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MRCS Part B - Paul Edit > Miscellaneous 1 > Flashcards

Miscellaneous 1 Flashcards

1
Q

What are the 4 main risks of IV contrast administration?

A

Anaphylaxis/allergy Renal impairment Lactic acidosis (secondary to metformin) Extravasation

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2
Q

What is the annual background radiation in Sieverts?

A

2.4mSV per year

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3
Q

What frequency would be used to look at deep structures in ultrasound?

A

Lower frequency

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4
Q

What is Duplex US?

A

Allows for velocity of a substance e.g. blood to be determined, assessing flow patters of blood within a vessel

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5
Q

Why is ultrasound not good at looking at bowel?

A

Waves don’t travel well through gas and become distorted resulting in significant artefact

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6
Q

What part of the adrenal is affected primarily in Addison’s disease?

A

Adrenal cortex - destruction via autoantibodies

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7
Q

4 causes of primary hypoadrenalism?

A

TB Bilateral adrenalectomy Metastatic Ca deposits WHFS (menigococcal sepsis)

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8
Q

What is the biochemical difference between primary and secondary hypoadrenalism? Why?

A

In secondary, e.g. due to long term steroids, aldosterone secretion is maintained and fluid/electrolyte disturbances less marked (aldosterone secreted in relation to RAS)

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9
Q

6 functions of glucocorticoid hormones?

A

Maintenance of immune system Stimulate gluconeogenesis Stimulate glycogenolysis Stimulate lipolysis Mobilise amino acids Inhibit glucose uptake by muscles

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10
Q

How would you manage adrenal insufficiency peri-operatively?

A

Pre-op assessment, do first on list Give usual AM medications and hydrocortisone IV at induction Depending on procedure and post-op recovery, double hydrocortisone dose for 24-48 hours before established back on usual oral medications Local hospital protocol

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11
Q

Management of Addisonian crisis?

A

ABCDE Correct hypoglycaemia IV Fluid resuscitation and correct electrolyte abnormalities Hydrocortisone 200mg stat then 100mg QDS Fludrocortisone 0.1mg OD Look for precipitants

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12
Q

Typical starting regime of steroids for primary adrenal insufficiency?

A

Hydrocortisone 20mg / 10mg per day Fludrocortisone 0.05-0.1mg OD

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13
Q

How is cardiopulmonary exercise testing performed?

A

Ramped protocol test using cycle ergometer, with cardiac monitoring attached and soft rubber facemask. Cycle for 3 mins unloaded then gradually increase load until symptomatic or after 10 minutes

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14
Q

What key piece of surgically relevant information does cardiopulmonary exercise give?

A

Anaerobic threhold, occuring at 47-64% of VO2Max - roughly equating to physiological reserve and risk of surgery

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15
Q

What is the relevance of VO2Max to surgical risk?

A

Over 20ml/kg/min = no increased risk 10-15ml/kg/min = increased risk Less than 10ml/kg/min = very high risk

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16
Q

How accurate is pulse oximetry to true HbSat level? When is it less reliable/not useful?

A

Accurate within 2%, however less at working out severity of hypoxia or in vasoconstriction or carbon monoxide poisoning. Also can’t provide information on alveolar hypoventilation

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17
Q

What 3 syndromes may phaeochromcytoma occur as part of?

A

NF1 VHL MEN2

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18
Q

Diagnosis of phaeochromocytoma is made by?

A

24 hour urine collection of catecholamine hormones and metabolites Plasma metanephrines

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19
Q

Imaging options for phaeochromoctyoma?

A

CT - contrast historically said to trigger crisis MRI I-MIG - radionucleotide scan to localise lesion and detect extra-adrenal lesions

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20
Q

Procedure of choice for phaeochromocytoma?

A

Laparosopic adrenalectomy

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21
Q

What is the biggest concern/operative risk for phaeochromcytoma surgery?

A

Hypertensive crisis - manage by ensuring alpha (phenoxybenzamine) then beta blockade

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22
Q

What is the order of blockade required in surgical management of phaeochromocytoma? What is used?

A

Alpha blockade first via phenoxybenzamine Then beta blockade

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23
Q

What BP changes can occur during phaeochromocytoma surgery? When?

A

Changes can occur during manipulation of gland (hypertensive) Hypotension may occur when adrenal veins secured

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24
Q

What forces govern the accumulation of fluid in the interstitium? What makes these up?

A

Starling’s Forces - capillary pressure, plasma colloid oncotic pressure vs interstitial fluid pressure and interstitial fluid osmotic pressure

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25
Q

What proportion of body fluid is interstitial?

A

1/6

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26
Q

What key part of plasma is not present in interstitial fluid? Why?

A

Protein - high molecular weight precludes filtration

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27
Q

How is excess interstitial fluid usually returned to vsacular system?

A

Lymphatics

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28
Q

4 factors favouring development of oedema (excess fluid in extracellular space)?

A

Increased hydrostatic pressure Hypoprotinaemia - low plasma oncotic pressure Venous/lymphatic obstruction Endothelial changes in capillary bed - acute inflammation or sepsis

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29
Q

Where is respiratory rhythm generated? What are these?

A

2 groups of neurones in medulla - dorsal inspiratory and ventral repiratory groups

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30
Q

Where do respiratory groups in medullar receive afferents from?

A

Cortex, pons, aortic and carotid bodies and lung (vagal nerve)

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31
Q

What is respiratory drive primarily influenced by? How?

A

PaCO2 CO2 generates hydrogen ions in CNS which stimulate central chemoreceptors - in periphery these are aortic and carotid bodies

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32
Q

How do catecholamine based inotropes work?

A

Beta adrenergic receptors to increase intracellular (myocyte) cAMP and mobilise calcium, or inhibit neuronal resorption of NA/Ad

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33
Q

What receptors do inotropes work on generally?

A

Beta 1 agonism directly on myocardium

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34
Q

When are inotropes best used?

A

Depresion of cardiac function to increase ouput and improve blood pressure, to in turn improve myocardial perfusion

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35
Q

How do vasoconstrictors/’pressors’ work? Receptors?

A

Alpha receptor agonism to act on peripheral tissues and cause constriction

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36
Q

Why are central lines required for inotropes?

A

Require MAP and CVP monitoring Direct entry to high flow system Reliable dosing

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37
Q

What is the difference in receptors between adrenaline and norad? How does this vary?

A

Adrenaline primarily beta 1 - cardiac, although is an alpha agonist at high doses Norad is alpha 1 agonist - pressor

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38
Q

How does dopamine work?

A

D1+2 receptor mediated renal and mesenteric vascular dilatation (and D2 - inhibits NA release) and beta 1 agonism at high doses to increase CO - good for cardiac issues and myocardial perfusion

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39
Q

How does dobutamine work?

A

Predominantly beta 1 agonism - weak beta 2 and alpha agonism

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40
Q

Phosphodiesterasae inhibitors - example and mechanism of action?

A

Milrinone Acts directly on cardiac phosphodiesterase to increase cardiac output

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41
Q

What effect do B2 agonism have?

A

Vasodilation

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42
Q

What does ABO incompatibility result in following transplant?

A

Early hyperacute organ rejection due to pre-existing antibodies

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43
Q

How does HLA matching impact on transplant outcomes? Which are most important clinically?

A

HLA A B C and DR are most important - greater number of mismatches the worse the outcome; T lymphocytes recognise antigens bound to HLA molecules, activate and then direct clonal response against the antigen

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44
Q

How long do fractures involving cancellous bone take to unite? How does this differ in cortical bone e.g. tibia, femur?

A

6 weeks Cortical takes 4-6 months (6 for femur)

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45
Q

Describe this image?

A

Displaced, comminuted fractured humerus with fracture callus surrounding site

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46
Q

What are the potential imaging modalities for suspected colorectal cancer? What is best?

A

Direct visualisation via colonoscopy is most sensitive and specific

Sigmoidoscopy

CT colonography

CT with faecal tagging

Barium enema

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47
Q

When would you perform an MRI for colorectal cancer?

A

If cancer below peritoneal reflection - MRI rectum

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48
Q

What is this and what does it show? What is the classic appearance?

A

Double contrast barium enema showing lesion of right colon

Classical apple core lesion suggesting colonic adenocarcinoma

49
Q

What is the treatment for colonic cancer generally? Alternatives?

A

Generally surgical resection as only shot at cure

Stents, bypass and diversion stomas are palliative adjuncts

50
Q

Why are colonic cancer surgeries chosen in the way they are?

A

Following lymphatic drainage, which follows arterial supply

51
Q

What chemotherapy may be offered post-resection for colonic cancer?

A

5FU and oxaliplatin

52
Q

What adjunct to surgery can be offered for rectal cancers and why?

A

Radiotherapy - as it is extraperitoneal

Often given neoadjuvant radiotherapy

53
Q

What is normal arterial pH and what does this correspond to?

A

7.35-7.45, corresponding to H+ ion concentration of 40nmol/L

54
Q

What is the main buffer system for pH? How does this work?

A

Bicarbonate present within blood, which can combine with hydrogen ions to form carbonic acid which then dissociates to CO2/H20

55
Q

What are the main sites of acid-base excretion and conservation? Outline these

A

Lung - changes in respiratory rate allow for retention/excretion of CO2

Kidneys - can retain bicarbonate short term, and increase H+ ion excretion longer term

56
Q

Outline how kidney manages acid-base balance?

A

PCT re-absorbs around 85% of filtered bicarbonate

Distal nephron secretes H+ ions into collecting duct, which are formed from carbonic acid dissociation in tubular cells

Result is excretion of H+ and retention of bicarb

57
Q

What is usual acid-base state of urine? How is this mediated?

A

pH5-6

Due to hydrogen ion excretion, buffered by e.g. ammonium ions

58
Q

What 6 things do ABG machines directly measure?

A

O2, CO2, pH, Na, K and Cl

59
Q

What is the difference between standard and regular bicarb?

A

Bicarbonate is that which is actually present at time of analysis

Standard bicarbonate is calculated by adjusting CO2 to 5.3kPa

60
Q

What is the anion gap and how is it calculated? Why is it useful?

A

AG = unmeasured anions - [Na + K] - [Bicarb + Cl]

Useful in metabolic acidosis as high AG suggests acid gain e.g. ketones, lactate vs normal AG which suggests bicarb loss

61
Q
A
62
Q

2 indications for cryoprecipitate?

A

Bleeding following massive transfusion

Haemophilia when factor concentrates not available

63
Q

How to manage bleeding from liver surface?

A

Try topical haemostatic agents

If not resolving, pack and remove 24 hours later

64
Q

Specific management of open fractures?

A

Take photo

Remove any obvious debris

Cover with soaked towel

Give broad spec antibiotics and tetanus toxoid

Prepare for theatre and consider specialist orthoplastic centre

65
Q

When and how should surgery be done for open fractures?

A

Ideally within 6 hours if possible with combined orthoplastic approach but do in daylight hours unless:

Immediate if vascular injury (consider CTA)

Within 12 hours if high velocity

Within 24 hours otherwise

66
Q

Is CVP affected in neurogenic shock? What about cardiac output?

A

Not primarily - unless concommitant hypovolaemia, which may be masked by nature of neurogenic shock (no tachycardia)

Cardiac output may be same or elevated

67
Q

At what level is neurogenic shock likely? Why?

A

T6 and above

Below this unlikely to cause sufficient sympathetic disruption

68
Q

What level of spinal cord injuries may be associated with bradycardia? Why?

A

T1 and above

Unopposed vagal activity on heart

69
Q

Management of neurogenic shock?

A

Vasopressor support e.g. NA on ICU with management of concomitant injuries

Often give fluids any way but will not work long term

Bradycardia may respond to atropine if present

70
Q

How much blood in pleura will blunt costophrenic angle on CXR? Problems with supine? Best scan for haemothorax?

A

400ml in pleural space

No meniscus on supine XR - hazy opacity

GAST scan better at detecting

71
Q

What is massive haemothorax usually due to?

A

Major vessel injury - hilar disruption

72
Q

Will parenchymal lesions cause massive haemothorax?

A

Not usually - low pressure and cease spontaneously

73
Q

Management of massive haemothorax?

A

Chest tube insertion

Thoracotomy

74
Q

What is biggest risk factor for tension pneumothorax? How is this seen in ventilated patients?

A

Penetrating chest injury plus mechanical ventilation

In ventilated patients presents as cardiovascular disturbance, subcutaneous emphysema and increasing O2 requirements

75
Q

6 CXR signs of tension pneumothorax?

A

Lung collapse towards hilum

Increased rib separation

Diaphragmatic depression

Increased thoracic volume

Ipsilateral heart border flattening

Contralateral mediastinal deviation

76
Q

Management of tension pneumothorax?

A

Immediate needle decompression (2ICS, MCL w 14-16G needle) + definite wide bore chest drain insertion

77
Q

Presentation, investigation and management of pyloric stenosis?

A

Presents aged 2-4 weeks with projectile vomiting, due to hypertrophy of circular muscles of pylorus

Diagnose via US/test feed

Ramstedt pyloromyomotomy

78
Q

What is the classical biochemical disturbance of pyloric stenosis? Why?

A

Hypochloraemic metabolic alkalosis with hypokalaemia

Because protracted vomiting causes hydrogen ion and chloride ion loss, increasing gastric production and H+/K+ pump. Also hypovolaemia and acidic urine

79
Q

How is acid produced in stomach? Explain the hypokalaemia in pyloric stenosis?

A

Parietal cells generate hydrogen and bicarbonate ions

H+ combines with chloride to form HCl whereas bicarbonate ions enter circulation

In kidney there is exchange between sodium and hydrogen ions - conserving sodium and excretion of hydrogen. As H+ loss progresses the kidney then exchanges sodium for K, resulting in loss of K

80
Q

Why is atelectasis seen post surgery and what is the significance of this?

A

Multiple reasons - especially abdominal surgery, pain post-op and inadequate analgesia causes underventilation and basal atelectasis

Significance is due to underventilation - risk of HAP

81
Q

4 ECG signs of PE?

A

Tachycardia - sinus, AF

S1Q3T3

RBBB

Signs of right heart strain

82
Q

Why may pain occur in pancreatic cancer? When?

A

Invasion of coeliac plexus - late on

83
Q

What is Trousseau’s sign?

A

Migratory superficial thrombophlebitis suggestive of pancreatitis

84
Q

What is CA19-9 and why is it used?

A

Carbohydrate antigen 19-9 used for monitoring (but not diagnosis) in pancreatic cancer

85
Q

2 side effects of Whipple’s procedure?

A

Dumping syndrome

Ulcers

86
Q

What does actual amount of oxygen transported in blood depend on?

A

Haemoglobin concentration

Haemoglobin O2 saturation

87
Q

What does globin bind to?

A

CO2 and H+ ions

88
Q

What is 2,3 DPG and what does it bind to?

A

2,3 diphosphoglycerate - binds to beta chains of globin; chronic anaemia causes raised 2,3 DPG

89
Q

How many oxygen molecules bind to each haemoglobin molecule?

A

4

90
Q

Discuss the oxygen dissociation curve? Why is it the shape it is?

A

Describes relationship between percentage of saturated Hb and partial pressure of oxygen in blood.

Shape is sigmoidal because when Hb binds with a single O2 molecule, it conformationally changes protein structure to facilitate binding of next molecule which is not dependent on Hb concentration

91
Q

What is the Bohr effect with relation to oxygen dissociation?

A

Shift in O2 dissociation curve to the right indicating reduction in oxygen affinity for Hb molecule, in metabolically more active tissue (and so facilitates oxygen release) - seen in high temp, high H+ concentration, high CO2 and high 2,3 DPG

92
Q

What is the Haldane effect?

A

Left shift of oxygen dissociation curve in circumstances of decreased oxygen delivery to tissues and so less metabolically active - O2 displaces CO2 from Hb. In low H+, low temp, low 2,3 DPG.

93
Q

7 things which cause left shift in O2 dissociation curve?

A

Low H+

Low temp

Low DPG

Low CO2

HbF

Methaemoglobin

Carboxyhaemoglobin

94
Q

Where are the main chemoreceptor centres modulating respiratory activity and what are they sensitive to?

A

Central chemoreceptors - central surface of medulla, sensitive to changes in CSF pH

Peripheral chemoreceptors - carotid bodies and aortic arch, sensitive to O2 levels

95
Q

How are central chemoreceptors stimulated? Where are they?

A

Stimulation via CO2 dissolution in CSF to carbonic acid and H+ ions, which stimulate receptors on medulla

96
Q

How are peripheral chemoreceptors stimulated with regards to respiration?

A

Bifurcation of carotids (bodies) and arch of aorta - fire more in response to reduced pO2, increased H+ and increased pCO2 in arterial blood

97
Q

In a well person, what is the single most important driver for increase in respiratory rate?

A

Increase in partial pressure of CO2

98
Q

There are 3 respiratory centres involved in respiration. Where are they and what do they?

A

Medullary respiratory centre - inspiratory (dorsal) and expiratory (ventral) neurones

Apneustic centre - lower pons - stimulates inspiration by activating and prolonging inhalation. Overriden by pneumotaxic centre to end inspiration

Pneumotaxic centre - upper pons - inhibits inspiration to fine tune respiratory rate

99
Q

What are the 2 main problems with laryngeal mask airways?

A

Potential for reflux of gastric contents because it doesn’t occlude trachea

Often not possible to use high pressure ventilation

100
Q

Advantages of LMA airway?

A

Easy to insert

Do not require paralysis

101
Q

What are tracheostomies used for? Why are they good?

A

Reduce work of breathing

Reduce anatomical dead space

Good for weaning intubated patients and facilitate awake ventilation

102
Q

5 main risks of ET intubation?

A

Damage to dentition

Accidental intubation of oesophagus

Damage to oropharynx or trachea

Single lung intubation

Pneumothorax formation with PPV

103
Q

What is the difference between paediatric and adult ET tubes other than size?

A

Paeds are uncuffed, adults are cuffed

104
Q

How to avoid intubation of oesophagus during ET intubation?

A

Training and familiarity with landmarks

Auscultation of chest and abdomen following intubation

Attaching end tidal CO2 monitor to circuit

105
Q

Describe this?

A

Intertrochanteric, displaced, angulated neck of femur fracture with comminution and separation of lesser trochanter

106
Q

General management of fractured neck of femur?

A

Combined orthogeriatric approach

Full trauma assessment and management of comorbidities

Fascia iliaca nerve block and analgesia

Surgery within 36 hours; delay of over 48 associated with increased morbidity and mortality

Early mobilisation post op and intensive physio

Manage underlying causes and treat osteoporosis - bisphosphonate and calcium

107
Q
A
108
Q

What forms does calcium exist in in body and what form of calcium is biologically active?

A

Protein bound

Complexed

Ionised - biologically active

109
Q

Where is the largest store of calcium in the body?

A

Skeleton

110
Q

Describe renal homeostasis of calcium and phosphate?

A

Normally calcium and phosphate freely filtered at glomerulus

Majority of calcium ions diffuse out of PCT, rest actively filtered in DCT

Majority of phosphate actively filtered at PCT, diffuse out in DCT

2% of filtered Ca excreted, 10% of filtered PO4 excreted

111
Q

3 actions of calcitonin?

A

Inhibits intestinal calcium absorption

Inhibits osteoclast activity

Inhibits renal tubular absorption of calcium

112
Q

4 actions of active form of vitamin D? What is it?

A

1,25 dihydroxycholecalciferol

Increases intestinal absorption of calcium

Increases renal tubular reabsorption of calcium

Increases osteoclastic activity

Increases renal phosphate reabsorption

113
Q

4 actions of PTH?

A

Increase bone resorption via activating osteoclasts

Increase renal tubular reabsorption of calcium

Increase synthesis of active form of vitamin D in kidney to increase gut absorption

Decrease renal phosphate reabsorption

114
Q

What markers are used in SOFA scoring? Where is it appropriate?

A

Used in ICU patients primarily

Pa/FiO2

Platelets (low)

Bilirubin

MAP/inotropes required

GCS

Creatinine

Urine output

115
Q

What 3 criteria are used in qSOFA?

A

Resp rate over 22

SBP under 100

GCS under 15

116
Q

Specific goals in treating sepsis in terms of CVP, MAP, UO, SVC O2 and lactate?

A

CVP 8-12mmHg

MAP over 65

UO over .5ml/kg/hour

SVC O2 conc over 70%

Normal lactate

117
Q

What haemodynamic parameters define septic shock?

A

MAP under 65 or lactate over 2 in presence of infective source

118
Q
A

MRCS Part B - Paul Edit (29 decks)

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