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20/6 Week Learning Points > 21/6 > Flashcards

21/6 Flashcards

1
Q

Describe protamine and its desired effects

A

Protamine is a polycationic peptide that binds to heparin to form a stable ion pair without anticoagulation activity.

Ionic complex is removed by reticuloendothelial system.

Returns ACT to baseline.
Can have weak anticoagulation effect at large doses

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2
Q

Describe the adverse effects of protamine

A

Type 1 - hypotension from histamine release. Avoid by slow injection

Type 2 - anaphylactic reaction. IgE or anaphylactoid

Type 3 - catastrophic pulmonary vasoconstriction from activation of heparin-protamine complex with leucocyte aggregation or arachidonic acid pathway released TXA

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3
Q

What is the normal range of activated clotting time?

A

ACT 70-120s

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4
Q

What is the MoA of gabapentinoids?

A

Binds to the alpha2 delta subunit of VG Ca Channel on the presynaptic membrane -> reduces glutamate release and decreases activation of NMDA receptors

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5
Q

Describe the side effects of gabapentin

A

Sedation, dizziness, withdrawal seizures

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6
Q

What is the MOA of paracetamol

A

COX inhibitor centrally -> inhibits PG synthesis in CNA

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7
Q

How many lung segments are there?

A

10 in right lung (3 upper, 2 middle, 5 lower)

  • Upper: apical, posterior, anterior (APA)
  • Middle: medial, lateral
  • Lower: add basal to the five segments above (apical basal)

9 in left lung (5 upper, 4 lower lobes)

  • Upper: apical, posterior, anterior, inferior division superior and inferior.
  • Lower: apical, anterior/lateral/posterior basal
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8
Q

What is the clinical diagnosis of inadequate reversal from NMB?

A

tidal volume <5ml/kg, vital capacity <20ml/kg, inspiratory force <40cmH2O, head lift <5s, hand grip <5s, sustained jaw clench.

Only sensitive for <50% receptor occupancy

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9
Q

Describe ToF

A

4 supra maximal stimuli over 2 secs, detection of fade, Ratio of >0.9 is adequate reversal.

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10
Q

Describe double burst stimulus

A

2 short bursts of 50Hz tetanus (3 impulses) separated by 750ms, more accurate for fade, able to detect up to 60% receptors occupancy.

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11
Q

How can one avoid increase in PVR under GA?

A

Blunt SNS response on laryngoscopy, which can increase PVR

Avoid nitrous
Avoid hypercapnia and acidosis
High FiO2
Optimal ventilation

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12
Q

What drugs can lower PVR

A

GTN, inhaled nitric oxide, inhaled prostacyclin (iloprost), milrinone, vasopressin

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13
Q

What is vasopressin

A

Vasopressin is a nonapeptide produced in the supra-optic and paraventricular nuclei of hypothalamus and stored in the posterior pituitary

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14
Q

Describe the action of vasopressin

What are the analogues?

A

V1 - vasoconstriction
V2 - insertion of aquaporin to collecting duct, increases plasma VWF and factor VIII
V3 - found mainly in pituitary

Vasopressin, DDAVP, terlipressin

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15
Q

Describe the use of vasopressin in the peri-op setting

A

Bleeding - DDAVP has 1500x VC activity, increases vWF by 4x, dose 0.3microg/kg

Variceal bleeding - terlipressing on V1, portal VC, also useful for hepatorenal syndrome

Shock - infusion of 1-4U/hr in catecholamine refractory shock

Diabetes insipidus - 2microg IV to treat cranial DI

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16
Q

What is laser and what does it comprise?

A

light amplification by stimulated emission of radiation and comprises 3 main components

  • energy source
  • lasing medium (solid, gas, liquid)
  • optical resonator
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17
Q

Describe the hazards of laser

A
  1. energy transfer to inappropriate location (eye damage, skin burn, fire risk from nearby fuel)
  2. Laser plume can cause bronchospasm / laryngospasm
  3. embolism
  4. Tissue/vessel perforation
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18
Q

What is microshock

A

low current that is delivered directly through heart muscle at 0.05 to 0.1mA

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19
Q

Structure the answer for how to minimise risk of microshock

A

Equipment

  • Grounding of equipment
  • Residual current device will protect against macro but not microshock
  • Line isolation monitors, also no protection from microshock.

Environment

  • General wiring standards to ensure safety of electrical equipments
  • isolation transformers
  • Equipotential earthing system

Patient

  • ensure patient is not earthed
  • Insulated from any metal
  • patient skin kept dry
  • on a non-conducting mattress
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20
Q

Describe the principle of an automated oscillometric non-invasive monitor

A

Oscillometry - variation in oscillatory amplitude of pressure within a deflating cuff overlying an artery

Cuff is inflated to completely occlude artery, slow deflate, and analyse oscillatory signals

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21
Q

What are the components of a non-invasive BP cuff

A
  1. cuff with inflatable bladder

2. Air insufflation port and pressure transduction port

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22
Q

Describe the oscillometric analysis

A

First onset - approximate systolic pressure

Point of maximal oscillatory amplitude - MAP

Point of maximum reduction in rate of change - DBP
- Can also assume diastole as a fixed fraction (3MAP - SBP)/2

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23
Q

Describe the sources of error from blood pressure cuff

A

Patient erros

  • Irregulat pulse rate
  • Excessive movement
  • Very low BP
  • Calcified non-compressible artery
  • Pain from high NIBP

Equipment

  • Wrong cuff size, which should be 20% larger than arm diameter
  • Placement (need to be at heart level)
  • External compression
  • Calibration or transducer errors
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24
Q

What is the shunt equation

What are the sources of physiological shunt?

A

Qs/Qt = (CcO2-CaO2) / (CcO2-CvO2)

Bronchial veins and Thebesian veins

25
Q

Discuss the factors that affect oxygen transport from alveoli to tissues

A

Oxygen cascade.
Fick’s law of diffusion at the alveolar level.
- Alveolar gas equation
- Pressure gradient: high supplemental FiO2, hyperbaric
- Decreased PaCO2
- High Hb, CO, pulmonary perfusion

Pulmonary -> systemic circulation

  • Venous admixture
  • V/Q mismatch and shunt

Systemic to tissues

  • pressure gradient by O2Hb curve, offloading capacity determined by degree of right shift.
  • P2 decreases if there is increased myoglobin or O2 extraction
  • Recruitment and distension to aerobic exercise, of capillary bed.

Cytotoxic
- Cyanide inhibition of oxidative phosphorylation.

26
Q

What is the effect of sevoflurane on the airway anatomy?

A

Bronchodilation and increases anatomical DS

Decrease airway reflex for toleration of LMA, increases aspiration risk

decreases pharyngeal dilator tone

Decreases ciliary activity

27
Q

What is the shelf lives of suxamathonium and rocuronium at room temp?

A

sux 2/52

roc 2/12

28
Q

What is the volume of distribution of muscle relaxants?

A

0.2L/kg

29
Q

What is the breakdown product of sux?

A

choline and succinic acid

30
Q

Describe the metabolism and eliminination of rocuronium

A

95% excreted unchanged

  • 60% via bile, 40% via kidneys
  • Reduced dose in either impairments, or prolonged blockade.
  • 5% liver metabolism into active 17-desacetylrocuronium
31
Q

What is the percentage change in cardiac output in pregnancy and what are the contributions

What is the change in blood pressure?

A

50% increased in cardiac output by third trimester

20% increased heart rate from baseline
40% increased in stroke volume from baseline

10% reduction in overall blood pressure (due to reduced SVR) - drop in DBP more than SBP, increased pulse pressure

32
Q

What changes lead to hypercoagulability in pregnancy

A

Increased level of factors I, VII, VIII, IX, X, XII, vWF

Reduced level of protein S

Due to oestrogen

33
Q

Outline the storage lesion changes for PRBCs

A

Cellular: spheroidal, rigid and fragile RBCs, 25% loss at 4/52, antigenic WBCs, PLTs inactive at 48 hrs.

Biochemical - pH 6.7 due to additives, K+ up to 30mM, 2.3 DPG at 50% by 2/52, 5% at 4/52, increase free haemoglobin

34
Q

How would you calculate the dose of protamine?

A

1mg per 100U heparin.
Lower dose used in cardiac theatre, around 50% of dose to account for metabolism for lapse of time.
Anti-coagulant effect at high dose.
According to ACT/APTT normalisation
Comparatively shorter half life of protamine may result in a heparin rebound.

35
Q

What amount of blood transfusion will constitute a massive transfusion

A

50% of blood volume over 4 hours, or 100% of volume over 24 hours

36
Q

Describe storage lesion

A

Adverse effects associated with the storage of blood.

Cellular

  • spherical red cells.
  • 25% loss at 4/52
  • Inactivated but still antigenic white cells.
  • Platelets inactivated at 48 hours

Coag factors - FV 50% at 3/52, FVIII 30% at 3/52

Metabolic - cold storage at 4 degrees, pH 6.7, K up to 30mmol, Citrate, reduced 2.3 DPG 5% at 4/52

37
Q

Describe the immunological effects of blood transfusion

A

acute - anaphylaxis, febrile non-haemolytic (cytokines), febrile haemolytic due to ABO/RhD, TRALI

delayed

  • alloimmunisation: delayed haemolysis (Kell/Kidd/Duffy), haemolytic disease of new born
  • Graft vs host donor WBC overwhelms host bone marrow.
  • Transfusion related immune modulation (TRIM): MOA unknown, due to WCC releasing cytokines.
38
Q

What is a competitive antagonist and how does it affect the quantal response curve?

A

Drugs with intrinsic activity of 0

Right shift of the quantal response curve. Reduce potency, but still able to achieve max efficacy at higher dose.

39
Q

What is the therapeutic index, LD50 and ED 50 of morhpine?

A

ED50 7mg
LD50 500mg /kg
TI = 70mg

40
Q

What is glomerulotubular feedback

A

A constant amount of Na/Cl/H2O reabsorbed from proximal tubule.

Reduce glomerular filtration -> increase oncotic pressure at the peri-tubular capillary which favours reabsorption

41
Q

Describe renal potassium handling

A

180L/day x 4mM/L = 720mM filtered per day.

Fixed reabsorption 95% (65% PCT, 30% LoH)

Compulsory excretion of 5%

Secretion stimulated by aldosterone

42
Q

How much acid can the renal phosphate system secrete daily?

A

30mmol/day at baseline
Up to 60mmol day

H2PO4 -> H+ + HPO4- at pKa 6.8

43
Q

List the regions important for autonomic innervation

A

Nucleus tracts solitarius - receives afferent signals.

RVLM - SNS
dorsal vagal nucleus / nucleus ambiguus - PNS

44
Q

How the the vagus nerve innervate the heart?

A

R branch - SA node
L branch - AV node

m2 receptors, Gi -> reduce cAMP

Fast onset compared to SNS

Minimal inotropic effect, but can reduce inotropy by interneuronal effect

45
Q

What is the mechanism of milrinone?

A

PGE3 inhibitor -> reduce cAMP breakdown

46
Q

Midazolam

  • PO bioavailability?
  • Onset and peak effect
  • Duration
  • Protein binding
  • VDSS
  • T1/2Ke0
  • Clearance
  • T1/2b
A 
50% 
2 and 10 mins 
1-6 hours 
98% 
1.5L/kg 
4 mins 
5-10ml/kg/min 
2 hours
47
Q

Describe the metabolism and excretion of midazolam

A

liver phase 1 via CYP3A4 then phase 2 conjugation

Active metabolite a-OH-midaz (50% active), oxazepam
- These undergo glucuronidation

<1% excreted unchanged.

48
Q

What hormones increase BGL?

A

glucagon, cortisol, catecholamines, growth hormones.

Ratio of insulin: glucagon determines effect

49
Q

List the key enzymes for glucose / glycogen metabolism

A

Glycolysis - glycogen phosphorylase

Glycogenesis - glycogen synthase

Lipolysis - hormone-sensitive lipase

Lipogenesis - lipase, acetyl-CoA carboxylase, fatty acid synthase

Ketogenesis - acetyl-coa thiolase

50
Q

Describe the stimuli that increase insulin secretion

A
  1. Increase BGL
  2. increase amino acid, fatty acid
  3. GIT secretagogues like GLP-1, GIP
51
Q

What is the mechanism for B-islet cells to secrete insulin?

A

Increase BGL -> increase ATP -> inhibition of K+ channel -> depolarisation -> calcium influx -> exocytosis

1st phase - preformed insulin, onset 2 mins, duration 15 mins

2nd phase - newly synthesised, onset 15 mins, duration 2 hours.

52
Q

Describe the effect of catecholamine on BGL

A

Generally increase BGL

  • binds to B2 receptor on a-islet cells -> increase glucagon
  • Also b2 on SKM -> stimulates glycogenolysis
  • B3 on brown fat -> lipolysis
  • B1 on what fat -> reduce glucose uptake
53
Q

What is the side effect of misoprostol?

A

diarrhoea

54
Q

Describe prostaglandins

A

Groups of arachidonic acid derivatives

  • Autocrine and/or paracrine
  • inhibitory or excitatory
  • PGs may have opposing effects
  • Different effect on different tissues.
55
Q

What is the effect of PGI2 on different tissues?

A

Vascular smooth muscle - vasodilation

Bronchiole - Bronchodilation

Uterus / GIT / Utreters - none

Renal - direct vasodilation / activation of RAAS for VC

56
Q

What are the different PGE receptors and GPCR?

A

EP1 - Gq
EP2,4 - Gs
EP3 - Gi

57
Q

what are the effects of PGE2 on different tissues

A

Bronchioles - EP2/4 BD, EP1/3 BC

Vascular SM - EP2/4 VD

Uterus / GIT - EP1/3 contraction
- Think misoprostolol

Ureters - dilation

Renal - direct VD, activation of RAAS for VC

58
Q

What are the effects of PGD2 and PGF2a

A

On bronchioles - BC

PGF2a also causes uterine and ureteric contraction

PGD2 in mast cells, which cause BC

20/6 Week Learning Points (4 decks)

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