Primary Flashcards
CSHT
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
3 causes of calcified CXR lesions
Asbestosis
Mitral valve disease
Chicken pox
Visual symptoms of papilloedema
Enlargement of blind spot
Blurring of vision
Mapleson A minimum flow (2)
SV: 0.8-1x MV
CV: 2-3x MV
Mapleson B minimum flow (2)
SV: 1.5-2x MV
MV: 2-3x MV
Mapleson C minimum flow (2)
SV: 1.5-2x MV
MV: 2-3x MV
Mapleson D minimum flow
SV: 2-3x MV
CV: 0.8-1x MV
Mapleson F minimum flow
2-3x MV
Mapleson E minimum flow
2-3x MV
Lack system
Co-axial Mapleson A
Bain system
Co-axial Mapleson D
Bain system FGF is carried through…
The inner tube
Closing capacity = FRC when?
Age 44 supine
Age 66 upright
Identify the structures of the descending tracts
Medial longitudinal fasciculus
Lissaur’s tract
Lateral corticospinal Tract
Rubrospinal tract
Pontine reticulospinal tract
Medullary reticulospional
Lateral vestibulospinal
Tectospinal
Ventral corticospinal
Identify the structures of the ascending tracts
Fasciculus gracilis
Fasciculus cuneatus
Dorsal spinocerebellar tract
Ventral spinocerebellar tract
Spinothalamic tract
Anion Gap (2)
[Na] + [K] - [HCO3] - [Cl]
Range 8 - 16 mEq/L
Causes of a high anion gap metabolic acidosis (3)
High unmeasured anions:
- Lactic acidosis
- DKA
- Alcohol, methanol, ethylene glycol
Clearance
Volume of plasma from whicha drug is completely removedina given time(mL/min)
Commonly indexed against body mass (mL/kg/min)
Clearance (formulas)
Cl = Vd / T
Since T = 1 / K
Cl = K.Vd
Pharmacokinetics
Absorption
Distribution
Metabolism
Excretion
Bioavailability
Fraction of a drug available to the systemic circulation compared with IV administration
Calculated by area under the curve
First pass metabolism
Metabolism by the gut wall or liver prior to reaching systemic circulation
PR, SL, TD, inhalational, IV etc - bypass 1st pass metabolism
First order kinetics
Rate of elimination of a drug is directly proportional to drug concentration
Time to reach steady state (first order kinetics)
5 half lives
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
Describe C0
The concentration of a drug at time = 0
C0= dose / Vd
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.
Half life
The time taken for plasma concentration to reach half its starting value
Relationship between half life and the time constant (T)
T½ = T.ln2
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
Why do you wake up quickly following a propofol infusion at steady state?
Conductancebetween the peripheral and central compartments islow. The terminal elimination take a long time, butplasma concentrations fall rapidlyand you wake
Michaelis constant
The concentration of a substrate at which an enzyme system is working at half its maximal capacity
What factors affect hepatic extraction of a drug? (3)
Protein binding
Blood flow
Michaelis constant
Volume of distribution
The theoretical volume into which a drug disperses to produce the observed plasma concentration
Vd = Dose / C0
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
Isomer
Molecules that have the same molecular formula but whose atoms are arranged differently
Structural isomer
Molecules with the same molecular formula but different chemical structure
Colloid
A substance that has large insoluble particles of one substance suspended/dispersed through a second substance
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
What is the embryological origin of the adrenal medulla?
Chromaffin cells derived from the ectodermal cells of the neural crest
What is the embryological origin of the adrenal cortex?
Mesoderm
What does the adrenal cortex secrete?
Steroid hormones:
Glomerulosa: glucocorticoids (cortisol)
Fasciculata: mineralocorticoids (aldosterone)
Reticularis: androgens
What are glucocorticoids? (1)
Steroid hormones that affect the metabolism ofcarbs, fats + proteins
Important in mediating the response to fasting and stress
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
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
Cardiovascular - none
Aldosterone is released in response to:
- Decreased Na⁺
- Decreased plasma volume
- Increased K⁺
- Activation of the RAAS
The final common pathway is thebinding of angiotensin IIto receptors in thezona glomerulosa - This acts viaG-proteinto activatephospholipase C
It facilitates the conversion ofcorticosterone → aldosterone
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
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)
What is SVR?
SVR = 80 x (MAP - CVP)/CO
1000 - 1500 dyne/s/cm5
What factors cause a right shift of the oxyhaemoglobin dissociation curve?
CADET:
CO₂
Acidosis / anaemia / altitude
DPG (raised) - e.g. in pregnancy
Exercise
Temperature
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
What are the “classical” anti-inflammatory cytokines?
IL4
IL-10
IL-13
IFN-α
TGF-β
Define osmolarity
Number of osmoles perlitreof solvent
2x (Na⁺ + K⁺) + urea + glucose
* Na⁺ + K⁺ are doubled because each has an associated anion (usually Cl⁻)
Affected by temperature + pressure
Define osmolality
Number of osmoles perkgof solvent
Maximum concentrating capacity of the kidneys
1200 mOsm/L
Minimum mandatory renal solute excretion
500-600 ml / day
