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Primary Flashcards

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1
Q

CSHT

A

Time taken for the plasma concentration of a drug to fall by half, when an infusion (designed to maintain a constant plasma concentration) is stopped

Context refers to the duration of the infusion

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2
Q

3 causes of calcified CXR lesions

A

Asbestosis
Mitral valve disease
Chicken pox

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3
Q

Visual symptoms of papilloedema

A

Enlargement of blind spot
Blurring of vision

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4
Q

Mapleson A minimum flow (2)

A

SV: 0.8-1x MV
CV: 2-3x MV

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5
Q

Mapleson B minimum flow (2)

A

SV: 1.5-2x MV
MV: 2-3x MV

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6
Q

Mapleson C minimum flow (2)

A

SV: 1.5-2x MV
MV: 2-3x MV

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7
Q

Mapleson D minimum flow

A

SV: 2-3x MV
CV: 0.8-1x MV

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8
Q

Mapleson F minimum flow

A

2-3x MV

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9
Q

Mapleson E minimum flow

A

2-3x MV

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10
Q

Lack system

A

Co-axial Mapleson A

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11
Q

Bain system

A

Co-axial Mapleson D

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12
Q

Bain system FGF is carried through…

A

The inner tube

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13
Q

Closing capacity = FRC when?

A

Age 44 supine
Age 66 upright

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14
Q

Identify the structures of the descending tracts

A

Medial longitudinal fasciculus
Lissaur’s tract
Lateral corticospinal Tract
Rubrospinal tract
Pontine reticulospinal tract
Medullary reticulospional
Lateral vestibulospinal
Tectospinal
Ventral corticospinal

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15
Q

Identify the structures of the ascending tracts

A

Fasciculus gracilis
Fasciculus cuneatus
Dorsal spinocerebellar tract
Ventral spinocerebellar tract
Spinothalamic tract

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16
Q

Anion Gap (2)

A

[Na] + [K] - [HCO3] - [Cl]
Range 8 - 16 mEq/L

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17
Q

Causes of a high anion gap metabolic acidosis (3)

A

High unmeasured anions:
- Lactic acidosis
- DKA
- Alcohol, methanol, ethylene glycol

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18
Q

Clearance

A

Volume of plasma from whicha drug is completely removedina given time(mL/min)
Commonly indexed against body mass (mL/kg/min)

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19
Q

Clearance (formulas)

A

Cl = Vd / T
Since T = 1 / K
Cl = K.Vd

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20
Q

Pharmacokinetics

A

Absorption
Distribution
Metabolism
Excretion

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21
Q

Bioavailability

A

Fraction of a drug available to the systemic circulation compared with IV administration
Calculated by area under the curve

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22
Q

First pass metabolism

A

Metabolism by the gut wall or liver prior to reaching systemic circulation
PR, SL, TD, inhalational, IV etc - bypass 1st pass metabolism

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23
Q

First order kinetics

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A

Rate of elimination of a drug is directly proportional to drug concentration

24
Q

Time to reach steady state (first order kinetics)

25
Elimination profile in a single compartment.
C = C0.e-kt where: C = concentration at time = t C0 = concentration at time = 0 k = rate constant t = time -kt is a dimensionless term
26
Describe C0
The concentration of a drug at time = 0 C0 = dose / Vd
27
What is the time constant (t)?
Time taken for plasma conc to fall to 1/e of it's current value Or the time taken to fall to 37% of initial value Or the time taken for a drug to be completely eliminated, had the original rate of decline continued The inverse of the rate constant.
28
Half life
The time taken for plasma concentration to reach half its starting value
29
Relationship between half life and the time constant (T)
T½ = T.ln2
30
Which is bigger? the time constant or half life?
Time constant > half life T is time taken to fall to 37% which is longer than t1/2 time taken to fall to 50% ALWAYS
31
Why do you wake up quickly following a propofol infusion at steady state?
Conductance between the peripheral and central compartments is low. The terminal elimination take a long time, but plasma concentrations fall rapidly and you wake
32
Michaelis constant
The concentration of a substrate at which an enzyme system is working at half its maximal capacity
33
What factors affect hepatic extraction of a drug? (3)
Protein binding Blood flow Michaelis constant
34
Volume of distribution
The theoretical volume into which a drug disperses to produce the observed plasma concentration Vd = Dose / C0
35
Seddon-Sunderland Classification
Classifcation of peripheral nerve injury 1. Neuropraxia - temporary interruption of conduction without loss of axonal continuity 2. Axonotmesis - loss of relative axon continuity and myelin covering, but preservation of the connective tissue framework 3. Neurotmesis - axon + endoneurium transection (preserved perineurium + epineurium) 4. Neurotmesis - axon + endoneurium + perineurium transection (preserved epineurium) 5. Neurotmesis with complete transection of nerve trunk
36
Isomer
Molecules that have the same molecular formula but whose atoms are arranged differently
37
Structural isomer
Molecules with the same molecular formula but different chemical structure
38
Colloid
A substance that has large insoluble particles of one substance suspended/dispersed through a second substance
39
Blood:gas coefficient
Ratio of amount of anaesthetic gas in blood to that in gas when the two phases are equal volume + pressure + in equilibrium at 37°C Describes the relative solubility of a gas in blood (water) Lower blood:gas coefficient → more in gas than in blood → faster onset/offset
40
What is the embryological origin of the adrenal medulla?
Chromaffin cells derived from the ectodermal cells of the neural crest
41
What is the embryological origin of the adrenal cortex?
Mesoderm
42
What does the adrenal cortex secrete?
Steroid hormones: Glomerulosa: glucocorticoids (cortisol) Fasciculata: mineralocorticoids (aldosterone) Reticularis: androgens
43
What are glucocorticoids? (1)
Steroid hormones that affect the metabolism of carbs, fats + proteins Important in mediating the response to fasting and stress
44
What are the primary effects of glucocorticoids?
Cardiovascular - Maintenance of response to catecholamines Liver - Protein catabolism - Gluconeogenesis Kidney - Weak mineralocorticoid activity Immune - Immunosuppresion - Slowed healing
45
What are the primary effects of mineralocorticoids?
Cardiovascular - none Liver - none Kidney - Resorbs Na⁺ in the Distal Convoluted Tubule at the expense of loss of K⁺ and H⁺ lost into the urine - Expansion of the intravascular compartment (water follows Na⁺) Immune - none
46
Cardiovascular - none
Aldosterone is released in response to: - Decreased Na⁺ - Decreased plasma volume - Increased K⁺ - Activation of the RAAS The final common pathway is the binding of angiotensin II to receptors in the zona glomerulosa - This acts via G-protein to activate phospholipase C It facilitates the conversion of corticosterone → aldosterone
47
What is hyperaldosteronism?
Excess circulating aldosterone: Primary causes - Conn’s Syndrome - adrenal adenoma (60%) - Bilateral adrenal hyperplasia (30%) - Carcinoma Secondary causes - Increased activation of the RAAS e.g. CCF or liver cirrhosis
48
What are the core features of hyperaldosteronism?
Hypertension (coz retention of water) Hypokalaemia (coz loss of H⁺ in kidneys) Metabolic alkalosis (coz loss of H⁺ in kidneys)
49
What is SVR?
SVR = 80 x (MAP - CVP)/CO 1000 - 1500 dyne/s/cm5
50
What factors cause a right shift of the oxyhaemoglobin dissociation curve?
CADET: CO₂ Acidosis / anaemia / altitude DPG (raised) - e.g. in pregnancy Exercise Temperature
51
Which components in PRC help prevent depletion of 2,3-DPG?
Adenosine Phosphate Glucose NB, mannitol helps prevent oxidative stress to RBC, but has no impact upon 2,3-DPG
52
What are the “classical” anti-inflammatory cytokines?
IL4 IL-10 IL-13 IFN-α TGF-β
53
Define osmolarity
Number of osmoles per litre of solvent 2x (Na⁺ + K⁺) + urea + glucose * Na⁺ + K⁺ are doubled because each has an associated anion (usually Cl⁻) Affected by temperature + pressure
54
Define osmolality
Number of osmoles per kg of solvent
55
Maximum concentrating capacity of the kidneys
1200 mOsm/L
56
Minimum mandatory renal solute excretion
500-600 ml / day

Final (21 decks)

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