General Review Flashcards
Antigen presenting cells:
macrophages
B-lymphocytes
Dendritic cells
T-cells:
T cytotoxic: killer T-cells
T helper cells:
T helper 1
T helper 2
T cytotoxic cells action.
killer T-cells, recognize MHC 1 = intracellular antigens
T helper cells general actions.
recognize MHC 2 on APCs → activate other cells. APC’s are not infected.
T helper 1 cells action.
activate macrophages, natural killer cells
T helper 2 cells action.
activate B-cells → Ab production
Complement pathways
Classical
Lectin
Alternative pathway
Classical complement pathway is activated by:
Ag-Ab complexes or acute phase proteins
Lectin complement pathway is activated by:
mannose binding protein (MBP) binding to Antigen
Alternative complement pathway is activated by:
foreign pathogens without antibody
Endpoint of complement pathways:
All 3 pathways end the same…
- Enhanced attachment or opsonization (C3b)
- Trigger inflammation/phagocyte chemotaxis (C5a)
- MAC → cell lysis (C5b and others)
Immunoglobulin structure- draw
Hypersensitivity reactions with examples:
Type 1: IgE mediated → eosinophils → anaphylaxis.
Ex: bee sting
Type 2: cytotoxic. Complement mediated or Ab mediated → cell or receptor destruction.
Ex: IMHA, transfusion reaction, myasthenia
Type 3: Ag-Ab complex deposition.
Ex: lupus, lyme GN
Type 4: Delayed: T-cell mediated with prior sensitization → Macrophage activation.
Ex: albumin rxn
List the Endognous pyrogens and their effects:
IL 1
IL 6
TNF-a.
→ cytokine release, macrophage stimulation, release of prostaglandin → hypothalamus → raise set point
Define SIRS & nSIRS
Systemic inflammation.
nSIRS = non-infectious
Define sepsis (OLD)
SIRS due to an infection.
Define sepsis (NEW)
- life-threatening organ dysfunction caused by a dysregulated host response to infection.
- Acute change in SOFA score >/= 2 from baseline (assumed 0 if previously healthy)
- qSOFA: RR > 22, Systolic BP < 100, altered mentation
Define severe sepsis (OLD)
- OLD definition, eliminated with sepsis 3.
- Sepsis + organ dysfunction, hypotension, or impaired perfusion.
- In sepsis 3, all sepsis is “severe”.
Define Septic Shock (OLD)
severe sepsis with hypotension requiring pressors
Define Septic Shock (NEW)
- Subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality.
- Requires pressors to maintain systolic BP > 65
- Lactate > 2 despite adequate volume resuscitation
- Hospitality rate > 40%
Define MODS (OLD)
sepsis or SIRS + 2 or more organ dysfunctions
Define MODS (NEW)
- Any acute change in total Sequential Organ Failure Assessment (SOFA) score >/= 2 points as a result of sepsis or nSIRS
SIRS criteria (cat)
3 or more
- T < 100 or > 103.5
- HR < 140 or > 225
- RR > 40
- WBC < 5K or > 19.5K
SIRS criteria (dog)
2 or more
- T < 100.6 or > 102.6
- HR > 120
- RR > 20
- WBC < 6K or > 16K or 3% bands
Endpoints of goal directed therapy (old stuff…)
- Macrocirculation: CVP 7-10, MAP > 65, UOP > 0.5ml/kg/hr
- Microcirculation: Lactate < 2.5, ScvO2 > 70
Inflammatory Cytokines in sepsis:
IL 1
IL 6
IL 8 (aka CXCL8)
IL 12
TNF-a.
Anti-Inflammatory Cytokines in sepsis:
IL 4
IL 10
TGF-b
Mechanisms of vasodilation in sepsis:
- Activation of ATP-K channels in smooth muscle due to inflammation → prevention of Ca influx
- Increase nitric oxide release
- Vasopressin depletion
Mechanisms of septic myocardial dysfunction:
- Global ischemia
- Unknown circulating myocardia depressant factor
- Cytokines
Mechanisms of hypocalcemia in critical patients
- Increased calciuresis
- Dilution
- Cellular uptake due to muscle damage
- Chelation with citrate or lactate
- Altered hormones (PTH, vit D)
- Saponificaiton of fat (pancreatitis)
Positive Acute phase proteins:
- mannose binding protein
- fibrinogen
- haptaglobin
- C-reactive protein
- Serum Amyloid A
- Ceruloplasmin
Negative Acute phase proteins:
- albumin
- antithrombin
- transferrin
Definitions of nosocomial infection: infection that is first diagnosed….
- > 48 hrs after admission
- Within 2 weeks of hospitalization
- After transfer from another facility
- < 30 days post op
Mechanisms of bacterial resistance transfer:
Transformation: pick up naked DNA laying around
Transduction: bacteriophage (virus) transfers DNA
Conjugation: plasmid transferred by bacterial “sex”. #1 method
Random mutation → Natural selection/replication
Briefly explain transformation in terms of bacterial resistance.
pick up naked DNA laying around
Briefly explain transduction in terms of bacterial resistance.
bacteriophage (virus) transfers DNA
Briefly explain transduction in terms of bacterial resistance.
plasmid transferred by bacterial “sex”. #1 method
Lab findings in tumor lysis syndrome:
hyperphosphatemia
hypocalcemia
increased uric acid
azotemia
hyperkalemia
metabolic acidosis
multiple organ failure
shock
Mechanisms of heat loss:
Radiation
Conduction
Convection
Evaporation
Briefly explain radiation as a mechanism of heat loss.
exchange b/w objects and environment
Briefly explain conduction as a mechanism of heat loss.
objects in direct contact
Briefly explain convection as a mechanism of heat loss.
movement of fluid or air over body
Briefly explain evaporation as a mechanism of heat loss.
heat energy turns liquid → gas (ie sweat)
Classification of surgical wounds:
Clean
Clean-contaminated
Contaminated
Dirty
Briefly explain a clean-contaminated surgical wound.
entered a lumen and kept it clean
Briefly explain a contaminated surgical wound.
overt leakage/contamination at sx
Briefly explain a dirty surgical wound.
already infected/contaminated prior to sx
RER=
RER= (30 x kg) + 70 = 70 kg^0.75
TPN calculations:
Protein: 4kcal/g
(Dog: 4-5g/100kcal, Cat: 6-8g/100kcal)
Dextrose: 30-50% of remaining Kcal.
50% dextrose = 1.7kcal/ml
Lipid: 50-70% of remaining Kcal.
20% lipid = 2kcal/ml
Anterior Pituitary sections:
Makes TSH
ACTH
LSH
FSH
prolactin
GH (not stored really)
Posterior Pituitary sections:
Stores and releases ADH/vasopressin and oxytocin (these are made in magnocellular neurons of the hypothalamus)
Transudate classification & examples
TP < 2.5, < 1000 cells/µL.
Low alb, portal hypertension, vasculitis
Modified Transudate classification & examples
TP > 2.5, 1000-5000 cells/µL.
CHF, vasculitis, lymph obstruction
Exudate classification & examples
TP > 2.5, > 5000 cells/µL.
Blood, chyle, suppurative, septic, neoplastic
Abdominal effusion chemistry ratios:
Uroabdomen
Creat > 2 abdomen : 1 peripheral
K > 1.4 abdomen : 1 peripheral
Abdominal effusion chemistry ratios:
Bile peritonitis
Bili > 1.2 abdomen : 1 peripheral
Septic abdomen
Abd glu > 20 less than serum
Abd lactate 2 x more than serum
A-Fast views:
Ideally R lateral recumbency
DH view (diaphragmaticohepatic)
Splenorenal (L)
Cystocolic
Hepatorenal (R)
T-Fast views:
R and L chest tube sites: probe horizontally, look for pneumo
R and L pericardial sites: probe both ways and scan, look for fluid, heart
DH view: pericardial effusion, ab effusion
Adrenal gland layers:
Medulla: Norepi (cat), epi (dog)
Cortex:
- Zona glomerulosa: outer, salt (mineralocorticoids)
- Zona fasciculata: middle, sugar (glucocorticoids)
- Zona reticularis: inner, sex
Zona glomerulosa:
outer, salt (mineralocorticoids)
Zona fasciculata
middle, sugar (glucocorticoids)
Zona reticularis
inner, sex
Renin-AT-Aldosterone system:
Angiotensinogen (from liver) →(via renin from JG cells) → AT I → (via ACE from lung) → AT II
AT II effects:
- Na reabsorption → H20 Reabsorption
- Vasoconstriction
- Sympathetic stimulation → Increased RH/inotropy, vasoconstriction
- Aldosterone release → H2O/Na retention
- ADH → H20 reabsorption and vasoconstriction
Phase 1 metabolism reactions:
oxidative
reductive
hydrolytic
Phase 2 metabolism reactions:
conjugation
(glucaronic acid, sulfate, glutathione, acetylation)
Causes of ascites in liver disease:
- Portal hypertension
- Splanchnic vasodilation
- RAAS sodium retention
- Hypoalbuminemia
Causes of PU/PD in liver disease:
- Encephalopathy
- RAAS sodium retention
- Medullary washout (no urea)
- Increased endogenous steroids
Hepatic encephalopathy mediators:
- ammonia
- manganese
- glutamate/glutamine
- GI toxins
- increased GABA
- endogenous benzos
- aromatic AAs
- Mercaptans
- Skatoles
- Indoles
- Bile acids
- Serotonin
- Phenol
- Tryptophan
Path of bile flow:
Cranial nerves:
- Olfactory
- Optic (vision)
- Oculomotor (PLR and most motor)
- Trochlear (dorsal oblique)
- Trigeminal
(a) Ophthalmic (sensory eye)
(b) Maxillary (sensory teeth)
(c) Mandibular (masticatory mm, tongue sensory) - Abducent (lateral rectus, retractor bulbi)
- Facial (face motor, tongue sensory)
- Vestibulocochlear (vestibular, hearing)
- Glossopharyngeal (swallowing, tongue taste)
- Vagus (parasympathetic)
- Accessory (neck mm)
- Hypoglossal (tongue motor and swallowing)
Modified Glasgow Coma Scale
- Level of consciousness (0-6)
- Brain stem reflexes (0-6)
- Motor reflexes (0-6)
- Total score 0-18 (higher is better)
Mechanisms of secondary brain injury
- Increased excitatory neurotransmitters (glutamate) → ATP depletion
- Ca/Na entry into cells (pumps fail) → swelling (cytotoxic edema)
- ROS → peroxidation injury
- Bleeding → iron → worse ROS
- Increased vascular permeability (leaky BBB) → vasogenic edema
- Loss of pressure autoregulation due to NO induction
- Increased ICP → ischemia → worsened injury
- Systemic hypotension or hypoxia → ischemia → worsened injury
Hind end nerve roots
Femoral: L4-6 (Patellar and hip flexors)
Sciatic: L6-S2 (withdrawal)
Pudendal: S1-3
CVP waveform: be able to draw, label, explain all parts.
A wave = RA contraction (highest pressure)
C wave = Bulging of TV into RA (early RV systole)
X descent= RV emptying
V wave= rapid atrial filling (TV closed)
Y descent= TV opens, ventricular filling
Capnogram: be able to draw, label, explain all parts (normal and some common abnormals)
A-B = phase 1 = dead space exhalation
B-C = phase 2 = intermediate airways
C-D = phase 3 = alveolar gas
D = ET CO2
D-E= inhalation
Abnormals: Curare cleft, obstruction to exhalation, rebreathing, death/severe hypotension
Draw curare cleft capnograph waveform
Breakthrough breathing during IPPV
Draw obstruction to exhalation capnograph waveform
Obstruction in expiratory limb of circuit
Also, Bronchospasms/Asthma, COPD, upper airway FB, partially kinked or occluded airway
Draw a rebreathing capnograph waveform
Draw a death/severe hyoptension capnograph waveform
Draw a hypoventilation capnograph waveform
Draw a hyperventilation capnograph waveform
Draw:
Flow volume loop normal
Draw:
Flow volume loop abnormal -jagged
Airway secretions
Draw:
Flow volume loop abnormal - scooped
small or medium airway obstructions
Draw:
Pressure volume loop normal
Draw:
Pressure volume loop normal - decreased compliance
Draw:
Pressure volume loop normal - changes in resistance
Draw:
Pressure volume loop normal - Leak
Draw:
Flow-time scalars with both volume and pressure controlled ventilation
Draw:
Pressure-time scalars with both volume and pressure controlled ventilation
Draw:
Volume-time scalars with both volume and pressure controlled ventilation
Compliance
Compliance = 𝝙V/𝝙P
Elastance
Elastance = 𝝙P/𝝙V
Haldane effect
O2 offloading → increased CO2 affinity
Bohr effect:
increased CO2 (acidosis) → decreased O2 affinity
PaO2/FiO2 ratio:
PaO2 should be 5x FiO2 (or PaO2/FiO2 as a decimal = 500)
Residual volume
= volume left in lungs after max expiration
Total lung capacity
= volume in lungs after maximal inspiration (everything)
Tidal volume
= normal volume of inspiration
Expiratory reserve volume
= extra amount you can expire (still can’t ever get RV)
Inspiratory reserve volume
= extra amount you can inspire
Functional residual capacity
= volume left in lungs after normal expiration = RV + ERV
Inspiratory capacity
= maximum amount you can inspire= TLC - FRC = IRV + TV
Vital capacity
= total moveable air, air expired after a maximal insp/exp = TLC - RV
Airway pressure during inspiration:
𝝙P = 𝝙TV/ compliance + (Resistance x 𝝙Flow)
O2 saturation left curve shifts:
= increased affinity
=
alkaline
cold
decreased 2,3 DPG (fetus)
CO
O2 saturation right curve shifts:
= decreased affinity = increased offloading
=
high (increased 2,3 DPG)
hot
acid
Fick’s law of gas diffusion:
Volume of gas/time = Area/thickness x diffusion constant x 𝝙PP
𝝙PP = partial pressure difference
Diffusion constant = solubility/ √MW
Equation of motion (ventilator):
pressure = (TV/compliance) + (resistance x flow)
A-a gradient
= PAO2 - PaO2
PAO2 = FiO2 decimal x (barometric pressure - 50) - (PaCO2 x 1.1)
Barometric pressure at sea level = 760
50 = water pressure
PaO2 comes from your blood gas
Normal A-a gradient = < 15
Causes of hypoxemia:
- decreased FiO2
- hypoventilation
- diffusion impairment
- V/Q mismatch
- shunt (severe V/Q mismatch)
Causes of tissue hypoxia:
PA pressure = 4 x TR2
PHT pathophysiologic causes (3):
- Increased pulmonary vascular resistance: vasoconstriction, occlusion, remodeling (chronic lung disease), polycythemia
- Increased blood flow (L → R shunt)
- Increased LA pressure (MR)
PHT categories based on new consensus statement?
— need answer
What are the ARDS/ALI Criteria:
- Acute onset
- No evidence of cardiac dysfunction (based on echo, heart size on rad, or PCWP < 18)
- Pulmonary infiltrate with high protein fluid
- Hypoxemia: PF ratio 300-200 is mild, 200-100 is moderate, < 100 is severe- all with 5 PEEP
- Risk factors (ie systemic inflammation)
Fill in this chart:
NEED STATISTICS CHART
Define Sensitivity.
= ability to correctly ID those with disease
= true pos / all disease pos
= true pos/(true pos + false neg)
Define Specificity
= ability to correctly ID those without disease
= true neg / all disease neg
= true neg/(true neg + false pos)
Define Positive predictive value
= likelihood that patient has a disease with a positive result
= true pos / all test pos
= true pos/(true pos + false pos)
Define Negative predictive value
= likelihood that patient doesn’t have a disease with a negative result
= true neg / all test neg
= true neg/(true neg + false neg)
Define accuracy.
= # correct tests/all tests
= (TP + TN)/(TP + FP + TN + FN)
Accuracy = [sensitivity (prevalence)] + [specificity (1- prevalence)]
Define Likelihood ratio
= how much more likely it is that a patient with a positive test has a disease compared to a patient with a negative test
= sensitivity/ (1-specificity)
CO equation & normals
= SV x HR
normal = 100-200 ml/kg/min
CI equation
= CO/body surface area in m2
O2 Deliver equation
DO2 = CO x CaO2
Arterial O2 content equation
CaO2 = (1.3 x SaO2 x Hb) + (PaO2 x 0.003)
= bound + unbound
O2 consumption equation
VO2 = CO x (CaO2 - CvO2)
Oxygen extraction ratio equation & normal
OER = VO2/DO2
= (SaO2-SvO2)/SaO2.
Normal = 25%
Higher = inadequate O2 delivery
Systemic vascular resistance equation
= (MAP - CVP) / CO
Fick principle equation (to calculate CO):
CO = VO2/(CaO2 - CvO2)
Normal heart pressures:
- RA mean 0-5
- RV 25/5
- PA 25/10
- LA mean 5-10
- LV 125/10
- Aorta 125/80
Cerebral perfusion pressure equation
= MAP - ICP
Coronary perfusion pressure equation
= Diastolic aortic pressure - RA pressure
Law of LaPlace (Wall tension) equation
Tension = pressure x radius/wall thickness
(I do not really understand where this applies)
Pouisselle’s Law equation
Flow = (𝛑 x 𝝙 P x r4)/8nL
n= viscosity
Flow = 𝝙 P/ resistance
Ohm’s law equation
= rearranged Pouiselle’s
= Pressure = blood flow x resistance
Starling’s Law equation:
Net filtration (OUT of vessel) = Kf [(Pcap - Pint) - 𝛔 (𝛑cap - 𝛑int)
Kf = permeability
𝛔 = reflection coefficient
Explain how to set up and test a direct arterial BP system. — NEED TO WRITE OUT ANSWER
Arterial system dampening:
Ideal
Ideal: 2-3 oscillations after the square wave, each drop by ⅔ to the next one
Arterial system dampening:
Overdamped
Too few oscillations, too flat
Compliant tubing, air in tubing, clot in catheter or tubing, narrow tubing
Arterial system dampening:
Underdamped
Too many oscillations, doesn’t drop enough
Stiff tubing, tachycardia or dysrhythmia, long tubing
Albumin deficit (in grams) equation:
= 3 x (desired Alb - current Alb) x kg
List Albumin products:
FFP = 3g/100ml
WB = 1.4g/100ml
HSA = 25g/100ml
Transfusion volume calculations:
Transfused volume
WB
pRBC
Transfused volume = 90ml/donor PCV x % rise x kg
WB (PCV 45)= 2 x % rise x kg
pRBC (PCV 60) = 1.5 x % rise x kg
Normal COP:
Dog 18-20
Cat 20-24
Massive transfusion definitions:
More than blood volume in 24 hours
Half of BV in 3 hrs
High rate/bolus: > 1.5ml/kg/min over 20min (> 30ml/kg in 20 min)
Metabolic acidosis compensation equation
0.7 DECREASE in PCO2 for each 1meq DECREASE of HCO3
Metabolic alkalosis compensation equation
0.7 INCREASE in PCO2 for each 1meq INCREASE of HCO3
Respiratory acidosis
Acute & chronic compensation equation
Acute: 0.15 increase HCO3 for every 1 up in pCO2
Chronic: 0.35 increase HCO3 for every 1 up in pCO2
Respiratory alkalosis
Acute & chronic compensation equation
Acute: 0.25 decrease HCO3 for every 1 down in pCO2
Chronic: 0.55 decrease HCO3 for every 1 down in pCO2
Things to remember about acid-base compensation
- Compensation is always LESS than the primary problem (so a percentage = the decimal).
- Primary problem is the 1.0.
- Kidneys are not as good at compensating as lungs.
- 0.15, 0.25, 0.35, 0.55 alphabetical (acute acid, acute alk, chronic acid, chronic alk)
Henderson Hasselbach equation
pH = 6.1 + log HCO3 / (0.03 x pCO2)
Bicarbonate buffer equation
CO2 + H20 ⟷ H2CO3 ⟷ H+ + HCO3-
CO2 + H20 ⟷ H2CO3 is mediated by carbonic anhydrase
H2CO3 ⟷ H+ + HCO3- is a fairly immediate dissociation (doesn’t hang out as H2CO3)
Strong Ion Difference equation
= strong cations - strong anions
= (Na + K + Ca + Mg) - (Cl + lactate + urate
Stewart independent variables
- PCO2
- Strong ion difference (SID= essentially Na - Cl)
- Total weak acids (Atot = Alb + phos)
Bicarb deficit equation
Meq HCO3 = kg x 0.4 x (24-patient HCO3)
24 = normal bicarb
Want to correct ¼ to ⅓ of the deficit at a time
K shift for acid/base equation (briefly discuss)
0.6mEq increase in K for every 0.1 unit drop in pH
Applies to MINERAL metabolic processes only
Basically: acidosis → hyperkalemia, alkalosis → hypokalemia (use Bicarb to drop K)
Anion Gap equation (briefly discuss)
= (Na + K) - (HCO3 + Cl)
= pos - neg
= essentially unmeasured anions (unmeasured cations are not variable)
Normal = 12-24
Unmeasured acids (anions):
MEG’s LARK (or LARD)
Methanol
Ethylene Glycol
Salicylate
Lactic Acid
Renal acids
Ketones (DKA)
Others: Propylene Glycol, ethanol, Sulfuric acid, metaldehyde, D-lactate
Types of lactate:
L-Lactate
D-Lactate
L- Lactate
Animal
Produced by anaerobic metabolism
D- Lactate
Bacterial
not generally measured.
Increased with short-bowel syndrome, DM, EPI, propylene glycol in cats)
Type A Lactic acidosis
Tissue hypoxia
Type B lactic acidosis
impaired cellular metabolism (abnormal mitochondrial dysfunction)
Congenital defect
Drugs/toxins
Lymphoma
Diabetes
Hypoglycemia
Liver/kidney failure
Sepsis
Lactate pathway
Types of ketones
Acetoacetate (ketostix)
Acetone
B-hydroxybutyrate (blood ketones, most abundant)
Free water Stewart Calculation
(& effect on base excess)
= (Measured Na - Normal Na)/4
High Na → Alkalosis (remember- contraction alkalosis)
Low Na → Acidosis
Chloride Stewart Calculation
(effect on base excess)
= Normal Cl - Corrected Cl
Remember- Hypochloremic metabolic alkalosis
Corrected Cl = measured Cl x (normal Na/measured Na)
Corrected Cl
= measured Cl x (normal Na/measured Na)
Phosphate Stewart Calculation
(effect on base excess)
= (Normal Phos - Measured Phos)/2
High Phos → Acidosis (Remember- renal failure acidosis)
Albumin Stewart Calculation
(effect on base excess)
= (Normal Alb - Measured Alb) x 4
Low Alb → alkalosis (Remember- masks metabolic acidosis in septic patients)
Lactate Stewart Calculation
(effect on base excess)
= (-1) x lactate
High lactate → acidosis
Water = ___ % BW
60%
ICF= ____ % BW
40% or ~(2/3)
ECF = _______% BW
20 % or (1/3)
- 3/4 interstitial (15% BW)
- 1/4 intravascular (5% BW)
Effects of hyperkalemia on resting membrane potential
increased RMP (more excitable)
Effects of hypokalemia on resting membrane potential
decreased RMP (less excitable)- ie hypokalemic ventroflexion
Effects of hypercalcemia on threshold membrane potential
increased TMP (less excitable)
Effects of hypocalcemia on threshold membrane potential
decreased TMP (more excitable)- ie eclampsia
Osmolarity definition
= # osmoles/L of solution
Osmolality definition
= # osmoles/kg of solution
Calculated Osmolality
=2 (Na + K) + Glu/18 + BUN/2.8
Normal osmolality
~300
290-330 cat
290-310 dog
Effective Osmolality
=2 (Na + K) + Glu/18
(leave out BUN- it is not an effective osmole)
Osmole Gap:
= Measured Osm - Calculated Osm
Gap = unmeasured Osmoles (essentially the same as unmeasured anions)
Normal < 15
Gibbs-Donnan Effect:
negatively charged proteins (albumin) attract anions (Na) which increases their effective oncotic pressure due to increased osmolarity
Corrected Na
= 1.6 mEq/L drop in Na for every 100mg/dl increase in Glucose (or mannitol)
Corrected Cl
= measured Cl x (normal Na/measured Na)
Free water deficit
= [(Current Na/Normal Na) - 1] x 0.6 x kg
Sodium deficit
= (Current Na - Normal Na) x 0.6 x kg
Hetastarch molecular weight…
Lower = increased osmotic effect (more molecules/mL)
Hetastarch degree of substitution…
HES = 0.7
VES = 0.4
Higher is longer lasting/more side effects.
Hetastarch C2:C6 ratios
Higher lasts longer, more side effects.
More C2 is slower to hydrolyze.
Describe Ultrafiltration in Dialysis:
movement of fluid (osmosis)
Describe Diffusion in Dialysis:
through a membrane down a concentration gradient
Describe convection in Dialysis:
movement of solutes with water flow
Describe adsorption in Dialysis:
stuff binds to membrane or a special filter (ie charcoal)
SCUF CRRT Mode:
- close continuous ultrafiltration
- just ultrafiltration (membrane, no dialysate, no replacement fluid)
CVVH CRRT Mode:
- continuous venovenous hemofiltration
- ultrafiltration + convection (membrane + replacement fluids, no dialysate)
CVVHD CRRT mode:
- continuous venovenous hemodialysis
- ultrafiltration + diffusion (membrane + dialysate, no replacement fluid)
CVVHDF CRRT mode:
- continuous venovenous hemodiafiltration
- ultrafiltration, diffusion, and convection (membrane, dialysate, and replacement fluid)
Renal Clearance equation
= [urine] x urine flow / [plasma]
Renal Plasma flow equation
= clearance of PAH
= [PAH urine] x urine flow / [PAH plasma]
GFR equation
= clearance of inulin
= [inulin urine] x urine flow / [inulin plasma]
RBF equation
= RPF / (1-Hct)
Fractional excretion (ie of Na) equation
FENa = (Urine Na x Plasma Creat)/ (Plasma Na x Urine Creat) x 100
Filtration fraction equation
= GFR/RPF
Excretion rate equation
= urine flow x [urine]
Filtered load equation
= GFR x [plasma]
Secretion rate equation
= excretion rate - filtered load
= (urine flow x [urine]) - (GFR x [plasma])
Reabsorption rate equation
= filtered load - excretion rate
= (GFR x [plasma]) - (urine flow x [urine])
Carbon monoxide toxicity MOA
competitive inhibition of O2-Hb binding (shifts Hb/O2 curve L, tighter O2 binding)
Cyanide toxicity MOA
inhibits cytochrome oxidase → impaired O2 utilization by tissues.
Tx with sodium nitrate.
Carbamates and Organophosphates toxicity MOA
ACH inhibition (muscarinic and nicotinic stimulation).
OP’s are irreversible
Carbamates (Tres Pasitos) are reversible.
Bromethalin toxicity MOA
Uncouples oxidative phosphorylation → decreased brain ATP → pump failure/edema
Anticoagulant rodenticides toxicity MOA
antagonize vitamin K epoxide reductase → inhibit carboxylation of vitamin K coag factors (2, 7, 9, 10)
Ivermectin toxicity MOA
inhibits GABA gated Cl-channels in CNS (with altered BBB or OD)
Strychnine toxicity MOA
inhibits the inhibitory interneurons (renshaw cells) → excitatory effect
Metaldehyde toxicity MOA
Serotonin and gaba antagonist → excitatory effect
Permethrin toxicity MOA
disruption of voltage/gated Na channels → early or extended depolarization
Amitraz toxicity MOA
alpha agonist
Tremorgenic mycotoxins MOA
Increase resting potential, increase duration of depolarization, decrease gaba → excitatory effect
Tremorgenic mycotoxins examples
Penitrem A
Roquefortine
Thomitrems
Aflatrem
Verruculogen
PPA toxicity MOA
Sympathomimetic (alpha and beta)
Digitalis toxicity MOA
Inhibits Na/K/ATPase → increased intracellular Ca → vagal stimulation
Ethylene glycol metabolism
EG → (via ADH) → glycoaldehyde → glycolate → glycoxalate → oxalate
Ethylene glycol stages
Stage 1: EG induced acidosis, hyperosmolarity, ataxia/nausea (0.5-12 hrs). Need to intervene by 3 hrs in cats and 6 hrs in dogs to avoid toxic metabolites
Stage 2: Signs mostly resolve as metabolites form (8-24 hrs)
Stage 3: Acute renal failure develops from the toxic metabolites (24-72 hrs)
Acetaminophen metabolism and toxic metabolites
- Conjugated with glucuronide and sulfate
- Unconjugated stuff gets bound to glutathione → rest is now toxic
- NAPQI → liver toxicity mostly
- Para-aminophenol (PAP) → Met Hb mostly
Toxins that don’t bind charcoal
EG
xylitol
ethanol and other alcohols
hydrocarbons (ie petroleum)
Metals
Inorganic toxins (cyanide, ammonia, nitrates, phos, bromide)
corrosive/caustic agents
others
