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Quick facts Flashcards

1
Q

4 types of lung receptors (peripheral afferents)

Respiratory

A
  • Pulmonary stretch receptors - discharge in response to distension of lung & activity is sustained with lung inflation - ie. They show little adaptation
  • Irritant receptors - Rapidly respond to airway irritants - eg. Cigarette smoke/noxious gases/cold air
  • J receptors - respond to chemicals injected into the pulmonary circulation –> results in rapid, shallow breathing
  • Bronchial C fibres - respond to chemical injected into the bronchial circulation –> results in rapid, shallow breathing
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2
Q

Hering-Bruer reflex

Respiratory

A

Stimulation of pulmonary stretch receptors results in slowing of respiration due to increase in expiratory time

[Opposite is true for expiration]

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3
Q

Normal compliance

Respiratory

A

100mL/cmH2O
* C(lung)= 200mL/cmH2O; C(chest wall) = 200mL/cmH2O

Specific compliance = 0.05/cmH2O

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4
Q

Malignant hyperthermia incidence

Pharmacogenetics

A

1:5,000 - 1:50,000

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5
Q

What is porphyria?

Pharmacogenetics

A

Mutation of haem synthesis enzymes which causes a build-up of neurotoxic intermediate metabolites (porphyrin precursors) in response to various drugs (anticonvulsants, antibiotics, thiopentone)
○ Autosomal dominant

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6
Q

Malignant hyperthermia mechanism

Pharmacogenetics

A

Mutation of the ryanodine calcium channel receptor which causes a hypermetabolic crisis in response to volatile anaesthetics

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7
Q

Malignant hyperthermia signs/symptoms

Pharmacogenetics

A

○ Initial - tachycardia, masseter spasm, hypercapnoea, arrhythmia
○ Intermediate - hyperthermia, sweating, combined metabolic and respiratory acidosis, hyperkalaemia, muscle rigidity
○ Late - rhabdomyolosis, coagulopathy, cardiac arrest

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8
Q

Malignant hyperthermia Mx

Pharmacogenetics

A

Cease volatile, start TIVA, give dantrolene 2.5mg/kg increments to 10mg/kg, Rx of complications

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9
Q

Atypical plasma cholinesterase/pseudocholinesterase

Congenital/acquired/both/neither?

Pharmacogenetics

A

Fails to metabolise suxamethonium and causes “sux apnoea”
○ Congenital - autosomal recessive
○ Acquired - due to loss of plasma cholinesterase. Can occur in pregnancy, organ failure (hepatic, renal, cardiac), malnutrition, hyperthyroidism, burns, malignancy, drugs (OCP, ketamine, lignocaine and ester Las, metoclopramide, lithium)
○ Note: acquired disease will have normal dibucaine no but just decreased quantity of enzyme

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10
Q

How to test for atypical plasma cholinesterase/pseudocholinesterase?

Pharmacogenetics

A

○ Measured by dibucaine number. Dibucaine is an amide LA, which inhibits plasma cholinesterase. Greater inhibition indicates a less severe mutation - so normal:normal dibucaine no = 80 (80% inhibited). Dibucaine resistant:resistant has a no of 20 (20% inhibited)

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11
Q

G6PD deficiency

Pharmacogenetics

A

Mutation of glucose 6-phosphate dehydrogenase which produces acute haemolysis in response to oxidative stress due to dapsone, methylene blue, fluoroquinolones, antimalarialas and rasburicase

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12
Q

Normal cardiac output and cardiac index values

A

CO = 5L/min; CI = 2.5-4L/min

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13
Q

LaPlace’s Law (cardiac)

A

sigma = Pr/2h

where sigma = myocardial wall stress
P = transmural pressure
r = radius
h = ventricular wall thickness

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14
Q

Outline determinants of preload

A

Vascular factors
* MSFP (venous blood volume + venous compliance)

Factors impeding venous return
* High intrathoracic pressure
* High intra-abdominal pressure (including caval compression syndrome in pregnancy)
* RAP (Guyton’s curves)

Myocardial factors
* Contribution of atrial kick (impaired in AF, arrhythmias)
* Valvular competence (mitral stenosis)
* Ventricular compliance
— pericardial compliance
— ventricular wall compliance
— end systolic volume (depends on afterload)

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15
Q

Outline determinants of contractility

A

Biochemical/cellular factors
* Calcium concentration
— Catecholamines –> increased i[Ca2+] (via cAMP etc)
— Extracellular calcium - contractility decreases linearly with decreasing extracellular [Ca2+]
* Temperature
— catecholamines lose affinity for receptors, decreased cardiac myofilament sensitivity to calcium

Myocardial integrity
* Ischaemia

CVS Parameters
* Cardiac reflexes - Anrep (afterload), Bowditch (HR), Woodworth (prolonged time between beats)

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16
Q

Outline determinants of afterload

A
  • Myocardial wall stress -(Laplace) - Pr/h
    ○ Radius
    ○ Ventricular transmural pressure - (cavity pressure minus ITP)
    ○ Thickness of wall - increased thickness decreases wall stress (
  • Input impedance
    ○ Ventricular outflow tract resistance
    ○ Arterial compliance - aortic + peripheral
    — Decreased proximal aortic compliance will increase wall stress and decrease flow (60% of stroke volume stored in arterial capacitance vessels (tunica media allows expansion))
    — Peripheral compliance:
    □ Pulse pressure wave–> distal circulation at 1m/s–> reflected from arterioles –>returns to heart during diastole (helps fill coronaries)
    □ Decreased compliance –>increases the speed of pulse wave propagation –> wave returns sooner, in systole –> adds pressure to aortic pressure
  • Inertia of blood column
  • Arterial resistance (can be described by Poiseuille equation), where vessel radius is most important variable (raised to power of 4)
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17
Q

Features of SA node and ventricular myocyte action potentials: resting, threshold, peak potentials

A

Ventricular myocyte:
* Resting potential: -90mV
* Threshold: -70mV
* Peak: +50mV

SA node:
* Max diastolic (nil real resting potential): -70mV
* Threshold: -40mV
* Peak: +20mV

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18
Q

Structure of fast cardiac Na+ channel

A

2xβ subunits
1x α subunit
* Has 4 domains - I-IV
* The N- & C- terminus are both intracellular
* Each domain has 6 transmembrane segments linked by intracellular and extracellular peptides
–Extracellular peptides linking segments 5-6 form the ion pore (responsible for ion selectivity - the Ca channel has similar structure but is Ca selective)
–Domain IV undergoes a conformational change in response to voltage & opens the pores (activation gate - ‘m’)
– The intracellular peptide loop connecting domain III & IV forms the inactivation gate ‘h’

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19
Q

What membrane potential does the absolute refractory period of a cardiac action potential go up to?

A

Absolute refractory period is up to ~-50mV. At this value, some fast Na+ channels have recovered from inactivation enough to permit response to stimulation

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20
Q

Time constant equation

A

(tau) = compliance x resistance

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21
Q

How do time constants affect the respiratory system?

A

Physiological:
* Compliance
— Observed difference between static and dynamic compliane - static compliance measured when all fast and slow alveoli have equilibrated
— Compliance in apical lung units is lower (as intrapleural pressure difference is lower). Therefore time constants are faster - ie. these alveoli fill up quickly
* V/Q matching - at high RR, slow alveoli don’t have time to fill and ventilation preferentially diverts to fast alveoli (V/Q mismatch for slow alveoli)

In disease:
* Asthma/COPD - increased airway resistance = increased time constant
* Emphysema - increased compliance = increased time constant
* Pulmonary fibrosis - decreased compliance = faster time constant

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22
Q

What are the functions of the FRC?

A
  • Oxygen reservoir - prevents rapid changes in alveolar oxygen tension and arterial oxygen content by maintaining gas exchange throughout expiration
    • Maintenance of small airway patency (N2 splinting)
    • Optimising respiratory workload - compliance maximal at FRC, WOB required from FRC is minimal
      ○ Keeps tidal volume over steep part of lung compliance curve
    • Minimises pulmonary vascular resistance & hence RV afterload/work/oxygen demand
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23
Q

What are the factors affecting FRC

A
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24
Q

Normal WOB

A

0.35J/L

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25
Q

Oxygen requirement of breathing

A

The oxygen requirement of breathing at rest is 2-5% of VO2 or 3ml/min

(tidal breathing uses <2% of BMR)

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26
Q

Normal osmolarity

A

~285mOsm/kg

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27
Q

Baroreceptor reflex

A
  • Sensor/stimulus: carotid sinus & aortic arch - circumferential and longitudinal stretch receptors detect change in BP
    ○ Decreased BP decreases firing rate of baroreceptor
    • Afferent: glossopharyngeal + vagus
    • Processor: NTS & Caudal ventral medulla/RVLM
      ○ Decreased BR firing rate –> decreases GABA secretion from caudal VM. This decreases inhibition of sympathetic output from RVLM (ie SNS activity increased)
    • Efferent/effectors: vagus nerve + sympathetic chain
      ○ Peripheral vessels - a1 mediated vasoconstriction
      ○ Decreased vagal input into SA
    • Effect: increased HR and BP in response to fall in BP
    • Note: Tends to override Bainbridge reflex when it comes to atrial stretch in hypovolaemia (except in spinal anaesthesia, where reverse Bainbridge reflex may predominate)
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28
Q

Bainbridge reflex

A
  • Sensor/stimulus: Stretch receptors in atria + pulmonary artery measure changes in pressure
    • Afferent: vagus
    • Processor: NTS & CVM
    • Efferent:
      ○ Sympathetic fibres to heart
      ○ Vagal efferents to gardiac ganglion
    • Effects
      ○ Increased RA pressure produces an increase heart rate
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29
Q

Chemoreceptor reflex

A
  • Sensor/stimulus: Carotid and aortic body detect low PaO2 and/or high PaCO2
    • Afferent: glossopharyngeal + vagus
    • Processor: NTS + Nucleus ambiguus
    • Efferents/effectors:
      ○ Sympathetic fibres to heart and peripheral smooth muscle
      ○ Vagal efferents to cardiac ganglion
    • Effects:
      ○ Primary effects - bradycardia, hypertension
      ○ Secondary effects - increased preload due to increased ventilation, thus activation of Bainbridge –> increased heart rate
      ○ Activation of pulmonary stretch receptors –> activation of Hering-Breuer reflex –> increases HR
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30
Q

Cushing reflex

A
  • Sensor/stimulus: intracranial pressure/cerebral ischaemia is detected by some unknown sensor
    • Afferent:
      ○ Fibres from the medullary mechanosensory areas, to sympathetic ganglia
      ○ Fibres from cerebral hemispheres, which exert descending inhibitory control on the medullary vasomotor sensor
    • Processor: rostral ventrolateral medulla
    • Efferents/effectors: Sympathetic fibres to heart and peripheral smooth muscle
    • Effects:
      ○ Hypertension + tachycardia
      ○ Secondary - baroreflex mediated bradycardia
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31
Q

Bezold-Jarisch Reflex

A
  • Sensor/stimulus: Multiple and heterogeneous stimuli interact with receptors in all cardiac chambers, including:
    ○ Mechanical: pressure and stretch (thus, inotropy preload and afterload)
    ○ Chemical: veratrum alkaloids, ATP, capsaicin, snake venom, other venoms
    • Afferent: unmyelinated C-fibres of vagus
    • Processor: NTS
    • Efferents/effectors: sympathetic fibres to heart and peripheral smooth muscle, vagus via cardiac ganglion
    • Effects: hypotension (vasodilation) & bradycardia
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32
Q

Occulocardic reflex

A
  • Sensor/stimulus: mechanoreceptors on the globe and in facial muscles detect pressure on the globe
    • Afferent: long and short ciliary nerves to trigeminal nerve (via Gasserian ganglion) to sensory nucleus of TN. From here, short internuclear fibres to NTS
    • Processor: NTS
    • Efferents/effectors: vagus nerve via cardiac ganglion to SA + AV node
    • Effects: bradycardia, if severe, to the point of arrest
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33
Q

Diving reflex

A
  • Sensor/stimulus: pain, temperature, chemical and mechanosensitive stretch receptors detect pressure to globe of eye, pain in trigeminal nerve distribution, cold temperature, or noxious stimulus of anterior ethmoidal nerve
    • Afferent: trigeminal nerve
    • Processor: NTS (vagal response), Rostral medulla (sympathetic response), ventral response (apnoea)
    • Efferents/effectors: Vagus nerve via cardiac ganglion to SA, AV nodes; phrenic nerve to respiratory muscles
    • Effects: bradycardia, cerebral vasodilation + systemic vasoconstriction, apnoea
      ○ Net effect is to prevent aspiration and maximise blood flow to CNS at the expense of skin, muscle and splanchnic organs
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34
Q

Barcroft-Edholm Reflex

A
  • Sensor/stimulus: Emotional distress/orthostatic changes, increased ITP (eg. Defecation, cough/sneeze, laughter)
    • Afferent: unknown
    • Processor: ?NTS/Nucleus ambiguus
    • Efferents/effectors: vagus & SNS to SA, AV nodes, peripheral smooth muscle
    • Effects: Vagal - bradycardia, sympathetic - systemic vasodilation
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35
Q

SvO2 from tissue beds: jugular, muscles, renal, IVC, SVC, Hepatic

A

Jugular - 55%
Muscles - 72%
Renal - 81%
IVC - 71%
SVC - 79%
Hepatic - 66%

36
Q

Normal mixed venous PO2 & SvO2

A

40mmHg & 70-75%

37
Q

Energy consumption of 1 MET

A

1 MET = 3.5 ml O2/kg/minute

38
Q

Aortocaval compression syndrome

A
  • Seen as early as wk 20
  • Compression of IVC by gravid uterus - decreases venous return & reduced CO
    * Blood returns to heart via paravertebral epidural veins draining into azygous
    * Uterine perfusion diminished secondary to increased uterine venous pressure
  • Compression of aorta may be present & associated with uterine arterial hypotension + reduced uteroplacental perfusion
  • Can be relieved by positioning mother to left side
39
Q

Changes in afterload during pregnancy

A

Afterload (reduced) –> TPR decreases by 30% by wk 12& 35% (by week 20th wk, then remains at 30% below non-pregnant values)
* Vasodilation mediated by progesterone, prostaglandins & downregulation of alpha-receptors
* SBP + DBP - decrease (~10%) & reach nadir at 20wks
* Vascular system as whole becomes more refractory to vasoconstrictors
* Note re: RV afterload
□ CVP + PCWP - remain stable throughout pregnancy. PCWP balance by decreased PVR

40
Q

Changes in preload during pregnancy

A

○ Preload (increased) –> By term, maternal blood volume increased by 35-40% (approx 1-1.5L)
§ Plasma volume increases by 45% - Na + H2O retention by oestrogen stimulation of RAAS
§ RBC volume increases by 20% due to renal erythropoietin synthesis
§ Disproportionate rise in plasma volume vs red cell mass accounts for fall of haematocrit to 33% (“anaemia of pregnancy”)

41
Q

Changes in CO, HR and SV during pregnancy

A

CO increases by 40-45% by 12-28wks, peaks at 50% 32-36wks, then reaches 47% at term
- Heart rate: HR increases by 17% at end of first trimester,(increases to 25% at middle of third trimester);
- Stroke volume increases by 20-30% (predom in 1st trim)

42
Q

Changes to distribution of CO in pregnancy (regional flow changes)

A
  • Distribution (regional flow changes)
    ○ Renal blood flow - increases by 80% in first trimester (may fall slightly towards term)
    ○ Large proportion of blood flow is directed to uteroplacental circulation, that increases its blood flow 10-fold to 750mL/min at term
    ○ Increased blood flow to breasts, GIT, skin
43
Q

Physical and mechanical changes to heart during pregnancy

A

Physical/mechanical changes:
- LV mass increases by 40g by 3rd trimester
- Heart is more rotated to left
○ May see Q waves + TWI in inferior leads
- Colloid oncotic pressure falls by 14% - may predispose to oedema

44
Q

CVS changes during PARTUITION + Post delivery:

A
  • Pressure:
    ○ Maternal SBP + DBP increase 10-20mmHg during uterine contraction
    • Volume:
      ○ Each uterine contraction squeezes ~300mL blood from uterus into central maternal circulation
    • Cardiac output:
      ○ CO increases by ~15% during latent phase of labour, by 30% during the active phase & 45% during the expulsive stage
      ○ Immediately after delivery, CO ~60-80% above pre-labour values as a consequence of autotransfusion & increase venous return associated with uterine involution
    • CO & SBP/DBP return to non-pregnant values by 2 wks post delivery
45
Q

Effect of pregnancy on drug absorption

A

Absorption:
- Oral absorption:
○ May decrease due to:
§ Nausea +/- vomiting
§ Higher gastric pH with delayed gastric emptying
○ May increase due to:
§ Slower gut transit
§ Increased GIT blood flow
- IM/SC/transdermal absorption:
○ May increase due to:
§ Increased CO, decreased SVR
- IV absorption - increased rate of onset
- Inhalational absorption:
○ Increases due to:
§ Increased progesterone mediated increase in MV
§ Increased pulmonary blood flow
○ Eg. Volatile anaesthetics have decreased time for onset
- Neuraxial absorption:
○ Increased due to venodilation
○ Less volume required
○ Decreased epidural space

46
Q

Effect of pregnancy on drug distribution

A

Distribution
- Increased volume of distribution
○ Increased total body water + plasma volume (RAAS activation) (need increase dose of hydrophilic drugs - eg NDMB)
○ Increase body fat % (possibly longer CSHT for lipophilic drugs)
- Protein binding
○ Dilution of serum proteins - increased unbound fraction (eg. LAs due to dilution of α1-glycoprotein)
§ Decreased dose required, increased transplacental transfer of drugs
○ Increased fatty acid levels - compete with drugs for binding sites on albumin
- Ionisation
○ Mild increase in pH (resp alkalosis)
○ Increased transplacental transfer of basic drugs (increased % in unionised form)
○ Increased ion trapping (of basic drugs) in more acidic fetal circulation

47
Q

Effect of pregnancy on drug metabolism

A

Metabolism
- Hepatic enzyme activity
○ Progesterone induces enzymes, Oestrogen inhibits
○ Depends on P:O ratio
○ Egs CYP2D6 induced in pregnancy - rapid metabolisers of codeine will have high plasma peaks of morphine –> transferred to breast milk. CYP3A induction –> increased metabolism of midaz –> decreased plasma conc
- Placenta has functioning CYP450
- Plasma cholinesterase (30% decrease) - although nil significant increase in DoA of sux
- Influence of changes in CO:
○ Increased CO will increase clearance of drugs with high HER

48
Q

Effect of pregnancy on drug elimination

A

Elimination:
- Increased renal clearance due to increased GFR - drugs cleared solely by filtration are most affected (eg. Cephazolin)
- Hepatobiliary clearance reduced by cholestatic effects of estrogen
- Increased volatile washout (increased MV)

49
Q

Effect of pregnancy on drug pharmacodynamics

A

Pharmacodynamics
- Increased sensitivity to volatile anaesthetics (decreased MAC), IV anaesthetics, Las
Changed therapeutic indices due to concerns re: fetal damage + teratogenicity

50
Q

Effect of pregnancy on upper airway

A

Upper airway
- Mucosal oedema in upper airway
○ increased Oestrogen –> capillary engorgement –> oedema –> increases airway resistance
§ Difficult airway and increased risk of airway collapse with sedation (can be significantly worsened during pre-eclampsia due to change in capillary dynamics)

51
Q

Effect of pregnancy on chest wall

A

Properties of the chest wall + lung mechanics
- Anatomical
○ Diaphragm:
§ progressive upwards displacement by gravid uterus (up to 4cm). Results in:
□ Reduced FRC (20% when standing, a further 30% when supine)
□ Reduced capacity for pre-oxygenation, rapid desaturation
□ Impaired ventilation/oxygenation when supine
§ increased diaphragmatic excursion (2cm) –> increases Vt
○ Rib cage:
§ Oestrogen-induced increased laxity of rib ligaments –> flaring of lower ribs (increased AP and lat dimensions of thorax)
§ Chest cavity becomes shorter, but other dimensions increase to maintain nearly constant TLC (reduced by only ~5%)
○ Anatomical dead space:
§ increased Progesterone –> Bronchodilation:
□ increases deadspace (45% - however, VD/VT remains the same)

52
Q

Effect of pregnancy on Lung volumes + respiratory control

A
  • Progesterone-mediated stimulation of respiratory centre in medulla oblongata (increased sensitivity to CO2)
    –> increased MV (up to 20-50%), due to:
    ○ increased Vt by up to 50% at term (~10mL/kg)
    ○ increased RR by up to 10% (15-17)
    ○ increased MV even further during labour due to pain
    • increased MV results in: chronic, completely compensated respiratory alkalosis:
      ○ decreased PaCO2 (26-32mmHg) with increases renal bicarb losses (plasma bicarb ~20mmol) to compensate
      § Slightly reduced ability to buffer a metabolic acid load
      ○ increased PaO2 (~100-104mmHg) (due to decreased CO2 (Dalton’s Law))
53
Q

Effect of pregnancy on Oxygen transport, consumption and CO2 production

A

Other
* O2 Transport: Oxygen-Haemoglobin dissociation curve shifted to right due to increased 2,3-DPG in maternal RBCs
○ p50 remains unchanged due to respiratory alkalosis
* O2 consumption increases (20% term, 60% during labour)
○ increased Maternal BMR and foetal consumption
* increased CO2 production (increased BMR)

54
Q

How long after birth do pregnancy-induced respiratory changes settle?

A

After birth:
* FRC and RV return to normal within 48h
* Vt returns to normal within 5 days

55
Q

Effect of pregnancy on lung mechanics

A
  • Compliance
    ○ increased adipose tissue and breast mass –> decreased chest wall compliance (lung compliance unchanged)
    • Resistance
      ○ Increases in early pregnancy - mucosal oedema
      ○ Progesterone-mediated bronchodilation - decreased resistance in later pregnancy (35%)
56
Q

Storage functions of the liver

A
  1. Storage
    • Metabolic fuel: Glycogen- ~100g & fat
    • Fat soluble vitamins
      ○ Vitamin A → stored in stellate cells –> converted to retinol (active form). Contains 1-2yr supply
      ○ Vitamin D → ~ 1-4 month supply
      ○ Vitamin E & vitamin K - minimal
    • Vitamin B12 + folate (50% of body’s storage for both)
    • Trace elements - iron (as ferritin), zinc, copper, selenium
    • Blood reservoir - ~ 500mL of blood
57
Q

Synthetic functins of the liver

A

Synthetic
- Plasma proteins- albumin, α+ β globulins, fibrinogen
- Nutrients - glucose, ketones, lipids, cholesterol, amino acids
- Regulatory molecules (thrombopoetin, angiotensinogen)
- Bile acids → stored in gallbladder

58
Q

Metabolic functions of the liver

A

Metabolic
- Carbohydrate metabolism
○ Liver is a glucostat –> maintains strict BSL
§ in conditions of ↑ glucose, glycogenesis & FFA synthesis will normalise BSL
§ in conditions of ↓ glucose, gluconeogenesis will normalise BSL
- Lipid metabolism → free fatty acids (FFA). synthesised & packaged with as lipoproteins be transported to adipose tissue for storage
§ FFA oxidation will also produce energy.
- Protein Metabolism - amino acids can be transaminated, deaminated or decarboxylated to give acetyl- CoA

59
Q

Detoxification/excretory functions of the liver

A

Detoxification & excretion
- Immunological detoxification:
○ Kupfer cells act as scavengers & phagocytes & secrete prostaglandins
- Ammonia → urea conversion via urea cycle
- Conjugation of bilirubin & excretion in bile
- Processing of drugs via:
○ Phase I (oxidation & hydrolysis) and
○ Phase II (conjugation) reactions

60
Q

Length, diameter, origin and termination of trachea

A

Length: 10-16cm
Diameter: (internal) 2.5cm
Origin: C6
Termination: carina, T4 (sternal angle)

61
Q

Classify generations of bronchial tree

A

Generation 1-4 - Bronchi (cartilaginous)
Generation 5-14 - bronchioles (non-cartilaginous)
Gen 15-18 - Respiratory bronchioles (some gas exchange)
Gen 23 - alveolar sacs

62
Q

Describe the muscles in the larynx involved with phonation, inspiration, expiration and effort closure

A

Muscles - various muscles attaching to the various structures. Important movements:
* Phonation: cricothyroid (brings cords together by moving thyroid down), interarytenoid (transverse + oblique), vocalis (subset of muscles from thyroarytenoid) - mediates tension in vocal ligament to modulate pitch
* Inspiration: + cricoarytenoid (posterior + lateral) - rotate arytenoids outwards
* Expiration: thyroarytenoid adduct cords to increase resistance and provide intrinsic PEEP (3-4 cmH2O), which maintains patency of small airways & maintains FRC
* Effort closure - aryepiglottic muscles contract strongly to act as a sphincter, allowing airway to withstand up to 120cmH2O pressure

63
Q

What is Dalton’s Law

A

Dalton’s Law:
* In a mixture of gases, the pressure exerted by each gas is the same as the pressure exerted if the gas was the only gas in that mixture:
* PTOTAL = PGas1 + PGas2 + PGas3

64
Q

What is Boyle’s Law?

A

Boyle’s Law:
* For a fixed mass of gas at constant temperature, the pressure (P) and volume (V) are inversely proportional, such that P ×V = k, where k is a constant.

65
Q

Henry’s Law

A

Henry’s Law
* The amount of a given gas dissolved in a given liquid is directly proportional to the partial pressure of the gas in contact with the liquid:

P = Hv × M

Where
* P is pressure
* M is the molar concentration of gas
* Hv is Henry’s Proportionality Constant

66
Q

Graham’s Law

A

Graham’s Law:

* The rate of diffusion is inversely proportional to the √MW
67
Q

Fick’s Law of diffusion

A

Fick’s Law of diffusion:
* Passive movement of molecule from an area of high concentration to low
- There are many different iterations of Fick’s Law
- V_gas∝A/T D (P_1− P_2)

V_gas  = Flow of gas
D∝ Solubility/√MW
MW = molecular weight 
A = surface area
P_1  − P_2= difference between partial pressure in alveolus vs capillary
T = diffusion distance (or thickness of membrane)
68
Q

Third gas law (Gay-Lussac’s Law)

A

The pressure of a fixed mass of gas at constant volume is directly proportional to its absolute temperature (P/T = k).

69
Q

Avogadro’s Law

A

Equal volumes of gases at the same temperature and pressure contain the same number of molecules (6.023 × 1023, Avogadro’s number).

70
Q

Universal (Ideal) Gas Law

A

The state of a fixed mass of gas is determined by its pressure, volume and temperature (PV = nRT)

71
Q

The Bohr equation for measuring dead space

A

VD/VT = (FACO2 - FECO2) / FACO2

Where:

VD = dead space volume
VT = tidal volume
FECO2 = fraction of expired CO2
FACO2 = fraction of alveolar CO2

		*Note: Enghoff modification: P_A 〖CO〗_2  is substituted by P_a 〖CO〗_2  as arterial CO2 is measurable (and arterial CO2 is the mixed product of all lung units (theoretically representative of the average CO2 of all alveoli put together))
72
Q

Alveolar gas equation

A

PAO2 = (FiO2 × (Patm - PH2O)) - (PaCO2 / RQ)

Where 

PAO2= Partial pressure of alveolar oxygen
FiO2 = fraction of inspired oxygen
Patm = Atmospheric pressure (usually 760 mmHg)
PH2O = partial pressure of water vapour at the alveolus (usually 47 mmHg)
PaCO2  = Partial pressure of arterial carbon dioxide
RQ = respiratory quotient, usually 0.8
73
Q

Oxygen content equation

A

(sO2 × ceHb × BO2 ) + (PaO2 × 0.03)

Where:

ceHb = the effective haemoglobin concentration (conc of hb species capable of carrying & releasing O2)
PaO2 = the partial pressure of oxygen in arterial blood
0.03 = the content, in ml/L/mmHg, of dissolved oxygen in blood (for a PaO2 of 100 mmHg, the O2 content is 0.03 × 100 = 3ml/L
BO2 =  the maximum amount of Hb-bound O2 per unit volume of blood (normally 1.39 of dry Hb, or 1.30 in "real" conditions)
sO2 = oxygen saturation:
74
Q

The shunt equation

A

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

Where
    Qs/Qt = shunt fraction (shunt flow divided by total cardiac output)
    CcO2 = pulmonary end-capillary O2 content, same as alveolar O2 content
    CaO2 = arterial O2 content
    CvO2 = mixed venous O2 content
75
Q

Starling equation

A

J_v=L_p S [(P_c − P_i) - σ(π_c− π_i)
Where:
Jv = filtration rate
Lp = Hydraulic permeability
S = Surface area
Pc = Capillary hydrostatic pressure
Pi = Interstitial hydrostatic pressure
σ = Reflection coefficient (protein permeability, range 0-1)
πc = Intracapillary plasma oncotic pressure
πi = Interstitial oncotic pressure

*Note: LpS = K = kf = capillary filtration constant*
**Note2: πi becomes πegl in the revised Starling model to represent the endothelial glycocalyx layer**
76
Q

Starling forces in lung

A

○ LpS - surface area ~140m2 (compared to 4000-7000m2 in systemic circulation)
○ Pc = 4-12mmHg
○ Pi = interstitial hydrostatic pressure - essentially equal to alveolar pressure = atm pressure. Increases during PPV
§ Surfactant decreases hydrostatic pressure by decreasing surface tension
○ πc = 25mmHg throughout circulation; affectd by blood protein count
○ πi = ~3mmHg at alveoli
○ σ= 0.5-0.7 in lung

77
Q

Normal airway resistance

A

2mLH2O/L/s

78
Q

MoA of aminoglycosides

A
  • Bind to 30s Ribosomal subunit, which interferes with protein synthesis by causing misreading and premature termination of mRNA translation.
  • Diffuse through porin channels in the outer membrane into periplasmic space. Transport through inner membrane is oxygen dependent (/electron dependent). Antimicrobial activity is markedly reduced in anaerobic conditions (eg. Abscess).
  • Concentration dependent killing - higher the concentration, the greater the rate at which bacteria are killed.
  • Post-antibiotic effect exists (bactericidal effect persists after conc<MIC). The duration of this effect is also concentration dependent
79
Q

Define antispectic and disinfectant

A
  • Disinfectants are chemical agents or physical procedures that inhibit or kill microorganisms
  • Antiseptics are disinfectants with sufficiently low toxicity to host cells that can be used directly on skin, wounds or mucosa
80
Q

Re: alcohol as an antispectic/disinfectant - what are its main action, onset/duration, advantages & limitations and spectrum of activity?

A

Main action: Likely act by denaturing proteins. Optimal bacteriocidal concentration is 60-90%
Onset/duration Rapid/ Lack residual action because they evaporate completely
Advantages: Evaporative effects are useful when sinks with running water are not available
Limitations: Flammable- must be allowed to dry fully before diathermy or laser surgery 2. Corneal damage; 3. Skin drying; 4. Ineffective against C. Dif spores
Spectrum of activity: - Gram positives and negatives, Acid fast bacteria are susceptible, - Lipophilic viruses may be susceptible, Many fungi
Ineffective against: Spores and prions. Hydrophilic viruses are less susceptible

81
Q

Re: Chlorhexidine as an antispectic - what are its main action, onset/duration, advantages & limitations and spectrum of activity?

A

Main action:Cationic biguanide -strongly adsorbs to bacterial membranes causing leakage of small particles and precipitation of cytoplasmic proteins
Onset/Duration: Delayed/Sustained residual activity
Advantages: Resistant to inactivation by blood and organic material; Low skin irritation
Limitations:
1. Neurotoxic
2. Delayed effect
3. No direct spore activity
4. Agents in moisturisers, neutral soaps, and surfactants may neutralised its action

Spectrum of activity
- Bacteria (G+ve>G-ve)
- Moderate fungal and viral activity
- Inhibits spore germination

Ineffective against
Spores and prions
Hydrophilic viruses are less susceptible

Other
Can be combined with 70% alcohol
Preferred antiseptic for central venous access
Not absorbed orally

82
Q

Re: Providone/Iodine as an antispectic/disinfectant - what are its main action, onset/duration, advantages & limitations and spectrum of activity?

A

Main action: Oxidative damage.
Onset/Duration: Onset: Iodine is bacteriocidal in 1 minute and kills spores in 15 minutes. However in povidine compounding it has a delayed onset/Duration: No sustained effect
Advantages:
1. Sporicidal
2. Cheap
3. Broad spectrum
Most effective for intact skin

Limitations:
1. Hypersensitivity reactions
2. Delayed onset without residual activity
3. Stains clothes and dressings

Spectrum of activity:
- Bacteria (G+ve and –ve and acid fast)
- Sporicidal
- Viruses
- Fungi

Ineffective against:
Prions
Hydrophilic viruses

Other:
Can be used as antiseptics or disinfectants (latter contains more iodine)

83
Q

What is the speed of sound in tissue

1540

A

1540m/s

84
Q

Define potency

(of a drug)

A
  • Potency is defined as the concentration (EC50) or dose (ED50) of a drug required to produce 50% of that drug’s maximal effect/a specified response in 50% of the population
    ○ Two drugs may have the same efficacy but one may achieve the effect at a lower dose
    ○ A drug with lower EC50 or ED50 has higher potency
85
Q

Define efficacy

(of a drug)

A
  • Efficacy - a measure of the magnitude of the effect once the drug is bound
    ○ Different agonists produce varying responses, even when occupying the same proportion of receptors
    ○ Efficacy can be expressed numerically - as a ratio of the drug’s maximal efficacy to the maximal efficacy of some known potent agonist (aka intrinsic activity or maximal agonist effect)
86
Q

What is a competitive antagonist?

A

A compound that competes with endogenous agonists for the same binding site - it may be reversible or irreversible
○ In the presence of a competitive antagonist, the Emax of the agonist is unaffected, but the potency is reduced

87
Q

What is a non-competitive antagonist?

A

A compound that binds at a different site to the natural receptor and produces a conformational change that prevents receptor activation

CICM Study (14 decks)

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