late august viva Flashcards
addisons
deficinet aldosterone secretion from adrenal
stewarts theory
CORE
Stewart stated that H+ and HCO3‐ ion concentration were
dependent variables, and thus acknowledged the
importance of other factors controlling the pH
ACID/BASE Balance should = (OH‐) / (H+)
The H+ and HCO3‐ ion concentrations in the body were
determined by 3 INDEPENDENT VARIABLES
1) SID = Na+, K+,Ca2+,Mg2+ minus
Cl‐, and all (Other Strong Anions)
2) A (total) –Weak non‐volatile acids – Inorganic
Phosphate, Plasma Proteins and Albumin
3) pCO2 – really CO2 concentration – however
solubility varies only slightly in the human temp
range and pCO2 is easily measured
stewart negative
COMPLEX Computer Algorithms
Lack of Clinical Correlation
SID reflects only Plasma, whereas SBE reflects Hb
influence and the Whole Body Status
– ISOHYDRIC PRINCIPLE
SBE –Well Validated clinically over a long period of
Time.
SID
Sum of Routinely Measured Strong Cations – MSC ‐ (Na+K)
MINUS Routinely Measured Strong Anions ‐ MSA ‐ (Cl)
= 42meq L.
SID and Plasma HCO3 have a direct relationship
↑ SID = ↑ Plasma HCO3 (Metabolic Alkalosis)
‐ Filling up SID Space caused by ⇓ Cl.
↓ SID = ↓ Plasma HCO3 (Metabolic Acidosis)
‐ SID Space occupied by Cl or Strong Acids (LTKR) not
routinely measured.
SID and IVF
In order to maintain Acid – Base Homeostasis with the
administration of NON Albumin containing fluids, the SID
of the infused 1L of fluid needed to decrease from
42 to 27 = NEUTRALITY
BENEFIT OF PLASMALYTE
Plasmalyte
–>SID of 50
high SID–>high HCO3–>alkalaemia
CSL
–>SID of 27–>neutral
SID of blood if 42 but vol explansion causes decreased albumin–>increased SID–>alkalaemia so less SID of 27–>neutral
buffer
BUFFER – is a mixture of a Weak Acid and its
Conjugate Base
Attenuates the change in H+ ion concentration when a
Strong Acid or Base is added
pka
pKa = the negative Log 10 of the Ionization constant
IONIZATION CONSTANT is the pH at which EQUAL
values of the Conjugate Base and the Weak Acid are
present.
Anion gap explained
Lethal Acids CONSUME HCO3, but do nothing to Cland
thus cause an ↑ in the AG
Buffer systems
ISF: H2CO3 Blood: Hb, Pr, H2CO3 ICF: HPO4, H2CO3 kidneys: NH4, HPO4 (titratable) Bone: CaCO3
law of mass action
Total Concentration‐‐ must equal the sum of all the dissociated components
Plus the sum of All the Undissociated Components
isohydric principle
The isohydric principle is the phenomenon whereby multiple acid/base pairs in solution will be in equilibrium with one another, tied together by their common reagent: the hydrogen ion and hence, the pH of solution.
mass action
Law of Mass Action states that the multiplication of the concentration of the Individual
constituents of a chemical reaction, divided by the concentration of the product of the
chemical reaction at equilibrium =a constant Ka
Ka = (H+) (HCO3‐)/H2CO3
Hb as buffer
Buffering is by the imidazole group of the histidine residues
– Pk = 6.8
imidazole is basic and a part of the AA histidine
Hb is 6x more important than plasma proteins as a buffer due to
1) Double the plasma concentration of Hb
2) Hb has 3x the amount of histidine residues per molecule
De –Oxy Hb has greater buffering power –Weak Acid
Pr buffer
Consists of Amino Acids that have Free Acidic Radicles
that can Dissociate into Base plus H+ ions.
PK ‐‐ 7.40
Most Important Buffer in ICF (large Protein conc in
ICF) – Thus contributes the MOST of all buffer
systems to Acid‐Base AbN
Contributes only 5% of Acute ECF Buffering due to the
Relative Impermeability of Cell Membranes to H+ and
HCO3‐ (delays buffering ability of Plasma Acid‐Base
AbN for several hours)
can be weak acids or weak bases
PO4 pka and site
Phos buffer pair very important in ICF
Phosphate conc much higher in ICF than ECF = 100x
pH of ICF is closer to the pK of the Phosphate Buffer
system, than is Ph of ECF
boen buffer
IONIC EXCHANGE
Bone can take up H+ in exchange for Ca+
Involved in buffering of Acute Metabolic Acidoses
without bone breakdown
OSTEOCLASTIC REABSORPTION of BONE
Release of CaCO3 which leads to HCO3‐ formation
Involved in Chronic Metabolic Acidoses – ESKD, RTA
meq/kg
A certain amount of univalent ions provides the same amount of equivalents while the same amount of divalent ions provides twice the amount of equivalents
Strong acids prod
1meq/kg/day
glutamine glutamate
glutamate punches you and it hurts T=transmitter
glutamine is an AMINoacide
NH4
glutamine (AMINOACID)–NH4 + HCO3
info on ABG for acid base
pH ‐ Measured directly
pCO2 – Measured directly
Actual HCO3 – Measures pH and pCO2 from blood sample and then
calculates HCO3 from the H‐H Equation
Standard HCO3 – Calculated parameter when the blood sample is
equilibrated with a gas mixture with PCO2 level of 40mmHg – attempt
to represent the True metabolic component in patients with dual Acid –
Base AbN.
BASE EXCESS = Amt of Acid or Base that must be added to the blood
sample to restore the pH back to 7.40 if the pCO2 is N (40mm)
STANDARD BASE EXCESS = As for BE but equilibrated with a
specimen of anaemic blood – Hb = 5,0
osmolar gap
10
uncharged particles that contribute to osmolarity but not measured
osmol define
an osmole is the amount of a substance that yields the number of particles that would depress the freezing point of the solvent by 1.86K
Avogadro’s number of particles in an ideal solution
NH4 system
The capacity of this system to excrete hydrogen ions in the urine exceeds that of phosphate
make urinary ph depression
The minimum urinary pH is 4.4, because the
mechanism of active transport of hydrogen
secretion is inhibited at higher hydrogen ion
concentrations.
minimum urine
maximally concentrating still needs to remove waste. –>0.3ml/kg/hr=430ml/day
nodes of ronvier mech
In some large-diameter nerves, the process of
action potential conduction is not continuous
along the length of the bre. Instead, action potentials jump along from point to point in a ‘saltatory’
manner (Figure 1.15a). is occurs in myelinated
nerves where a fatty layer composed of overlapping Schwann cells covers the axon apart from at
the regularly spaced nodes of Ranvier.
RMP of different tissues
SA -55
Vent-90
Nerve 70
m. -90
hyperpolarization cause
If all the sodium channels are open, however, then the neuron becomes ten times more permeable to sodium than potassium, quickly depolarizing the cell to a peak of +40 mV.[2] At this level the sodium channels begin to close and voltage gated potassium channels begin to open. This combination of closed sodium channels and open potassium channels leads to the neuron re-polarizing and becoming negative again. The neuron continues to re-polarize until the cell reaches ~ –75 mV,[2] which is the equilibrium potential of potassium ions. This is the point at which the neuron is hyperpolarized, between –70 mV and –75 mV. After hyperpolarization the potassium channels close and the natural permeability of the neuron to sodium and potassium allows the neuron to return to its resting potential of –70 mV.
RMP and Na
Hypernatremia:-generally change of sodium doesn’t affect RMP, The permeability of it is
low , so Na will accumulate(more distribution) extracellulary,
RMP and K
INCREASED (Hyperkalemia):-hyperpolarized because of more incurrent K+, SO the RMP will
be at new level further from the Threshold, so the probability to have an Action potential is
less. This will affect the heart and muscles in general, weakness, ascending paralysis, and If
untreated cardiac arrhythmias.
DECREASED (hypokalemia):-Weakness, fatigue, motor paralysis, Myopathies
(Myotonia:delay relaxation or continuous spasm after voluntary contraction).
RMP and Ca
Ca++ competes with Na so if there is more Ca+2 this means more blocked channels so less
Na influx and less depolarization , but when Ca++ is low so the competition is less and Na
influx increased and so the depolarization.
Ester link
COO
NOOT CCO
CVS and CNS LA ratio
CC/CNS ratio
PEEP effect
R and L
And Starling
Interdependence
USS depth and vision
High freq–> better resolution as smaller wave length but more absorption (attenuation) –> shallow pentration
Freq wave eqn
V=wave.freq
V is constant
Daba vs rivarox
Evernote
Oxycodone met
Oxymorphone is active met weakly
Hm met
HM3g and HM6G
NEUROTOXIC and accumulate in renal
Buprenorphine met
Hep then bilary excretion with only a touch of renal so good in shitty kidneys
This class
Barbiturate
Barbiturate moa
Augment cl flow indep of GABA
Decrease NT release and response
Thiopentone structure function
Thio is sulfur analog of oxybarbituatuate
Pentone is substition at 5–>hypnotic
Thio and ketamine isomers
Ketamine has S and R enantiomers
Thio has enol tautomerism to keto in acidity of blood!
Play ketamine and thio
7.5 and 7.6
Theory of alb
Oncotic
Antioxidant
Acid buffer
Won’t work in leaky
Non essential
Allergy
countercurrent
conc hair pin!!! dilute ascending!
The active transport of sodium and chloride in
the ascending limb and the water permeability of
the descending limb produce, as described earlier, an osmolality of 400 mOsmol/kg H2O in the
descending limb and the interstitial fluid, and an
osmolality of 200 mOsmol/kg H2O in the ascending limb. The processes of fluid flow down and
back up the loop, active sodium reabsorption from
the ascending limb and water reabsorption from
the descending limb are continuous and move the
more concentrated tubular fluid down into the
hairpin of the loop. The effect is to increase interstitial osmolality at the hairpin tip of the loop in the
medulla and dilute the fluid leaving the ascending
limb of the loop of Henle (Figure 7.14).
The long loops of Henle reach from
Frusemide moa
Furosemide inhibits the sodium-potassium-chloride (Na+-K+-2Cl-)
Frusemide PK
Approximately 50% of the furosemide load is excreted unchanged in urine, and the rest is metabolized into glucuronide in the kidney.
The bioavailability of torsemide is predictable. It is extremely well absorbed (80-90%), regardless of the presence of edema, because it undergoes substantial hepatic elimination. The dosage of intravenously administered furosemide is usually half of that of the oral dose; oral bioavailability is approximately 50%(10-90%)
The half-life of the various loop diuretics are not the same: 1-1.5 hours for furosemide
colloid def
A colloid is defined as a high molecular weight (MW) substance that largely remains in the intravascular compartment, thereby generating an oncotic pressure.
colloid types and SE
anaphylaxis and coag common to all
AKI spec to dextan and starch
b1 rec
https://en.wikipedia.org/wiki/Beta-1_adrenergic_receptor
b2 rec
https://en.wikipedia.org/wiki/Beta-2_adrenergic_receptor
CCF Mx chronic
spiro–>inhibit remodel
BB–>decreases Preload and work
RB digoxin in arrhythmia
WOB curves
elastic=lung recoil and ST
normal resp compliance
It is usually about 100ml/cm H2O.
500ml/5cmH20=100
1/200+1/200
hysteresis cx
Hysteresis develops due to: The effect of surfactant Relaxation of lung tissue Recruitment and derecruitment of alveoli Gas absrption during measurement Differences in expiratory and inspiratory air flow (for dynamic compliance)
Entropy negatives
no motor
alertness changes with stimulation hence fine then awake.
ADH secrtion graph
increased osmo–>increased ADH
threshold decreased in hypovol
dead space Cx
Factors that increase dead space:
General anesthesia – multifactorial, including loss of skeletal muscle tone and bronchoconstrictor tone
Anesthesia apparatus/circuit
Artificial airway
Neck extension and jaw protrusion (can increase it twofold)
Positive pressure ventilation (i.e. increased airway pressure)
Upright posture as opposed to supine (because of decreased perfusion to the uppermost alveoli)
Pulmonary embolus, PA thrombosis, hemorrhage, hypotension, surgical manipulation of pulmonary artery tree – anything that decreases perfusion to well-ventilated alveoli
Emphysema (blebs, loss of alveolar septa and vasculature)
Age
Anticholinergic drugs
fowlers method why midpoint
A plot of expired nitrogen concentration by volume is generated, producing a graph with four phases:
Phase 1 (Pure Dead Space)
Gas from the anatomical dead space is expired. This contains 100% oxygen - no nitrogen is present.
Phase 2
A mix of anatomical dead space and alveolar (lung units with short time constants) is expired. The midpoint of phase 2 (when area A = area B) is the volume of the anatomical dead space.
Phase 3
Expired nitrogen reaches a plateau as just alveolar gas is exhaled (lung units with variable time constants).
Vd contributers
“Patient factors could include age, gender, muscle mass, fat mass and abnormal fluid distribution (oedema, ascites, pleural effusion). The drug factors would include tissue binding, plasma protein binding and physicochemical properties of drug (size, charge, pKa, lipid solubility, water solubility).”
Preg: Recent studies have shown that anatomical dead
space increases by 45% due to the larger conducting airways,
haemasol
same conc as ideal blood essentially
rule of 5s
acute is small!
HITS Rx
Fondaparinux (Arixtra) is a synthetic anticoagulant based on the pentasaccharide sequence that makes up the minimal antithrombin (AT) binding region of heparin. Similar to low molecular weight heparins, it is an indirect inhibitor of factor Xa, but it does not inhibit thrombin at all
no effect on platelet or fibrinolysis or directly on thrombin
HITS
2 points if >50% fall in platelet count to a platelet count nadir of ≥20 × 10⁹/L (≥20 × 10³/microlitre)
4/8=10% risk of HITS
warfarin
inhibits Vitamin K epoxide reductase
req to reduce vit K
req as coenzyme for carboxylation of vit k dep CF
N20
OXIDATION of cobalt of B12 which is a cofactor for methionine synthase req for folate synth.
SUBACUTE DEGEN OF CORD
weak, paraesthesia, spasticity, altered mental state.
pancytopenia, megaloblastic aenaemia
heparin vs clexane
x
anticlot
To prevent uncontrolled disseminated coagulation, there are a number of physiological inhibitors
of coagulation. Serine protease inhibitors include
antithrombin III (inhibits IIa and Xa), C1 inhibitors (inhibit contact factors), α2-macroglobulins
(inhibit IIa and contact factors), α2-antiplasmin
and α2-antitrypsin, which inhibit circulating serine proteases.
Factors Va and VIIIa are regulated by proteins
C and S, which are vitamin-K-dependent serine
proteases. Protein C destroys factors V and VIII,
while protein S enhances protein C by binding it
to the platelet surface. Protein C is activated by
thrombomodulin formed by the binding of thrombin to the endothelial cell surface
Undamaged
vascular endothelial cells prevent clotting
by releasing natural anticoagulants, such
as heparin and prostacyclins, and by
expressing thrombomodulin, a protein that
binds thrombin and activates protein C, an
activator of plasmin.
prothrombinex
has heparin in it #HITS
heparin define
mucopolysach
daba vs rivar
evernote
why amide last longer
Prb
preg spiro actually draw
evernote
dynamic air trapping
starling resister TMP instead of alv vs atm.
Flow vol loop–>scooped out as late exp limited as equal pressure point is closer to alv.
hormones preg resp
relaxin
Progesterone
stimulates the respiratory centres and shis the
ventilation–carbon dioxide response curves to
the le
coag preg
Pregnancy is associated with increased coagulability and platelet turnover. ere is a signicant
increase in the concentrations of factors VII, VIII,
IX, X and brinogen. Greater platelet production
matches the increase in platelet activation and
consumption. Overall, the platelet count is slightly
reduced (5%–8%) during pregnancy. Fibrinogen
levels may double from 3 to 6 g/L.
Plasminogen concentration is markedly raised,
but this is oset by plasminogen activator inhibitors produced by the placenta. Antithrombin III
levels decrease. ere is an increase in brinolysis
and brin formation in late pregnancy.
Total circulating proteins increase during pregnancy, but the concentrations of total proteins and
albumin decrease as a result of haemodilution. ere
is an increase in total globulins, especially α-globulin
Serum pseudocholinesterase
activity is reduced by 20%–30% at the end of the rst
trimester and remains at that level until term.
DKA
The elevated blood glucose in DKA creates an osmotic gradient which @pically results in hyponatremia
medulla conc
1400 mOsmol/kg H2O in the inner medulla.
frusemide
luminal Na-K-Cl cotransporter in the thick
lose everythink
VD decrease preload and afterload and PHTN
increase RBF
nil BSL change
chloride loss–>HCO3 gain #SID–>alkalosis
met liver and kidney
elim liver and kidney
hormone define
A hormone (from the Greek participle ὁρμῶν, “setting in motion”) is any member of a class of signaling molecules, produced by glands in multicellular organisms, that are transported by the circulatory system to target distant organs to regulate physiology and behavior.[1] Hormones have diverse chemical structures, mainly of three classes:
eicosanoids
steroids
amino acid/protein derivatives (amines, peptides, and proteins)
The glands that secrete hormones comprise the endocrine signaling system. The term “hormone” is sometimes extended to include chemicals produced by cells that affect the same cell (autocrine or intracrine signaling) or nearby cells (paracrine signalling).
Hormones serve to communicate between organs and tissues for physiological regulation and behavioral activities such as digestion, metabolism, respiration, tissue function, sensory perception, sleep, excretion, lactation, stress induction, growth and development, movement, reproduction, and mood manipulation.[2][3] Hormones affect distant cells by binding to specific receptor proteins in the target cell, resulting in a change in cell function. When a hormone binds to the receptor, it results in the activation of a signal transduction pathway that typically activates gene transcription, resulting in increased expression of target proteins; non-genomic effects are more rapid, and can be synergistic with genomic effects.[4] Amino acid–based hormones (amines and peptide or protein hormones) are water-soluble and act on the surface of target cells via second messengers; steroid hormones, being lipid-soluble, move through the plasma membranes of target cells (both cytoplasmic and nuclear) to act within their nuclei.
define enzyme
x
stim of ATII
barorec in JGA!
adrenal cortex
zona Glomerulosa reticularis fasciulatar
Minero-ald
glucocort eg cortisol
sex
ultrafiltrate
solution and solute hrough SP memb (nil colloids)
BM charge change
nephritis lose charge–>pr loss
nephrotic Sx–>larger poor size–>pr loss
bowman cap
cap endo with split, BM with cahrge, podocyte
critically damped vs over
over is +++++ slow
critically is just at that point where it doesnt cross
issues with art line
res
-Nat freq superimposing peaks on 8th harmonic or less
NF proportional to stiff.r^2/density.l
damping-too much is slow. too little–>resonance
-diameter
damping
Damping is the process of the system absorbing the energy (amplitude) of oscillations
opitmal damping coeff
0.7
o2 cascade
capillaries higher than veins
mitochondria 5mmHg
photophlethysmograph absorption
DARL
Deox absorbs red light!
isobesic point
Isosbestic points are used in medicine in a laboratory technique called oximetry to determine hemoglobin concentration, regardless of its saturation. Oxyhaemoglobin and deoxyhaemoglobin have (not exclusively) isosbestic points at 586 nm and near 808 nm.
Cor BF humeral
HR!
CorVR governed by factors that alter coronary artery radius, which include:
(i) metabolic autoregulation ! vasodilator (NO, PGI2) release triggered by
local metabolites (↓ O2, ↑ CO2, ↑ H+
, ↑ K+
, ↑ adenosine, etc)
(ii) myogenic autoregulation ! smooth muscle stretch results in contraction
and vice versa
(iii) autonomic + hormonal control ! SNS, PSNS + adrenaline, ADH
(iv) extrinsic compression
(v) intrinsic narrowing ! coronary artery disease, vasospasm
current unit and measurement
amps
Current can be measured using an ammeter.
Electric current can be directly measured with a galvanometer,
changed EM filed moved needle
http://www.partone.litfl.com/drug_interactions.html
Drug interactions gold
Xx
baro rec range
threshold mean arterial blood pressure at which
baroreceptors begin to re is around 60 mmHg.
low pressure baro rec
↑vol (↑CVP) ~10% → afferents via CN X to medulla → Overall inhibitory effect on heart (stimulation PNS, inhibition SNS)
shock–>acidosis
increased lactate production and decreased clearance (less BF to liver–>Cori)
CSHT at infinity trend
terminal elimination halflife
after an instant==alphahalflife
limitations of half life
The concept of half-life has limitations in terms of its bedside utility to the pragmatic intensivist. If the effect of the drug has only a minimal relationship with its plasma concentration, the half-life becomes only marginally important. An excellent example of this is the relationship of aminoglycoside dosing to antibiotic effect against urosepsis and the plasma half-life of the drug. Gentamicin has excellent post-antibiotic effect and will continue to exert this effect long after the plasma concentration has half-lived down to minute fractions of the administered dose.
Half-life (in its conventional form) also has the limitation of being unfairly plasma-centric. Again using gentamicin and urosepsis as an example, the plasma half-life has relevance to systemic toxicity but will probably have little relevance to the “killing power” of the antibiotic against the bugs in the urine, where this renally excreted drug will rapidly be concentrated to massive levels (perhaps several orders of magnitude above MIC).
Half-life typically refers to elimination half-life, which is the half-life derived during the terminal elimination phase of a drug’s distribution. This makes no sense for widely and rapidly distributed drugs. For instance, the rapid distribution of thiopentone into the fat partition results in a rapid offset of clinical effect, but the elimination half-life will not give you that impression, as it is prolonged by the slow distribution of the drug back out of the fatty tissue. To some extent, this can be ameliorated by discussing half-life in terms of the exponent of interest, i.e separating half-life into a distribution half-life and an elimination half-life.
ropivocaine
S enantiomer
tiny Vd
15% unioninse pka 8.1
hydroxyropivocaine via hydroxylation via CYP450
EMLA
prilocaine 2.5 amd 2.5
toludene
monroe kelly pressures
normal is 5-15
20=trouble regional
50=fucked global
ACEi role
Conclusion: ACE inhibitors can prevent the LV remodelling process that accompanies cardiac dysfunction after MI, even in AT1 KO mice.
resistance
viscosity
re number
velocity.DIAMETER.DENSITY/VISCOSITY
error in pneumotacograph
(1) Deviation from laminar flow
Poiseuille law of laminar flow no longer holds ! flow rate and pressure drop no
longer follow simple linear relationship
Laminar flow more likely when Reynold’s number is low (< 2000)
Re = flow rate × vessel diameter × gas density / gas viscosity
(2) Resistance deviates from known constant
For laminar flow,
€
R = 8ηL
πr
4
Variations in above parameters ! alters resistance ! introduces error in calculated
flow rate
Alterations in viscosity of gas: ↑η ! ↑resistance
∴ calibration required for various gases compositions (e.g. air, N2O, volatiles, etc)
Alterations in temperature: ↑T ! ↑η ! ↑resistance
also, ↓T ! condensation of water vapour ! ↑resistance of barrier
∴ intrinsic heating coil maintains constant temperature of gas inflow and prevents
condensation in resistor
(3) Errors in measurement + errors introduced by measurement
If flow is too low ! resistor results in large decrease in flow rate ! introduces error
in measured flow rate
If flow rate too high ! resistor results in very small pressure differential ! difficult
to accurately measure ! error introduced
pneumotacogram
(1) Fleisch pneumotachograph → Fine bore parallel tubes (bulky)
(2) Lilly/screen pneumotachograph → Layer of metal or plastic gauze
(3) Pitot tubes → 2 pressure sampling tubes in the centre of gas flow measure the
potential difference between the upstream & downstream (static) pressures
pneumotachogram
venturi–>lamina
pitot–>more accurate
P proprotiaonl to square of flow
bernoulli
P1/density+V1^2/2=P2/density +V2^2/2
sfent potency
++++
buprenoprhine rec
Mu ag
kappa antag
NIL NMDA OR SSRI
METHADONE
Mu agonist
NMDA antage
SSRI
cerebral o2 consumption
The normal human brain consumes 3.5 ml of O2 per 100 g of brain tissue per minute, a value which remains constant throughout periods of wakefulness and sleep. This relatively high rate of oxygen consumption is appreciable when compared to the metabolic rate of the entire body.
why measure INR for warfarin
Why use intrinsic PT—>INR fro warfarin no
PT or/and INR explore the extrinsec pathway of coagulation that involves all vitamin K dependent coagulation factors. Factor 7 is more sensitive to vitamin K deficiency (nutritional or by oral anticoagulants). It’s T1/2 is shorter than for factor 2 for example.
The half-lives of the vitamin K-dependent factors are factor II, 60 h; factor VII, 6 h; factor IX, 24 h; factor X, 48 h. For the control proteins, protein C’s half-life is 7 hours, the protein S half-life has not been defined.
