investigation Flashcards

Question

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

Answer 1

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

Answer 2

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/

Answer 3

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

Answer 4

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.

Answer 5

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

Answer 6

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/

Answer 7

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

Answer 8

c. myasthenia gravis

Answer 9

d) Von willebrand disease - autosomal dominant inheritance - may have normal or prolonged APTT, PT is normal *Haem A: X-linked recessive disorder; would expect prolonged aPTT, and normal PT *Haem B: X-linked recessive disorder; would expect normal aPTT and normal PT Up to date: Inheritance patterns — Most cases of VWD are transmitted as an autosomal dominant trait; this includes types 1 and 2B, and most types 2A and 2M. Baseline hemostasis assessment — Most patients will have a complete blood count (CBC) with platelet count and coagulation studies during the initial evaluation for excessive bleeding or bruising. ●Individuals with VWD generally have a normal CBC and a normal platelet count, with the exception of those with type 2B VWD, most of whom will have mild thrombocytopenia (eg, platelet count 100,000 to 140,000/microL). ●Individuals with VWD may have a normal or prolonged activated partial thromboplastin time (aPTT), depending on the degree of reduction of the factor VIII level. The prothrombin time (PT) is normal in VWD. Up to date: ●Hemophilia A – Inherited deficiency of factor VIII (factor 8 [F8]); an X-linked recessive disorder. ●Hemophilia B – Inherited deficiency of factor IX (factor 9 [F9]); also called Christmas disease; an X-linked recessive disorder. Laboratory findings — Hemophilia is characterized by a prolonged activated partial thromboplastin time (aPTT). However, the aPTT may be normal in individuals with milder factor deficiencies (eg, factor activity level >15 percent), especially in hemophilia B (factor IX deficiency), where even individuals with moderate disease may have a normal aPTT. In some individuals with hemophilia A, factor VIII levels may increase with stress, leading to a normalization of the aPTT or mis-categorization of factor levels and disease severity. In patients with hemophilia, the aPTT corrects in mixing studies, unless an inhibitor is present, which only applies to individuals who have received factor infusions or who have an autoantibody such as a lupus anticoagulant or an acquired factor inhibitor. Mixing studies that do not show correction of a prolonged aPTT suggest an alternative diagnosis such as an acquired factor inhibitor. The platelet count and prothrombin time (PT) are normal in hemophilia. Thrombocytopenia and/or prolonged PT suggest another diagnosis instead of (or in addition to) hemophilia. Measurement of the factor activity level (factor VIII in hemophilia A; factor IX in hemophilia B) shows a reduced level compared with controls (generally <40 percent). One exception is an individual with mild hemophilia A who undergoes testing when stressed or pregnant and has a falsely elevated factor level. If this is suspected, factor activity testing should be repeated under conditions of low stress. The plasma von Willebrand factor antigen (VWF:Ag) is normal in hemophilia. If VWF:Ag is reduced, this suggests the possibility of von Willebrand disease (VWD) rather than (or in addition to) hemophilia. Urinalysis is not done routinely, but if performed it may sometimes (but not always) show microscopic or macroscopic hematuria.

Answer 10

B. 29 PaCO2= 1.5 x 14 + 8 PaCO2= 21 + 8 PaCO2= 29 Winter’s formula: expected PaCO2 = [1.5 x (serum HCO3)] + [8±2] if PaCO2 lower, there is a concomitant primary respiratory alkalosis if PaCO2 higher, there is a concomitant primary respiratory acidosis

Answer 11

d) Pulmonary hypertension Normal spirometry + low DLCO Asthma: obstructive pattern and normal DLCO Obesity: restrictive pattern and normal DLCO Sarcoid: restrictive pattern and low DLCO

Answer 12

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.

Answer 13

Acromegaly IGF-2 is consistently elevated GH should be suppressed by glucose load in healthy pt. The continued elevation of GH despite glucose is suggestive of acromegaly

Answer 14

a. Proceed with lobectomy or pneumonectomy FEV1 surgical suitability: - >80% or >2l pneumonectomy ○ no further testing required - >80% or >1.5l lobectomy ○ no further testing required - <80% or <2l for pneumonectomy ○ -> calculate ppoFEV1 - <80% or <1.5l for lobectomy ○ -> perform DLCO and express as % of predicted DLCO ○ Saturations on air - ppoFEV1 < 40% and DLCO <40% = High Risk - ppoFEV1 >40% and DLCO >40% and SaO2 >90% = Average risk (no further testing)

Answer 15

b) Myasthenia Gravis

Answer 16

b) Variable extra-thoracic obstruction

Answer 17

a) Closing capacity see graph in Millers

Answer 18

a) Variable intra-thoracic obstruction Dynamic (or variable, nonfixed) intrathoracic obstruction: flow limitation and flattening are noted on the expiratory limb of the loop.

Answer 19

b) severe dermatographia

Answer 20

Anaemia of chronic inflamation with iron deficiciency

Answer 21

albumin ALBUMIN AND PHOSPHATE the normal anion gap depends on serum phosphate and serum albumin the normal AG = 0.2 x [albumin] (g/L) + 1.5 x [phosphate] (mmol/L) albumin is the major unmeasured anion and contributes almost the whole of the value of the anion gap. every 1g/L decrease in albumin will decrease anion gap by 0.25 mmoles a normally high anion gap acidosis in a patient with hypoalbuminaemia may appear as a normal anion gap acidosis. this is particularly relevant in ICU patients where lower albumin levels are common Effects of albumin: Anion gap may be underesitmated in hypoalbuminaemia, because if albumin decreased by 1g/L then the anion gap decreases by 0.25 mmol To overcome the effects of the hypoalbuminaemia on the AG, the corrected AG can be used which is AG + (0.25 X (40-albumin) expressed in g/L

Answer 22

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.

Answer 23

Postpone 3 months and give oral iron

Answer 24

d) Sarcoidosis Pulmonary hypertension: Normal spirometry + low DLCO Asthma: obstructive pattern and normal DLCO Obesity: restrictive pattern and normal DLCO Sarcoid: restrictive pattern and low DLCO

Answer 25

30ml/cm H2O 600/32-8+4 = 30 Static lung compliance (Cstat), mL/cm H2O = TV / (Plateau pressure (Pplat) – TotalPEEP) remembered parameters included PEEP = 8 and autop PEEP = 4 if actual answer states TotalPEEP= 8 then no need to add 4 to the calculation

Answer 26

e. Obstructive w/ reduced FEV1 Mucous narrowing airways = obstructive Parenchymal damage = restrictive Obstructive PFP remains the most common pulmonary function pattern in adult CF and is associated with -decrease FEV1 & FVC/FEV1 For patients with CF, an obstructive pattern is generally seen, with a decrease in forced expiratory volume in 1 s (FEV1), and forced vital capacity (FVC) to FEV1 ratio. https://academic.oup.com/bjaed/article/11/6/204/263786

Answer 27

Repeat d) Sarcoidosis Normal FEV1/FVC ratio = no obstruction Low FVC = restrictive pattern Low DLCO = interstitial lung disease Asthma and emphysema would have obstructive pattern. Myasthenia gravis would have normal DLCO Pulmonary HTN would have normal spirometry and low DLCO.

Answer 28

Answer: b. rocuronium anaphylaxis NB RadioAllergoabsorbentSpecificTesting is a serum test for specific IgE antibodies RAST morphine is both more sensitive and more specific than the RAST for individual NMBDs (due to reaction with quaternary ammonium) and is being used increasingly to determine NMBDs as cause of anaphylaxis. IKR! http://www.anzaag.com/anaphylaxis-management/testing-guidelines.pdf

Answer 29

b. von willebrand's disease - autosomal dominant inheritance - may have normal or prolonged APTT, PT is normal *Haem A: X-linked recessive disorder; would expect prolonged aPTT, and normal PT *Haem B: X-linked recessive disorder; would expect normal aPTT and normal PT REPEAT | vWD can have prolonged APTT or normal APTT. Haemophilias are X-linked

Answer 30

c) FEV1 43% In pulmonary function testing, a post-bronchodilator FEV1/FVC ratio of <0.70 is commonly considered diagnostic for COPD. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) system categorises airflow limitation into stages. In patients with FEV1/FVC <0.70: GOLD 1 - mild: FEV1 ≥80% predicted GOLD 2 - moderate: 50% ≤ FEV1 <80% predicted GOLD 3 - severe: 30% ≤ FEV1 <50% predicted GOLD 4 - very severe: FEV1 <30% predicted.

Answer 31

b) Alcoholic liver disease - AST>ALT In hepatitis and paracetamol toxicity would expect ALT>AST. In cholecystitis, would expect a cholestatic picture with raised conjugated bilirubin and raised GGT/ALP. LITFL: Overall analysis of Liver Function Tests (LFT) Transaminitis: Aminotransferases (AST, ALT) - Generally associated with hepatocellular damage - Generally not associated with cholestasis Ratio of AST and ALT can be useful in differential ALT is more specific for liver damage than AST AST: ALT =1 -> Associated with ischaemia (CCF and ischaemic necrosis and hepatitis) AST: ALT >2.5 -> Associated with Alcoholic hepatitis -> Alcohol induced deficiency of pyridoxal phosphate AST: ALT <1 -> High rise in ALT specific for Hepatocellular damage -> Paracetamol OD with hepatocellular necrosis -> Viral hepatitis, ischaemic necrosis, toxic hepatitis -> Elevation with cholestasis (ALP, GGT) ALP – primarily associated with cholestasis and malignant hepatic infiltration Marker of rapid bone turnover and extensive bony metastasis GGT – sensitive to alcohol ingestion Marker of hepatocellular damage but non-specific Sharpest rise associated with biliary and hepatic obstruction

Answer 32

b) 90 PAO2: 0.4 (760 - 47) - 48/0.8 = 285 - 60 = 225mmHg 225 - 135 = 90mmHg.

Answer 33

Hereditary spherocytosis. Auto-haemolytic, intraplenic haemolysis. High reticulocyte count (6-20%) (normal range 0.5-2%)

Answer 34

renal tubular acidosis-> NAGMA HAGMA: Causes CATMUDPILES - CO/CN - Alcoholic ketoacidosis/ starvation ketoacidosis - Toluene (paint thinners) - Metformin/Methanol - Uraemia - DKA - Pyroglutamic Acidosis/paracetamol/ phenformin/propylene glycol/paraldehyde - Iron/ Isoniazid - Ethylene glycol (anti-freeze) - Salicylic Acid NAGMA: Causes CAGE: - Chloride - Acetazolamide and Addison's - GI causes (vomiting, diarrhoea, fistula) Extras: RTA

Answer 35

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

Answer 36

c) Lower airway obstruction Peripheral or lower airways obstruction: expiratory limb demonstrates concave upward, also called "scooped-out" or "coved" pattern.

Answer 37

E. 100 mcg/L ?? < 30mcg/L < 100mcg/L IF CRP > 5 and/or Transferrin saturation < 20 https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.13773#:~:text=Recommendations%20for%20best%20clinical%20practice,-Physicians%20should%20consider&text=The%20presence%20of%20anaemia%20should,identification%20of%20absolute%20iron%20deficiency.

Answer 38

Tracheal stenosis

Answer 39

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.

Answer 40

Category GFR ml/min/1.73 m2 Terms G1 ≥90 Normal or high G2 60-89 Mildly decreased* G3a 45-59 Mildly to moderately decreased G3b 30-44 Moderately to severely decreased G4 15-29 Severely decreased G5 <15 Kidney failure Assign Albuminuria category as follows: Albuminuria categories in CKD Category ACR (mg/g) Terms A1 <30 Normal to mildly increased A2 30-300 Moderately increased* A3 >300 Severely increased** Abbreviations: ACR, albumin-to-creatinine ratio; CKD, chronic kidney disease. *Relative to young adult level. **Including nephrotic syndrome (albumin excretion ACR >2220 mg/g) **Collectively referred to as “CGA Staging” REPEAT

Answer 41

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.

Answer 42

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

Answer 43

b) Pulmonary hypertension Up to date: Overview of pulmonary function testing in adults Diffusing capacity — Measurement of the single-breath diffusing capacity for carbon monoxide (DLCO; also known as transfer factor or TLCO) is quick, safe, and useful in the evaluation of restrictive and obstructive lung disease, as well as pulmonary vascular disease. The technique and interpretation are discussed separately. In the setting of restrictive disease, the diffusing capacity helps distinguish between intrinsic lung disease, in which DLCO is usually reduced, and other causes of restriction, in which DLCO is usually normal. In the setting of obstructive disease, the DLCO helps distinguish between emphysema, in which it is usually reduced, and other causes of chronic airway obstruction, like asthma or chronic bronchitis, where it is usually normal. The DLCO is also used in the assessment of pulmonary vascular disease (eg, thromboembolic disease, pulmonary hypertension), which typically causes a reduction in DLCO in the absence of significant restriction or obstruction

Answer 44

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

Answer 45

HCO3- is derived from pCO2 and pH Base excess is derived from pH SaO2 is derived from oxyHb and Hb Source LITFL

Answer 46

b) IgE mediated (i.e. anaphylaxis) rocuronium allergy Morphine RAST is most sensitive (88%) and specific (100%) test for NMBD as cause of anaphylaxis (quaternary ammonium epitope)

Answer 47

d) Pulmonary haemorrhage Rewording of 21.2 Question Won't increase in Myasthenia Gravis Causes of HIGH value include: Asthma Left-right intracardiac shunt polycythaemia Pulmonary haemorrhage Obesity - Dlco will increase but kco will not

Answer 48

24hrs Oxford handbook

Answer 49

a) Iron transfusion Iron infusion (ferric carboxymaltose) – can cause renal wasting of phosphate resulting in severe hypophosphataemia Vitamin D deficiency and hyperparathyroidism can also cause hypophosphataemia. Vitamin D deficiency would result in low calcium whereas hyperparathyroidism would result in hypercalcaemia. Fanconi syndrome: rare defect of proximal tubule leading to decreased reabsorption -> results in hypokalaemia, hypophosphataemia, hyperchloraemic metabolic acidosis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6689119/