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Ch 1-21 > 5a > Flashcards

5a Flashcards

1
Q

Body fluid composition

A

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%

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2
Q

Movement of fluid within the body depends on…..

A

… 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

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3
Q

Define dehydration

A

Hypohydration= loss of bodily fluidsCauses: GI, renal, burns/skin, respiratory tract, saliva, third spacing, hemorrhage

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4
Q

Dehydration and PE chart

A

<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

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5
Q

Shock dose dog vs cat

A

Dog 90ml/kgCat 50 ml/kg= to one blood volume

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6
Q

hyper vs hypotonic fluid losses

A

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

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7
Q

guidelines for calculating rehydration for patient

A

KG x % dehyd (replacement) +estimated losses + maintanence

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8
Q

osmolarity of plasma

A

290-310 mOsm/L

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9
Q

isotonic fluids contain which types of bicarbonate precursors

A

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

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10
Q

Fluid choice for patients with hypoNa, hypoCl, metabolic alkalosis

A

0.9% NaCl

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11
Q

T/FLarge quantities of acetate containing fluids can cause vasodilation and decr in BP

A

trueLarge quantities of acetate containing fluids can cause vasodilation and decr in BPsecondary to adenosine release (potent vasodilator) from muscle

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12
Q

fluid choice for head trauma patients

A

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

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13
Q

replacement vs maintenance fluids

A

replacement—isotonic (hi NaCl)maintenance–hypotonic (low NaCl, hi K)

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14
Q

option to treat free water deficit

A

hypotonic fluid252 mOsm/L (slightly lower than plasma)5% dextrose with sterile water

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15
Q

fluid choice for patients with diabetes insipidus or hypernatremia

A

sterile water with 5% dextrose

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16
Q

T/FD5W can be given as a bolus

A

FALSEhypotonicif given as a bolus will distribute to all body fluid compartments, cause acute decreases in osmolarity and lead to cerebral edema.

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17
Q

Why administer hypertonic fluids slowly

A

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

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18
Q

goal of hypertonic saline solutions

A

draw extravascular water into the intravascular spaceosmotic diuresis

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19
Q

contraindications of HTS use

A

do not given in already dehydrated animalsphlebitis/hemolysisavoid right atrium (leads to arrhythmias)

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20
Q

How are synthetic colloids described

A

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

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21
Q

side effects of colloid administration

A

disrupt normal coagulationdecr factor VIII, vWFimpair platelet fxinterfer w fibrin clot stability–>increased finbrinolysis

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22
Q

hydroxyethyl starch colloids are characterized by what?

A

contain highly branched starch, amylopectinweight average (Mw)–low, med, hiconcentration %# substitutions (more substitutions last longer)

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23
Q

T/F Total protein refractometer readings are a valid way of monitoring colloidal therapy

A

FALSEcolloids do NOT increase TP

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24
Q

Characteristics of oxyglobin

A

Hb based oxygen carrying fluidsterile, ultrapure, bovine Hb solutionnonantigenic40 mm Hg oncotic P13 ml/dL Hb concentration

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25
Q

Side effect of oxyglobin administration

A

NO scavenging affectsvasoconstriction

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26
Q

How much blood can most animals lose prior to blood transfusion

A

most can lose 10-15%acute hemorrhage > 20% often requires blood transfusion

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27
Q

dose of pRBC, FFP, or whole blood

A

pRBC 10-15 ml/kgFFP 10-15 ml/kgwhole blood 20-25 ml/kg

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28
Q

blood volume in dog vs cat

A

90 ml/kg dog50 ml/kg cat

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29
Q

calculation of volume of pRBC to be deliveredShort et al JVECCS 2012

A

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)

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30
Q

What does whole blood contain

A

clotting factors (no longer present if stored >24hr)plateletsRBCplasmause within 8 hr

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31
Q

pRBC characteristics

A

PCV ~ 80%shelf life 20 daysONLY RBCreadily available, low risk overload, reduced exposure to plasma antigens

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32
Q

What does plasma contain?

A

Protein (alb, globulins)Clotting factorsFFP within 6 hr-1yrFP >1yr–no longer has clotting factors

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33
Q

What does cryoprecipitate contain

A

vWf VIIIfibrinogenfibronectin

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34
Q

sequele of administering citrate containing blood products too quickly

A

chelation of Ca and clinical hypoCa

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35
Q

optional good products for vWF patients

A

cryoprecipitate (most effective)FFPplasma donors from dogs treated with desmopressin (DDAVP)

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36
Q

dose of DDAVP

A

1 mcg/kg SQ once before surgeryMOA: induces release of vWF

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37
Q

how many dog blood antigens

A

8 know canine blood antigens

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38
Q

how many dogs can tolerate a first blood transfusion

A

15% have reaction first time85% tolerate first transfusion fine

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39
Q

MOA of EACA

A

epsilon aminocaproic acidEACA binds lysine residues on fibrin–>BLOCKS activation of plasminogen to plasmin–>keeps clot longerantifibrinolytic used to treat greyhound bleeders

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40
Q

EACA and amputation in GHMarin 2012

A

5.7x more likely to bleed without EACA28% delayed post op bleeding GH

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41
Q

EACA and gonadectomy in GHMarin 2012

A

30% bleeding in placebo group/ 10% EACA groupEACA sign decr bleeding post op by increasing clot strength (TEG–MA)

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42
Q

feline blood typing

A

A–DSHB–persian, british, himalayanType A cats rarely have large quantities of antiB antibodiesType B cats OFTEN have STRONG antiA antibodies

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43
Q

Why is auto transfused blood not a dependable source of clotting factors

A

with hemorrhage into a body cavity, all clotting factors and fibrin are rapidly depleted

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44
Q

how to perform autotransfusion

A

mix aspirated blood with 10 ml of CPDA-1 or 3.8% citrate with 90 ml blood

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45
Q

anticoagulant used in blood transfusions

A

CPDA-1citrate phosphate dextrose adenine-1

46
Q

potential risks of human albumin transfusion

A

fatal acute or delayed hypersensitivityvolume overloadcoagulopathyantibody formation (avoid repeat exposures)

47
Q

regulation of Na and serum osmolarity

A

Osmoreceptors/Baroreceptors sense incr osmolarity or hypovolemiastimulate ADH/Vasopressin releaseJG apparatus RAASincreases aldosteronerenal Na/water retention

48
Q

causes of hypoNa

A

-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)

49
Q

correcting low Na too quickly leads to

A

demyelination and central pontine myelinolysisDO NOT EXCEED 0.5 mEq/L/hr

50
Q

correcting hi Na too quickly

A

cerebral edemaDO NOT EXCEED 1 mEq/L/hr

51
Q

causes of hyperNa

A

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)

52
Q

calculation of a free water deficit

A

free water deficit (L) = 0.6 x KG x (Na present/Na normal-1)

53
Q

normal resting membrane potential and cation in charge

A

intracellular K+–90mV inside the cell relative to outside the cell

54
Q

regulation of body K

A

GIKidneyTranscellular shifts

55
Q

list two fluids that contain acetate

A

Plasmalyte-148Norm-R

56
Q

What are side effects of low oncotic pressure

A

negative effect on wound healingpredispose to bacterial translocationinterstitial edemadecrease tissue perfusionincrease distance for oxygen and nutrients to travel

57
Q

when does K move from extracellular to intracellular

A

during presence of glucose, insulin, catecholamines, metabolic alkalosis

58
Q

when does K move from IC to EC

A

during metabolic acidosis, hyperosmolarity

59
Q

total body hypoK causes

A

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)

60
Q

define paradoxical aciduria

A

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)

61
Q

what mineral should be checked with refractory hypoK and hypoCa

A

magnesium

62
Q

EKG changes of hyperK

A

spiked T waveprolonged PR intervalbradycardiawidened QRSdisappearance of P wavesV fib/asystole

63
Q

general clinical signs of hypoK

A

< 3 muscle weakness, arrythmias2 rhabdomyolysis<2 respiratory muscle paralysis

64
Q

classical clinical signs of hypoK in cats

A

cervical ventroflexionstiff stilted gaithindlimb weaknessplantigrade stance

65
Q

what effect does low K have on pancreatic islet cells

A

low K impairs insulin release from beta pancreatic cells

66
Q

treatment of hypo K

A

K supplementationKCl or KPhosDO NOT EXCEED 0.5 mEq/kg/hr

67
Q

causes of hyperK

A

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

68
Q

define pseudo hyper K

A

occurs as a result of severely elevated WBC (>100,000)hemolysis ( ESS, Akitas–with hi IC K)thrombocytosis

69
Q

most common cause of hyper K

A

impaired renal excretion

70
Q

what syndrome occurs if serum Na increases too fast

A

central pontine myelinosis(demyelination)

71
Q

T/F Boag JVIM 2005linear FB (not discrete FB) were associated with low Na, Low Cl and metabolic alkalosis

A

Truelinear FB (not discrete FB) were associated with low Na, Low Cl and metabolic alkalosis

72
Q

most clinically relevant adverse effect of hyper K

A

decrease in RMP (makes it more negative)more negative (less than threshold potential)therefor cannot depolarize

73
Q

tx hyper K

A

K deficient fluidsCa gluconate (0.5-1 ml/kg SLOWLY)Dextrose/InsulinCatecholamines –Beta2 agonist (albuterol)Na bicarbHemodialysis

74
Q

Mx of calcium gluconate for treatment of hyperK

A

does not alter K levelsraises threshold membrane potential to restore cell excitability

75
Q

where is 99% of Ca found

A

hydroxyapatite of bone

76
Q

forms of calcium and which is most active

A

ionized, protein bound, chelatedionized is most active; doesn’t always correlate w other forms

77
Q

T/Fhypoalbuminemia affects total body Ca levels

A

true but NOT active ionized form

78
Q

three hormones regulating Ca homeostasis

A

calcitonin–senses hi Ca, GOAL to lower Cavitamin D (cholecalciferol)–aims to incr Caparathyroid hormone–senses low Ca. GOAL to incr Ca

79
Q

3 body systems involved in Ca homeostasis

A

boneGIkidney

80
Q

PTH ROLE

A

senses low Caincr Ca from bone, incr resorption from kidneyactivates vit D from kidney (incr Ca absorption from gut)

81
Q

Calcitonin role

A

senses hi Ca, GOAL to lower Cainhibits bone resorption and release of Ca

82
Q

causes of hypoCa

A

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)

83
Q

mechanism of acute/chronic renal failure on bit D synthesis

A

renal failure decreases the ability of kidney to convert25-hydroxycholecalciferol to to vit D (cholecaciferol)

84
Q

clinical signs of hypoCa

A

muscle tremors, hyperexcitability, restless, facial rubbing, stiff, seizures, hyperthermia, vomiting

85
Q

tx hypoCa

A

calcium gluconate 0.5-1.0 ml/kg slowly 10-20 minwatch ECG for bradyarrythmias

86
Q

causes of hyper Ca

A

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)

87
Q

how does malignancy lead to hyper Ca

A

paraneoplastic syndromelymphoma, anal sac adenocarcinomaPTH-related peptide synthesismost common cause of hyper Ca in DOGS

88
Q

most common cause of hyper Ca in cats

A

IDIOPATHIC

89
Q

tx of hyperCa

A

Ca free fluids—NaCl diuresisloop diuretic–promotes calciuresis furosemideGCCBisphosphonatesCalcitoninCa channel blockersNabicarbdecr calcium in diet

90
Q

Magnesium plays an important role in what homeostatic mechanism

A

PTH and vitamin D maintenance of Ca levelsif low Mg PTH does not work normally

91
Q

Phosphorous less that < 1 mg/dl leads to what

A

hemolysis, rhabdomyolysisMost dogs (other than Japanese or Koren–Akita, Shiba Inu, Kindo) have phosphorous independent RBC regulation and may NOT develop hemolysis

92
Q

when does soft tissue mineralization occur with hyperP

A

Ca x P&raquo_space; 60-70= soft tissue dystrophic mineralization

93
Q

What is pseudo hyperchloridemia

A

automated analytical assays measure halides all under Cl(ex. KBr patient)

94
Q

how are brain cells unique when it comes to glucose utilization

A

brain cells are permeable to glucosedo NOT require insulin to bring into cellsneuronal cells also don’t synthesize their own glucose

95
Q

hormones involved in glucose homeostasis

A

insulin–pancreatic B islet cellsglucagon–pancreatic alpha islet cellscortisolepinephrinegrowth hormone

96
Q

liver role in glucose homeostasis

A

hypogly conditions:liver is stimulated via glucagon to make glucose (glycogenolysis, gluconeogensis)

97
Q

How do glucometers work

A

need normal patient (not anemic)whole bloodAnemic patients or serum samples will read erroneously high

98
Q

what is Whipple’s triad

A

low BGclinical signs corresponding to low BGresolution of signs with glucose therapy

99
Q

causes of hypoglycemia

A
  1. 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
100
Q

paraneoplastic hypoglycemia

A

hepatomashepatocellular carcinomas leimyomas/myosarcomas

101
Q

Drugs/toxins that cause hypoglycemia

A

sulfonylureasbeta blockersinsulin overdosexylitol

102
Q

tx hypoglycemia

A

dextrose bolus (0.5-1.0 g/kg) diluted 1:1 to prevent phlebitis(can worsen insulinomas)GCC, frequent meals

103
Q

how common is stress induced hyperglycemia

A

16% critically ill dogs54% critically ill cats

104
Q

discuss the mechanisms by which hyperglycemia has adverse effects on the body

A
  1. 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)
105
Q

T/Fprogesterone causes hyperglycemia

A

TRUEP causes hyperglycemia during diestrus

106
Q

in insulinoma patients ________administration may be more harmful and instead __________administration is used

A

dextrose is harmful because stimulates more insulinconsider glucagon CRI

107
Q

what is the molecular weight of albumin and its half life

A

69,000 daltons16 hours

108
Q

what is colloid oncotic pressure of plasma vs HES

A

plasma 25 mm HgHES 30 mm Hg

109
Q

Aarnes et al AJVR 2009 administration of HES rather than LRS is recommended for treatment of isoflurane induced hypotension in dogs

A

TRUE

110
Q

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

A

FALSE

Ch 1-21 (19 decks)

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