5a Flashcards
Body fluid composition
Water makes up 60% of weightIntracellular water–40% of weight, 2/3 of total body water, high K +Extra cellular water–20% of weight, 1/3 of total body water, high Na +EC water is1. Intravascular/plasma 25%2. Extravascular/interstitial 75%
Movement of fluid within the body depends on…..
… The balance btwn 1. Filtration (incr hydrostatic P, decr oncotic P)2. Resorption (decr hydrostatic P, incr oncotic P)occurs at the level of the capillary
Define dehydration
Hypohydration= loss of bodily fluidsCauses: GI, renal, burns/skin, respiratory tract, saliva, third spacing, hemorrhage
Dehydration and PE chart
<5% non-detectable5-8% decr skin turgor, dry MM8-10% + eyes sunken, prolong CRT10-12% + severe skin tent, eyes sunken, prolong CRT, dry MM, +/- shock12% life threatening
Shock dose dog vs cat
Dog 90ml/kgCat 50 ml/kg= to one blood volume
hyper vs hypotonic fluid losses
hypotonic fluid losses (loss of water >solutes)–>tonicity of extracellular fluid incr–>water shifts from intracellular to extracellular–>intracellular dehydrationhypertonic fluid losses (loss of solutes >water)–>tonicity of intracellular fluid will be higher or hypertonic and fluid to shift from extracellular to intracellular–>extracellular dehydration
guidelines for calculating rehydration for patient
KG x % dehyd (replacement) +estimated losses + maintanence
osmolarity of plasma
290-310 mOsm/L
isotonic fluids contain which types of bicarbonate precursors
alkalinizing effect1. lactate–metabolized by liver (D-lactate is not mx)2. acetate–metabolized by muscle (more profound effect)3. gluconate–metabolized by many cells
Fluid choice for patients with hypoNa, hypoCl, metabolic alkalosis
0.9% NaCl
T/FLarge quantities of acetate containing fluids can cause vasodilation and decr in BP
trueLarge quantities of acetate containing fluids can cause vasodilation and decr in BPsecondary to adenosine release (potent vasodilator) from muscle
fluid choice for head trauma patients
0.9% NaClbecause of high Na content (154 mEq/L) and is least likely to cause decr in osmolarity and subsequent water movement into brain interstitium
replacement vs maintenance fluids
replacement—isotonic (hi NaCl)maintenance–hypotonic (low NaCl, hi K)
option to treat free water deficit
hypotonic fluid252 mOsm/L (slightly lower than plasma)5% dextrose with sterile water
fluid choice for patients with diabetes insipidus or hypernatremia
sterile water with 5% dextrose
T/FD5W can be given as a bolus
FALSEhypotonicif given as a bolus will distribute to all body fluid compartments, cause acute decreases in osmolarity and lead to cerebral edema.
Why administer hypertonic fluids slowly
if hypertonic fluids are given too fast (> 1 ml/kg/min) osmotic stimulation of pulmonary C fibers results in vagal mediated bradycardia, bronchoconstriction, hypotensionbc monocyte dehydration and subsequent friction btwn monocytes
goal of hypertonic saline solutions
draw extravascular water into the intravascular spaceosmotic diuresis
contraindications of HTS use
do not given in already dehydrated animalsphlebitis/hemolysisavoid right atrium (leads to arrhythmias)
How are synthetic colloids described
by their weight average (Mw) or number average (Mn) molecular weightpolydispersity index Mw/Mn ratiohigher molecular weight molecules are not metabolized or excreted as quickly as smaller particlespersist longer
side effects of colloid administration
disrupt normal coagulationdecr factor VIII, vWFimpair platelet fxinterfer w fibrin clot stability–>increased finbrinolysis
hydroxyethyl starch colloids are characterized by what?
contain highly branched starch, amylopectinweight average (Mw)–low, med, hiconcentration %# substitutions (more substitutions last longer)
T/F Total protein refractometer readings are a valid way of monitoring colloidal therapy
FALSEcolloids do NOT increase TP
Characteristics of oxyglobin
Hb based oxygen carrying fluidsterile, ultrapure, bovine Hb solutionnonantigenic40 mm Hg oncotic P13 ml/dL Hb concentration
Side effect of oxyglobin administration
NO scavenging affectsvasoconstriction
How much blood can most animals lose prior to blood transfusion
most can lose 10-15%acute hemorrhage > 20% often requires blood transfusion
dose of pRBC, FFP, or whole blood
pRBC 10-15 ml/kgFFP 10-15 ml/kgwhole blood 20-25 ml/kg
blood volume in dog vs cat
90 ml/kg dog50 ml/kg cat
calculation of volume of pRBC to be deliveredShort et al JVECCS 2012
volume of RBC to be delivered = blood volume x kg x (PCV goal-PCV current)/PCV donor blood1.5 x %PCV rise x kg (both gave accurate predictions in PCV post pRBC transfusion)
What does whole blood contain
clotting factors (no longer present if stored >24hr)plateletsRBCplasmause within 8 hr
pRBC characteristics
PCV ~ 80%shelf life 20 daysONLY RBCreadily available, low risk overload, reduced exposure to plasma antigens
What does plasma contain?
Protein (alb, globulins)Clotting factorsFFP within 6 hr-1yrFP >1yr–no longer has clotting factors
What does cryoprecipitate contain
vWf VIIIfibrinogenfibronectin
sequele of administering citrate containing blood products too quickly
chelation of Ca and clinical hypoCa
optional good products for vWF patients
cryoprecipitate (most effective)FFPplasma donors from dogs treated with desmopressin (DDAVP)
dose of DDAVP
1 mcg/kg SQ once before surgeryMOA: induces release of vWF
how many dog blood antigens
8 know canine blood antigens
how many dogs can tolerate a first blood transfusion
15% have reaction first time85% tolerate first transfusion fine
MOA of EACA
epsilon aminocaproic acidEACA binds lysine residues on fibrin–>BLOCKS activation of plasminogen to plasmin–>keeps clot longerantifibrinolytic used to treat greyhound bleeders
EACA and amputation in GHMarin 2012
5.7x more likely to bleed without EACA28% delayed post op bleeding GH
EACA and gonadectomy in GHMarin 2012
30% bleeding in placebo group/ 10% EACA groupEACA sign decr bleeding post op by increasing clot strength (TEG–MA)
feline blood typing
A–DSHB–persian, british, himalayanType A cats rarely have large quantities of antiB antibodiesType B cats OFTEN have STRONG antiA antibodies
Why is auto transfused blood not a dependable source of clotting factors
with hemorrhage into a body cavity, all clotting factors and fibrin are rapidly depleted
how to perform autotransfusion
mix aspirated blood with 10 ml of CPDA-1 or 3.8% citrate with 90 ml blood
anticoagulant used in blood transfusions
CPDA-1citrate phosphate dextrose adenine-1
potential risks of human albumin transfusion
fatal acute or delayed hypersensitivityvolume overloadcoagulopathyantibody formation (avoid repeat exposures)
regulation of Na and serum osmolarity
Osmoreceptors/Baroreceptors sense incr osmolarity or hypovolemiastimulate ADH/Vasopressin releaseJG apparatus RAASincreases aldosteronerenal Na/water retention
causes of hypoNa
-hypervolemia (CHF, Nephrotic synd, severe liver dz, kidney failure-normovolemia (psychogenic PD, inappropriate ADH, ADH drugs, myxedema, hypotonic fluid admin-hypovolemia (GI loss–V,d, Third spacing, burns, renal loss–addisons, ADH)
correcting low Na too quickly leads to
demyelination and central pontine myelinolysisDO NOT EXCEED 0.5 mEq/L/hr
correcting hi Na too quickly
cerebral edemaDO NOT EXCEED 1 mEq/L/hr
causes of hyperNa
usually from free water losses–hypovol (GI loss–V,d, Third spacing, burns, renal loss, diuresis)–normovol (Diabetes insipidus, inadequate H2O, incr insensible losses)–hypervol (excessive salt ingestion, HTS, Cushings, hyperaldosterone)
calculation of a free water deficit
free water deficit (L) = 0.6 x KG x (Na present/Na normal-1)
normal resting membrane potential and cation in charge
intracellular K+–90mV inside the cell relative to outside the cell
regulation of body K
GIKidneyTranscellular shifts
list two fluids that contain acetate
Plasmalyte-148Norm-R
What are side effects of low oncotic pressure
negative effect on wound healingpredispose to bacterial translocationinterstitial edemadecrease tissue perfusionincrease distance for oxygen and nutrients to travel
when does K move from extracellular to intracellular
during presence of glucose, insulin, catecholamines, metabolic alkalosis
when does K move from IC to EC
during metabolic acidosis, hyperosmolarity
total body hypoK causes
decreased intake (insufficient diet, K depleted fluids)Increased losses (GI, Renal, drug induced diuretics, Penicillins, amino glycosides, hyperadrenocorticism/aldosteronism–mineralocorticoid excess)Translocation (alkalemia, insulin/glucose, TPN, catecholamines, hyperthyroid, HKPP)
define paradoxical aciduria
with GI loss of fluids with are K and Cl rich–> hypoK, hypoCl, hypoNa–>kidneys attempt to maintain Na and rid K,H–>worsens hypoK and metabolic alkalosis but H in urine (paradoxical aciduria)
what mineral should be checked with refractory hypoK and hypoCa
magnesium
EKG changes of hyperK
spiked T waveprolonged PR intervalbradycardiawidened QRSdisappearance of P wavesV fib/asystole
general clinical signs of hypoK
< 3 muscle weakness, arrythmias2 rhabdomyolysis<2 respiratory muscle paralysis
classical clinical signs of hypoK in cats
cervical ventroflexionstiff stilted gaithindlimb weaknessplantigrade stance
what effect does low K have on pancreatic islet cells
low K impairs insulin release from beta pancreatic cells
treatment of hypo K
K supplementationKCl or KPhosDO NOT EXCEED 0.5 mEq/kg/hr
causes of hyperK
decreased renal excretion (obstruction, uroab, oligo/anuric renal fail)GI dz–whipwormsChylothoraxdrugs (ACE inhibits, NSAIDS, K sparing diuretics, heparin)Translocation (acidosis, tumor lysis syndrome)increased intakePseudohyperKAddisons
define pseudo hyper K
occurs as a result of severely elevated WBC (>100,000)hemolysis ( ESS, Akitas–with hi IC K)thrombocytosis
most common cause of hyper K
impaired renal excretion
what syndrome occurs if serum Na increases too fast
central pontine myelinosis(demyelination)
T/F Boag JVIM 2005linear FB (not discrete FB) were associated with low Na, Low Cl and metabolic alkalosis
Truelinear FB (not discrete FB) were associated with low Na, Low Cl and metabolic alkalosis
most clinically relevant adverse effect of hyper K
decrease in RMP (makes it more negative)more negative (less than threshold potential)therefor cannot depolarize
tx hyper K
K deficient fluidsCa gluconate (0.5-1 ml/kg SLOWLY)Dextrose/InsulinCatecholamines –Beta2 agonist (albuterol)Na bicarbHemodialysis
Mx of calcium gluconate for treatment of hyperK
does not alter K levelsraises threshold membrane potential to restore cell excitability
where is 99% of Ca found
hydroxyapatite of bone
forms of calcium and which is most active
ionized, protein bound, chelatedionized is most active; doesn’t always correlate w other forms
T/Fhypoalbuminemia affects total body Ca levels
true but NOT active ionized form
three hormones regulating Ca homeostasis
calcitonin–senses hi Ca, GOAL to lower Cavitamin D (cholecalciferol)–aims to incr Caparathyroid hormone–senses low Ca. GOAL to incr Ca
3 body systems involved in Ca homeostasis
boneGIkidney
PTH ROLE
senses low Caincr Ca from bone, incr resorption from kidneyactivates vit D from kidney (incr Ca absorption from gut)
Calcitonin role
senses hi Ca, GOAL to lower Cainhibits bone resorption and release of Ca
causes of hypoCa
decr PTH release ( hypoPTH, postopthyroidectomy/PTectomy, suppression from chronic hyperCa, hypoMg)decr vit D (renal failure, malabsorption, liver insufficiency)Chelation (eclampsia, UT obstruction, saponification-pancreatitis, anticoag in blood transfusions, ethylene glycol))Critical illnesshypoAlb (does not change ionized, only total)
mechanism of acute/chronic renal failure on bit D synthesis
renal failure decreases the ability of kidney to convert25-hydroxycholecalciferol to to vit D (cholecaciferol)
clinical signs of hypoCa
muscle tremors, hyperexcitability, restless, facial rubbing, stiff, seizures, hyperthermia, vomiting
tx hypoCa
calcium gluconate 0.5-1.0 ml/kg slowly 10-20 minwatch ECG for bradyarrythmias
causes of hyper Ca
G (granulomatous dz)O (osteoclastic dz/osteomyelitis/osteoporosis)S (spurious)H (hyperPTH–primary or secondary)D (vit D toxicosis–cholecalciferol toxicosis)A (Addisons)R (renal failure)N (neoplasia–AGAC, lymphoma, MM, mets–carcinomas; nurtritional secondary renal hyperPTH)I (iatrogenic, idiopathic)T (toxins)
how does malignancy lead to hyper Ca
paraneoplastic syndromelymphoma, anal sac adenocarcinomaPTH-related peptide synthesismost common cause of hyper Ca in DOGS
most common cause of hyper Ca in cats
IDIOPATHIC
tx of hyperCa
Ca free fluids—NaCl diuresisloop diuretic–promotes calciuresis furosemideGCCBisphosphonatesCalcitoninCa channel blockersNabicarbdecr calcium in diet
Magnesium plays an important role in what homeostatic mechanism
PTH and vitamin D maintenance of Ca levelsif low Mg PTH does not work normally
Phosphorous less that < 1 mg/dl leads to what
hemolysis, rhabdomyolysisMost dogs (other than Japanese or Koren–Akita, Shiba Inu, Kindo) have phosphorous independent RBC regulation and may NOT develop hemolysis
when does soft tissue mineralization occur with hyperP
Ca x P»_space; 60-70= soft tissue dystrophic mineralization
What is pseudo hyperchloridemia
automated analytical assays measure halides all under Cl(ex. KBr patient)
how are brain cells unique when it comes to glucose utilization
brain cells are permeable to glucosedo NOT require insulin to bring into cellsneuronal cells also don’t synthesize their own glucose
hormones involved in glucose homeostasis
insulin–pancreatic B islet cellsglucagon–pancreatic alpha islet cellscortisolepinephrinegrowth hormone
liver role in glucose homeostasis
hypogly conditions:liver is stimulated via glucagon to make glucose (glycogenolysis, gluconeogensis)
How do glucometers work
need normal patient (not anemic)whole bloodAnemic patients or serum samples will read erroneously high
what is Whipple’s triad
low BGclinical signs corresponding to low BGresolution of signs with glucose therapy
causes of hypoglycemia
- excess insulin (iatrogenic, insulinoma, paraneoplastic, toxins-xylitol)2. increased glucose utilization (infection, exercise induced, paraneoplastic, pregnancy, polycythemia)3. decreased glucose production (liver fail, pediatric, toy breed, PSS, counter regulatory hormone deficiency, Addison
paraneoplastic hypoglycemia
hepatomashepatocellular carcinomas leimyomas/myosarcomas
Drugs/toxins that cause hypoglycemia
sulfonylureasbeta blockersinsulin overdosexylitol
tx hypoglycemia
dextrose bolus (0.5-1.0 g/kg) diluted 1:1 to prevent phlebitis(can worsen insulinomas)GCC, frequent meals
how common is stress induced hyperglycemia
16% critically ill dogs54% critically ill cats
discuss the mechanisms by which hyperglycemia has adverse effects on the body
- osmotic force–can pull IC fluids out2. increased glucose goes into urine and osmotic diuresis occurs dehydrating patients 3. tissue damage (retinopathies, heart attacks, renal dz)
T/Fprogesterone causes hyperglycemia
TRUEP causes hyperglycemia during diestrus
in insulinoma patients ________administration may be more harmful and instead __________administration is used
dextrose is harmful because stimulates more insulinconsider glucagon CRI
what is the molecular weight of albumin and its half life
69,000 daltons16 hours
what is colloid oncotic pressure of plasma vs HES
plasma 25 mm HgHES 30 mm Hg
Aarnes et al AJVR 2009 administration of HES rather than LRS is recommended for treatment of isoflurane induced hypotension in dogs
TRUE
Gebhardt et al JVECCS 2009T/F there is a sign difference btwn non septic SIRS and sepsis survival rates in dogs base on initial C reactive protein concentrations
FALSE
