
2. fluid restrict
3. incremental increase in Na+ if indicated to avoid central pontine myelinolysis
4. medications to decrease ADH secretion
>Demeclocycline
>Tolvaptan / Conivaptan
23.1 A 24-year-old man has been brought into the emergency department with a traumatic fracture of the femur. His observations are: heart rate 90 beats per minute; blood
pressure 120/80 mmHg; respiratory rate 25 breaths per minute. A peripheral VENOUS blood gas sample shows a pH of 7.29. The arterial blood pH can be estimated to be
A. 7.29
B. 7.32
C. 7.35
D. 7.4
B. 7.32
https://emj.bmj.com/content/18/5/340
The values of pH on arterial and venous samples were highly correlated (r=0.92) with an average difference between the samples of −0.4 units. There was also a high level of agreement between the methods with the 95% limits of agreement being −0.11 to +0.04 units.
https://litfl.com/vbg-versus-abg/
pH
- Good correlation
- pooled mean difference: +0.035 pH units
23.1 During standard diagnostic nocturnal polysomnography for investigation of obstructive sleep apnoea, apnoea is defined as cessation of airflow for
A. 10 sec
B. 20 sec
C. 30 sec
D. 10 sec with 3% desat
E. 20 sec with 3 % desat
A
Apnea is defined as the cessation of airflow for ten or more seconds.
Hypopnea is defined as a recognizable, transient reduction, but not a complete cessation of, breathing for ten or more seconds.
Hypopnea requires a 4% fall in SpO2
https://www.ncbi.nlm.nih.gov/books/NBK441909/#:~:text=Obstructive%20Sleep%20Apnea%20(OSA)%2C,for%20ten%20or%20more%20seconds.
A 35-year-old male, three days post laparoscopic sleeve gastrectomy has ongoing nausea and vomiting. His arterial blood gas measurement is as follows: (ABG shown) The best initial therapeutic option would be
Blood gas given:
hypokalaemia
hypochloraemia
alkalosis
normal lactate
a Laparoscopy
b IV fluids and KCL
c 4% albumin
d HCl infusion
e Acetazolamide
b IV fluids and KCL
UTD Stricture post Lap Sleeve Gastrectomy management
Although sleeve strictures have been reported in 0.26 to 4 percent of LSG operations, <1 percent result in symptoms that require endoscopic or surgical intervention
A stricture can manifest acutely, early after surgery, or more chronically.
Although strictures can occur anywhere along the long staple line, they are most often located at the level of the incisura angularis for anatomic reasons.
The etiologies of post-LSG strictures are either mechanical or functional. Mechanical strictures usually derive from the use of small bougies, stapling too close to the bougie (especially at the incisura angularis), twisting of the staple line creating a “spiral” sleeve, or aggressive imbrication of the staple line.
Functional stenoses derive from edema or hematomas at the staple line. As a result, functional stenoses are transient, which present immediately following LSG and resolve spontaneously with expectant treatment.
Patients who present with obstructive symptoms during the early postoperative period should be resuscitated with hydration and antiemetic medications and studied with an upper gastrointestinal (UGI) series.
Stable patients with a stricture can be observed to allow postsurgical mucosal edema to resolve, typically in 24 to 48 hours. Patients who cannot handle their own secretions require nasogastric tube decompression, preferably placed under fluoroscopic guidance.
Patients with an acute stricture who do not respond to conservative management require early surgical reintervention. Laparoscopy could demonstrate kinking of the gastric tube, a tight suture, or a compressing hematoma.
●Endoscopy is a good initial treatment for short-segment strictures, most of which can be dilated with balloons. Multiple treatments in four- to six-week intervals are sometimes needed to treat the stricture and improve patient symptoms. Stents have also been tried but are not effective for post-LSG strictures.
●Laparoscopic seromyotomy is a treatment option for long-segment strictures . In a small retrospective study, patients treated with laparoscopic seromyotomy had good symptomatic relief.
●Conversion to an RYGB is the last option for patients with a refractory stricture who have failed all other treatments.
20.1 A 64-year-old man presenting for elective surgery is on thyroxine 100 mcg daily. His thyroid function tests are: (Thyroid function tests shown). These results are most consistent with
TFTs thryoxine TSH < .05 T4 and T3 completely normal
a) Hypophysectomy
b) Subclinical Hyperthyoirdism
c) Sick euthyroid
d) Toxic Multinodular goitre
b) Subclinical Hyperthyoirdism
Subclinical hyperthyroidism: low TSH, normal T3 + T4
Clinical hyperthyroidism: low TSH, high T3, high/normal T4
Subclinical hypothyroidism: high TSH, normal T3 + T4
Clinical hypothyroidism: high TSH, low/normal T3, i T4
Amiodarone: high/normal TSH, low T3 (2o to inhibition of pituitary T4 to T3 conversion)
Sick euthyroid: low TSH, low T3
Hypophysectomy (central hypothyroidism): low/normal TSH/T3/T4
Compliant on thyroxine: normal TSH, high/normal T3, low T4
Non-compliant w thyroxine (pt taking several tabs prior to Dr’s appointment): high TSH, normal T4
23.1 A 60-year-old woman presents for thrombectomy with left lower leg ischaemia. She has not received any medications since presentation and takes none at home. The sole abnormality on laboratory testing is an activated partial thromboplastin time (APTT) of 52 seconds. The most likely cause of the raised APTT is
a. Cold agglutinins
b. Erroneous reading
c. Lupus anticoagulant
d. Factor VII deficiency
e. Haemophilia A
c. Lupus anticoagulant
(normal PT, raised APTT)
Lupus anticoagulant (more likely to be associated with thrombosis than bleeding)
https://www.uptodate.com/contents/image?imageKey=HEME%2F79969
The amount of intravenous potassium chloride required to raise the plasma potassium level from 2.8 mmol/L to 3.8 mmol/L in a normal adult is approximately
a. 10mmol
b. 20mmol
c. 30mmol
d. 100mmol
e. 200mmol
e. 200mmol
K+ < 3.0 mmol/L: 200-400 mmol of potassium are required to raise it by 1 mmol/L
K+ > 3.0 mmol/L: 100-200 mmol of potassium are required to raise it by 1 mmol/L
Hypokalaemia P. GLOVER
https://www.cicm.org.au/CICM_Media/CICMSite/CICM-Website/Resources/Publications/CCR Journal/Previous Editions/September 1999/05-Sept_1999_Hypokalaemia.pdf
If the serum potassium level is greater than 3 mmol/L, 100-200 mmol of potassium are required to raise it by 1 mmol/L; 200 - 400 mmol are required to raise the serum potassium level by 1 mmol/L when the potassium concentration is less than 3mmol/L, assuming a normal distribution between cells and the intracellular space, and a linear relationship between plasma potassium and body deficit (which has been described, i.e. 0.27 mmol/L/100 mmol deficit/70 kg), exists. The rate of administration of potassium will be influenced by the presence and seriousness of the pathophysiological changes caused by hypokalaemia. The underlying disorder should also be treated simultaneously.
21.1 A 45-year-old man has the following results on his blood biochemistry testing (Liver function tests shown). The most likely diagnosis is
a. Cholecystitis
b. Metastatic liver disease
c. Hepatitis C
d. Chronic liver disease
e. Paracetamol toxicity
a. Cholecystitis
Example and explanation taken from RACGP:
The raised AlP relative to Alt suggests cholestasis and the high GGt confirms liver origin. The mild hyperbilirubinaemia confirms the clinical impression of jaundice. Biliary disease is highly likely with gallstones the most likely differential diagnosis. however, this clinical picture may also occur in drug reactions or infiltrative conditions. After a careful history, abdominal ultrasound is the most appropriate next investigation.
20.2 A 55 year old man with no past history of ischaemic heart disease is 3 days post total hip replacement surgery. He has an episode of chest pain that sounds ischaemic, began at rest and lasts thirty minutes before resolving fully. There are no ECG changes nor troponin rise. The diagnosis is
a. No diagnosis made
b. Unstable angina
c. STEMI
d. NSTEMI
e. MINS
b. Unstable angina
Not a Repeat, no Tropnin rise in this question making the answer unstable angina as opposed to NSTEMI
UTD:
Unstable angina (UA) and acute non-ST elevation myocardial infarction (NSTEMI) differ primarily in whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injury (troponins):
●UA is considered to be present in patients with ischemic symptoms suggestive of an ACS and no elevation in troponins, with or without electrocardiogram changes indicative of ischemia (eg, ST segment depression or transient elevation or new T wave inversion).
●NSTEMI is considered to be present in patients having the same manifestations as those in UA, but in whom an elevation in troponins is present.
MINS: Myocardial injury after non-cardiac surgery (up to 30 days post-op):
1. Elevated postop troponin
2. Resulting from myocardial ischaemia (i.e. no evidence of a non-ischaemic aetiology), not requiring an ischaemic feature (i.e. no chest pain, no ECG change)
VISION studies (Vascular Events in Noncardiac Surgery Patients Cohort Evaluation) demonstrated that severity of MINS strongly associated with 30-day mortality after NCS.
hs-cTnT
<20ng/L ~ 0.5% 30 day mortality
20-64ng/L ~3% 30 day mortality
65-999 ng/L ~9% 30 day mortality
>1000ng/L ~30% 30 day mortality
Whilst VISION trial identified MINS in at risk patients, the question now becomes what interventions are available to prevent this complication?
22.1 A 45-year-old man presents on the day of surgery for an elective inguinal hernia repair. He is well
but is noted to be mildly jaundiced. He takes simvastatin for hyperlipidaemia and has no other medical history. He consumes about three standard drinks of alcohol per day and does not smoke. He briefly experimented with illicit drugs more than ten years ago. His laboratory results show: (supplied) The most likely diagnosis is
Normal electrolytes
ALP 85 N
ALT 31 N
AST 31 N
GGT 15 N
Urea 10 [4-9]
Creatinine 103 N
Total protein 74 N
Albumin 40 N
BSL 4.2 N
Bilirubin 29 [0-20]
Conjugated 5
Unconjugated 24
A. Fatty liver
B. Hepatitis
C. Cholestasis
D. Gilbert syndrome
E. Drug induced
Gilberts
Gilbert’s syndrome is a benign genetic condition that commonly presents as incidental
hyperbilirubinaemia or painless jaundice.
It is relatively common with a population frequency of approximately 2–10%.
Gilbert’s syndrome is caused by defective bilirubin clearance by the hepatic conjugating enzyme UDP-glucuronosyltransferase
https://www.rcpa.edu.au/getattachment/8b9a8acf-f7f5-4088-951c-3f65f0c2f8fe/Interpreting-liver-function-tests.aspx
22.1 A man has symptomatic carbon monoxide poisoning. His pulse oximetry (SpO2) and arterial blood gas (PaO2) would be expected to show
a. Normal SpO2, Normal PaO2
b. Normal SpO2, reduced PaO2
c. Reduced SpO2, normal PaO2
d. Reduced SpO2, reduced PaO2
a. Normal SpO2, Normal PaO2
ABG
HbCO (elevated levels are significant, but low levels do not rule out exposure) lactate (tissue hypoxia) PaO2 should be normal, SpO2 only accurate if measured (not calculated from PaO2) MetHb (exclude)
https://litfl.com/carbon-monoxide-poisoning/
During a routine preoperative examination of a patient’s heart, you note exaggerated splitting of the second heart sound with inspiration. This is characteristically heard in
A. Aortic Reguritation
B. HOCM
C. Left bundle branch block
D. Mitral Stenosis
E. Pulmonary Stenosis
E. Pulmonary Stenosis
DERANGED PHYSIOLOGY:
Splitting of the first heart sound
Right bundle branch block can produce a split first heart sound - because the contraction of the right ventricle is delayed- the conduction occurs via the left ventricle rather than the bundle of His- and thefore the closure of the tricuspid valve occurs after a substantial delay.
Atrial septal defect can result in a fixed split of the first heart sound
Splitting of the second heart sound
It is normal for this sound to be split. The high pressure in the systemic circulation slams the aortic valve shut rather abruptly, almost angrily. In contrast, low pressure of the pulmonary circulation tends to close the pulmonary valve gently, and therefore the pulmonary component of the second heart sound (P2) is usually delayed by about 20-30 milliseconds.
It is also normal for increased right ventricular filling to cause a widening of the split. The more blood in the RV, the longer it takes to eject, and therefore the greater the delay until pulmonary valve closure.
n the spontaneously breathing patient, the delay is greatest during inspiration. Naturally, in the patient ventilated with positive pressure the delay is greatest during expiration (positive pressure being a barrier to diastolic filling).
Increased normal splitting of S2
Anything that delays the end of right ventricular systole can cause this sort of picture.
Right bundle branch block - the delay in conduction via the left ventricle causes a delay in right ventricular contraction, and therefore a delay in pulmonary valve closure. The S1 will also be split.
Ventricular septal defect - because the right ventricle receives a large volume load directly from the left ventricle, and therefore takes longer to complete its systolic contraction.
Pulmonary valve stenosis - because the right ventricle takes longer to empty though a narrowed valve
Mitral regurgitation- not because right ventricular contraction is delayed, but because left ventricular contraction is shortened (as the LV empties in both the aortic and the atrial directuion, systole is over very quickly).
Fixed splitting of S2
Atrial septal defect - the atria, joined by a gaping hole in their seput, act as one atrium. The result is a reasonably equal distribution in volume betweent the right and left atrium. This way, both sides of the circulation share the same diastolic filling pressure. Dragging more volume into the right atrium with respiratory activity will not cause an inequality of ventricular filling (between the right and left ventricles) because the venous return will be “shared”.
Reversed splitting of S2
In this situation, P2 occurs before A2, and splitting widens during expiration (or inspiration in the mechanically ventilated patient). This only happens if the conduction to the left ventricle is delayed, or if the left ventricle is massively volume overload (and the right ventricle is not).
Left bundle branch block - the left ventricle depolarises after the right ventricle, and A2 is delayed
Aortic stenosis - the left ventricle empties slowly though a narrow valve
Large patent ductus arteriosus - the left ventricle receives a backflow of blood from the aorta, which causes it to become volume-overloaded
21.1 A 45-year-old man has the following results on his blood biochemistry testing (Liver function tests shown). The most likely diagnosis is
a. Cholecystitis
b. Metastatic liver disease
c. Hepatitis C
d. Chronic liver disease
e. Paracetamol toxicity
a. Cholecystitis
Example and explanation taken from RACGP:
The raised AlP relative to Alt suggests cholestasis and the high GGt confirms liver origin. The mild hyperbilirubinaemia confirms the clinical impression of jaundice. Biliary disease is highly likely with gallstones the most likely differential diagnosis. however, this clinical picture may also occur in drug reactions or infiltrative conditions. After a careful history, abdominal ultrasound is the most appropriate next investigation.
22.1 A 45-year-old man presents on the day of surgery for an elective inguinal hernia repair. He is well
but is noted to be mildly jaundiced. He takes simvastatin for hyperlipidaemia and has no other medical history. He consumes about three standard drinks of alcohol per day and does not smoke. He briefly experimented with illicit drugs more than ten years ago. His laboratory results show: (supplied) The most likely diagnosis is
Normal electrolytes
ALP 85 N
ALT 31 N
AST 31 N
GGT 15 N
Urea 10 [4-9]
Creatinine 103 N
Total protein 74 N
Albumin 40 N
BSL 4.2 N
Bilirubin 29 [0-20]
Conjugated 5
Unconjugated 24
A. Fatty liver
B. Hepatitis
C. Cholestasis
D. Gilbert syndrome
E. Drug induced
Gilberts
Gilbert’s syndrome is a benign genetic condition that commonly presents as incidental
hyperbilirubinaemia or painless jaundice.
It is relatively common with a population frequency of approximately 2–10%.
Gilbert’s syndrome is caused by defective bilirubin clearance by the hepatic conjugating enzyme UDP-glucuronosyltransferase
https://www.rcpa.edu.au/getattachment/8b9a8acf-f7f5-4088-951c-3f65f0c2f8fe/Interpreting-liver-function-tests.aspx
22.1 A man has symptomatic carbon monoxide poisoning. His pulse oximetry (SpO2) and arterial blood gas (PaO2) would be expected to show
a. Normal SpO2, Normal PaO2
b. Normal SpO2, reduced PaO2
c. Reduced SpO2, normal PaO2
d. Reduced SpO2, reduced PaO2
a. Normal SpO2, Normal PaO2
ABG
HbCO (elevated levels are significant, but low levels do not rule out exposure) lactate (tissue hypoxia) PaO2 should be normal, SpO2 only accurate if measured (not calculated from PaO2) MetHb (exclude)
https://litfl.com/carbon-monoxide-poisoning/
20.2 The flow volume loop is most consistent with (Flow-volume loop shown)
a) Variable intra-thoracic obstruction
b) Variable extra-thoracic obstruction
c) Lower airway obstruction
d) Fixed upper Airway obstruction
e) Mixed pattern
d) Fixed upper Airway obstruction
Fixed upper airway obstruction (can be intrathoracic or extrathoracic): flow limitation and flattening are noted in both the inspiratory and expiratory limbs of the flow-volume loop.
20.1 The flow volume loop is most consistent with
a) Variable intra-thoracic obstruction
b) Variable extra-thoracic obstruction
c) Fixed large airway
d) Restrictive lung pattern
e) Mixed pattern
b) Variable extra-thoracic obstruction
23.1 The parameter that changes most with increasing age in the otherwise normal lung is the
a. Closing capacity
b. Residual volume
c. FRC
d. Lung capacity.
a) Closing capacity
see graph in Millers
20.2 The flow volume loop is most consistent with (Flow-volume loop shown)
a) Variable intra-thoracic obstruction
b) Variable extra-thoracic obstruction
c) Lower airway obstruction
d) Fixed upper Airway obstruction
e) Mixed pattern
a) Variable intra-thoracic obstruction
Dynamic (or variable, nonfixed) intrathoracic obstruction: flow limitation and flattening are noted on the expiratory limb of the loop.
23.1 An absolute contraindication to skin prick testing for the diagnosis of allergies is
a. Pregnancy
b. Severe dermatographia
c. Concurrent antihistamine use
d. Concurrent beta blocker
e. Asthma
b) severe dermatographia
21.1 A 50-year-old man is seen prior to his hip revision surgery. His blood results are
Hb 110 (130-170 normal range)
Ferritin 31 (30-100 range)
Transferrin saturation 21% (normal 20-80)
CRP 10 (0.1-10 normal)
The most likely diagnosis is
a) iron deficiency anaemia
b) anaemia of chronic disease
c) anaemia of chronic inflammation
d) anaemia of chronic inflammation with iron deficiency
e) megaloblastic anaemia
Anaemia of chronic inflamation with iron deficiciency
21.2 In pulmonary function testing the presence of airflow limitation is defined by a post- bronchodilator FEV1/FVC ratio less than
a) 0.5
b) 0.6
c) 0.7
d) 0.8
c) 0.7
21.2 Of the following, the LEAST likely cause of high anion gap metabolic acidosis is
a) Pancreatic fistula
b) DKA
c) Cardiac failure
d) Anti-retroviral
e) Methanol
pancreatic fistula
-> should cause NAGMA
HAGMA:
Lactate
Toxins
Ketones
Renal failure
NAGMA
Chloride
Addison’s, adrenal insuffiency, acetazolamide
GI loss (pancreatic fistula)
Extra: RTA
Anion gap:
- Anion Gap = Na+ – (Cl- + HCO3-)
- The Anion Gap (AG) is a derived variable primarily used for the evaluation of metabolic acidosis to determine the presence of unmeasured anions
- The normal anion gap is assumed to be 12, and the normal HCO3 is assumed to be 24
Delta ratio:
- can check delta ratio in the presence of a high anion gap metabolic acidosis (HAGMA) to determine if it is a ‘pure’ HAGMA or if there is coexistant normal anion gap metabolic acidosis (NAGMA) or metabolic alkalosis.
22.1 A 65-year-old man presents to the preadmission clinic two weeks prior to his total knee replacement. His blood results include haemoglobin 100 g/L, ferritin 20 μg/L and normal C-reactive protein. The best course of action is to
a. Proceed
b. EPO and iron
c. Iron tablet and delay 3 months
d. Iron transfusion and proceed
e. PRBC
Postpone 3 months and give oral iron
20.2 Severe obstructive sleep apnoea in adults is confirmed if during polysomnography if the apnoea/hypopnea index (AHI) is greater than or equal to
A) 10
B) 20
C) 30
D) 40
E) 50
C) 30
22.1 A 45-year-old woman is reviewed in the preadmission clinic. She is scheduled to undergo a microwave endometrial ablation for menorrhagia in one week’s time. Her preoperative laboratory investigations include the following blood results (full blood examination and iron studies shown).
The most appropriate course of action would be to
a. Proceed
b. Iron IV then proceed
c. Transfuse 2 RBC intraop
d. Use cell saver intraop
e. Defer and refer to haematology for further Ix
22.1 A 72-year-old female smoker with hypertension presents to the emergency department with a wrist fracture after a fall. She has been increasingly tired and confused over the previous week. Her serum and urine electrolytes are (supplied). The most likely diagnosis is
(Low K, low Na, Normal Ur and Cr, Ur sodium <10mmol/L)
a. SIADH
b. Addison’s
c. Diuretic
Uncertain
SIADH:
1. hypotonic hyponatraemia
2. urine osmolality > plasma osmolality (<275mOsm/kg) (i.e. concentrated urine despite hypotonic blood)
3. urinary Na+ > 20mmol/L
4. normal renal, hepatic, cardiac, pituitary, adrenal and thyroid function
5. euvolaemia (absence of hypotension, hypovolaemia, and oedema)
6. correction by water restriction
Addison’s
Hypo natraemia
HYPER kalaemia
Hypo glycaemia
Acidosis
Diuretics
Hypo natraemia
Hypo kalaemia
High urinary Na and K
https://www.derangedphysiology.com/files/Electrolyte%20Disturbance.pdf
JAMA article on hyponatraemia
https://emergencymed.org.il/wp-content/uploads/2022/08/jama_adrogu_2022_rv_220011_1657919726.49616.pdf
20.2 The flow volume loop is most consistent with (Flow-volume loop shown)
a) Variable intra-thoracic obstruction
b) Variable extra-thoracic obstruction
c) Lower airway obstruction
d) Restrictive lung pattern
e) Mixed pattern
c) Lower airway obstruction
Peripheral or lower airways obstruction: expiratory limb demonstrates concave upward, also called “scooped-out” or “coved” pattern.
22.2 The curve labelled ‘b’ is most likely to represent the flow–volume loop of a patient with
a) Asthma
b) Post lung transplant
c) Pulmonary fibrosis
d) Tracheal stenosis
e) VC palsy
Tracheal stenosis
23.1 The following pressure-volume loop is displayed on your ventilator screen. The
shape of this loop indicates
a. Over-expansion
b. Under-expansion
c. Normal ventilation
d. PEEP too high
e. PEEP too low
a) over-expansion
The first graphic (loop a) shows the pattern of a typical pressure-volume loop, which rises in a counterclockwise direction until forming a complete loop. It also displays inflection points, which display rapid changes to the slope of the limb.
The lower inflection point (LIP) occurs due to the opening of collapsed alveoli, resulting in a sharp increase in volume. The upper inflection point (UIP) occurs near the end of inspiration when more pressure leads to only a minimal increase in volume.
The second graphic (loop b) displays how overdistension and hysteresis appear on a pressure-volume loop. Overdistention occurs when the lungs receive too much volume or pressure and can result in injury. Hysteresis refers to lung tissue that behaves differently on inspiration and expiration.
In other words, it takes more energy for the lungs to inflate than it does to deflate. Therefore, hysteresis on a pressure-volume loop refers to the space between the inspiratory and expiratory limbs. When the patient’s lung compliance or airway resistance changes, so will the hysteresis and, thus, the appearance of the loop.
Note: A pressure-volume loop under normal conditions should resemble the shape of a football (American). A curve with a flat appearance indicates decreased lung compliance. A steep curve, on the other hand, indicates increased lung compliance. A wide curve indicates increased airway resistance, whereas the opposite is true if the loop appears more narrow.
https://www.respiratorytherapyzone.com/ventilator-waveforms/#:~:text=Note%3A%20A%20pressure%2Dvolume%20loop,hand%2C%20indicates%20increased%20lung%20compliance.
20.1 70 year old patient for revision THR, in clinic 10 days prior
Hb 110
Ferritin 51
CRP 10
What should you do?
a Transfuse 2u pRBC
b Give oral iron therapy and continue with surgery
c Give oral iron therapy and defer surgery for 6 weeks
d Give IV iron
e Do nothing
c Oral iron and defer
or
d give IV iron
- most assume its IV iron and proceed but
- Assuming IDA and raised CRP then iron therapy but
‘deferable’ surgery? then oral and come again in 6 weeks
if not deferrable then IV iron - surely a revision THR is deferable?? - If give IV iron and defer was an option I would choose that one, it would allow assessment of inflammatory process and to confirm Hb and ferritin are at an acceptable level
International consensus statement on the peri-operative management of anaemia and iron deficiency
https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.13773
However, many patients will not respond to oral iron, especially those with functional iron deficiency and chronic illness or infection and those with ongoing blood loss 15, 25. Others will not tolerate oral iron due to gastro-intestinal side-effects. Once oral iron has been commenced, the Hb should be measured again, at least 4 weeks before surgery. In the absence of an increased Hb or if the patient is intolerant, i.v. iron is the preferred replacement route. If surgery is planned in less than 6 weeks time, i.v. iron may also be the most effective option.
22.2 A raised (> 140% predicted) single-breath diffusing capacity of the lung for carbon monoxide (DLCO) can be caused by
a. Emphysema
b. COPD
c. interstitial lung disease
d. Asthma
e. Sarcoidosis
d. Asthma
What are the causes of an elevated DL CO ?
The causes of an elevated DLCO are numerous, but is most commonly caused by asthma and obesity (increased pulmonary blood flow). Pulmonary hemorrhage is an additional important cause.
https://www.atsjournals.org/doi/pdf/10.1513/AnnalsATS.201605-355CC
22.1 Anaesthesia-induced rhabdomyolysis differs from malignant hyperthermia in that it is NOT
a. Reduced myoglobinuria
b. Less increase in ETCO2
c. Less muscle rigidity
a. Reduced myoglobinuria
weird double negative question, answers don’t quite fit grammatically, however
- There is NOT reduced myoglobinuria with AIR compared to MH (both have myoglobinuria)
- There IS less increase in ETCO2
- There IS less muscle rigidity
Anesthesia-induced rhabdomyolysis or malignant hyperthermia: is defining the crisis important?
College library drop “is defining the crisis important?” from search
https://onlinelibrary-wiley-com.ezproxy.anzca.edu.au/doi/full/10.1111/pan.13130?sid=worldcat.org
