Misc Flashcards

(107 cards)

1
Q

SIRS

A

-Systemic inflammatory response syndrome
-clinical state of systemic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of SIRS

A

-Infectious
-Non-infectious (panky, polytrauma, burns, heatstroke, neoplasia, immune-mediated disease, post-op)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

SIRS criteria

A

Diagnosis of SIRS consist of fulfilling 2 out of the following 4 criteria in dogs and 3 out of 4 criteria in cats:
(1) increased or decreased temperature
(2) tachycardia (or bradycardia in cats)
(3) tachypnea
(4) leukon abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Sepsis-2

A
  • categorizes patients into 3 groups: sepsis, severe sepsis, septic shock based on the presence of infection, SIRS, MODS, and refractory hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sepsis-3

A

-Categorizes patients into 2 groups (sepsis and septic shock) based on the presence of infection with organ dysfunction, refractory hypotension, and persistently increased lactate despite appropriate resuscitation
-Selects for patients with more severe cases of sepsis and higher risk of death compared to Sepsis-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Branched amino acids

A

leucine, isoleucine, valine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Gq receptors

A

-activates IP3, DAG
-Alpha 1, endothelin, V1, M1, M3, M5, H1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Gs receptors

A

Activates cAMP -> PKA
- B1
-B2
-V2
-Adenosine
-H2
-glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Gi receptors

A

-prevents conversion to cAMP
-M2
-M4
-alpha 2
-opioids
-D2
-Somatostatin
-GABA b

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Metabolic derangements seen with refeeding syndrome

A

Hypophosphatemia, hypomagnesemia, hypokalemia, hyponatremia, hypocalcemia, hyperglycemia, and vitamin deficiencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Processes body uses to maintain acid-base balance

A

1) regulation of PCO2 by alveolar ventilation
2) buffering of acids by bicarbonate and non- bicarbonate buffers
3) changes in renal excretion of acid or base

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Traditional acid base approach

A

Uses the Henderson - hasselbach equation for carbonic acid and uses pH, PCO2, and bicarb concentration.

PH has a direct relationship with bicarb concentration and an inverse relationship with PCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Purpose of anion gap

A

To identify the cause of a metabolic acidosis

Unmeasured anions are more abundant than unmeasured cations, the AG is essentially a marker of the amount of unmeasured cations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Measured cations

A

Sodium, potassium

Account for 95% total cations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Measured anions

A

Bicarb, chloride

Accounts for 85% total anions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Unmeasured cations

A

Albumin, lactate, phosphates, sulfates, ketones

Some drugs and toxins can also account for it, including methanol, salicylate, and ethylene glycol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes of increased ion gap metabolic acidosis

A

DUEL
-DKA
-Uremia
-Ethylene glycol
-Lactic acidosis

-Salicylate, Methanol (toxins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes of hyperchloremic metabolic acidosis

A

-Renal bicarb loss
-GI bicarb loss
-NaCl administration
-Addison’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Metabolic acidosis

A

Decreased pH, HCO3-, PCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Metabolic alkalosis

A

Increased pH, HCO3-, PCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Normal anion gap for dogs and cats

A

10-15 mEq/L

> 25 = acidotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Data Types

A

1) Categorical
-Nomial (order doesnt matter)
-Ordinal (order matters)
Includes: frequencies, proportiins, percentages, pie charts

2) Numerical
-Discrete (counted, not measured)
- Continuous (measured)
Includes: percentiles, means, medians, modes, box plots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Standard error

A

How far is the samole mean likely to be away rrom the actual (population) mean, describes the sampling process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Standard deviation

A

Describes the variation within the population/sample, how far an individual is from the population mean

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Type I errors
False positive Rejection of the null hypothesis when you shouldn't
26
Type II errors
False negative Acceptance of the null hypothesis when you shouldn't
27
Sensitivity
(True positive/ (true + false negative)) x 100
28
Specificity
(True negative/(true positive+ false negative)) x 100
29
PPV
(true positive/ (true positive + false positive)) x 100
30
NPV
(true negative/ (true negative + false negative)) x 100
31
Hospital-associated infection (HAI)
-nosocomial -infectious event diagnosed >48 hours after hospital admission, or more specifically, on or after the third hospital day without proven prior incubation
32
How common are nosocomial events?
-16.3% in dogs -12% in cats
33
True or False: HAIs in ICU are thought to originate either from the patient's own endogenous flora or from exogenous sources
True
34
What bacteria is a serious threat to critically ill animals?
Carbapenem-resistant Enterobacteriaceae
35
36
Massive Blood Transfusion
Replacement of one entire blood volume within 24 h Transfusion of >10 units of packed red blood cells (PRBCs) in 24 h Transfusion of >20 units of PRBCs in 24 h Transfusion of >4 units of PRBCs in 1 h when on-going need is foreseeable Replacement of 50% of total blood volume (TBV) within 3 h.
37
Sepsis
Defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection
38
Septic shock
Subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality.
39
What is a potential complication of parenteral nutrition?
Hyperglycemia
40
SOFA Score
Sequential Organ Failure Assessment -used to assess organ dysfunction in several different ICU settings -correlates with survival -assigns between 0-4 points to each of the 6 individual organ systems (total score 24) -higher scores = worse outcome
41
ATT
Animal Triage Score Higher score = poorer prognosis 6 categories, 18 points total
42
ATT
-Animal Trauma Triage -profusion, cardiac, respiratory, eye/muscle/integument, skeletal, neuro - out of a total of 18 points -higher = more severe -each point increase indicates a 2.3 to 2.6x decrease in survival rate
43
Pain vs Nociception
-Pain is the unpleasant sensory and emotional experience associated with actual or potential tissue damage (conscious experience) -Nociception is the detection of a noxious stimulus at the tissue level by nociceptors (mechanical, thermal, chemical)
44
Inflammatory mediators that induce pain sensation
Bradykinin, prostaglandins, leukotrienes, serotonin, histamine, substance P, thromboxanes, IL, TNF
45
Nociceptive Pathway
-transduction, transmission, modultaion, projection, perception
46
Analgesic effects of transduction
- local anesthetics - opioids - NSAIDs - corticosteroids
47
Analgesic effects on transmission
-local anesthetics -alpha 2 agonist
48
Analgesic effects on modulation
-local anesthetics -alpha 2 agonist -opioids -NSAIDs -benzodiazepines -NMDA antagonist -TCA antidepressants -anticonvulsants
49
Analgesic effects on perception
- general anesthesia - opioids - alpha 2 agonist - benzodiazepines - phenothiazines
50
Complications of transfusion reactions
Infectious versus more commonly non-infectious Non-infectious breaks down into acute (<24 hours) versus delayed Acute non-immune: Transfusion related sepsis Transfusion related circulatory overload (TACO) Metabolic derangements Dilutional coagulopathy Acute immune: Acute hemolytic transfusion reactions Febrile non-hemolytic transfusion reaction Allergic reactions TRALI Delayed non-immune: Iron overload Delayed immune: Delayed hemolytic transfusion reaction Post transfusion purpura Transfusion associated graft versus host disease
51
Incidence of reaction
0-38%
52
TACO
Transfusion associated circulatory overload Acute non-immunologic reaction secondary to increases in blood volume mediated by transfusion -acute respiratory distress -hydrostatic pulmonary edema -occurs within 6 hours of transfusion Evidence of left atrial overload
53
TRALI
Closely mimics taco but is different in the sense that it is a inflammatory trigger that increases capillary permeability and causes exudative pulmonary edema Antigen-antibody reaction in the lungs No prior lung injury No evidence of left attial hypertension
54
TRALI I
No risk factors for ARDS PF < 300 Clear evidence of bilateral pulmonary edema on rads No evidence of left atrial hypertension Onset within 6 hours
55
TRALI II
Similar to type one but also includes patients that are at risk for ARDS
56
TRALI vs TACO
57
CURATIVE guidelines for FATE
Recommend treatment for thrombophylaxis Recommends use of clopidogrel, UFH, LMHW Recommends AGAINST aspirin as the sole anti thrombotic Warfarin should not be used Rivaroxaban recommended Apixaban not mentioned but has shown to be well tolerated in cats
58
Adrenoreceptor function
Alpha1- contraction of smooth muscle (vascular smooth muscle, GI, bladder sphincters, radial muscle iris) Beta 1- involved in metabolic functions such as gluconeogenesis, lipolysis, run in secretion, functions in the heart Beta2- dilation or relaxation of smooth muscle in bronchioles, wall of the bladder, GI tract
59
Action of autonomic receptors
Alpha1- Gq receptor, increases intracellular calcium Alpha2- Gi, decreases cAMP Beta 1 and 2- stimulates cAMP
60
61
What medications can be given via aerosolized route in smoke inhalations?
Epinephrine: causes bronco dilation and vasoconstriction and aids in the breakup of airway secretions NAC: is a mucolytic but may cause bronco constriction Heparin: can reduce airway fibrin cast formation and the incidence of pulmonary edema
62
Hypothermia causes
- bradycardia, hypotension, cardiac dysrhythmias -decreased RR and depth -neurological changes -mixed respiratory and metabolic acidosis -thrombocytopenia and decreased coagulation factor activity
63
64
Heat stroke begins with the production and release of which inflammatory cytokines
IL-1, IL-6 from muscles Endotoxins from GI
65
Ethylene glycol MOA
Ethylene glycol is a CNS depressant and can cause GI irritation. The metabolites of ethylene glycol are responsible for AKI and metabolic acidosis. Glycolaldehyde is responsible for CNS signs
66
Blood gas of EG toxicity
Normal chlorinemic metabolic acidosis with decreased by carb and increased anion gap May have hypocalcemia Be cautious of high lactate because may actually be an elevation in glycolate which can also affect anion gap
67
68
Which inflammatory cytokines are released in response to smoke inhalation?
IL-1, TNFalpha, IL-6, IL-8
69
MOA of carbon monoxide
Binds hemoglobin to form carboxyhemoglobin resulting in a functional anemia also competitively inhibits cytochrome p450 to prevent aerobic metabolism
70
Clinical signs of carbon monoxide toxicity
Acute and delayed clinical signs Acute clinical signs associated with respiratory. Delayed clinical signs are usually neurological changes.
71
Loxoscelism
Bite of spiders from Loxoceles, known commonly as recluse spiders Mostly found in South America but can also be in Central and Southern US. Causes dermonecrosis. Bite reportedly not painful. Skin necrosis seen 72 hours or more after bite.
72
Lacrodectism
Widow spider group Has alpha latrotoxin and has an effect on nerve endings leading to flaccid paralysis
73
Main components of hymenoptera venom
Mellitin and PLA2 work together to cause red blood cell, platelet, leukocyte, vascular endothelial cell lysis May also cause myelinolysis of the spinal cord
74
Initial clinical signs with hypothermia
1 to 2° C below normal Causes a release of catecholamines which results in increased respiratory rate, minute ventilation, and oxygen consumption along with increased heart rate, cardiac output and MAP Blood work will show an increase in cortisol, lactate, ketones, glucose
75
76
77
Heatstroke definition
Characterized by core temperatures exceeding 41° C and CNS dysfunction
78
What toxicants do not bind activated charcoal?
Heavy metals (iron, zinc) Xylitol Alcohols
79
80
5-FU
Fluorouracil Chemotherapeutic agent Causes GI sloughing, pulmonary edema, seizures, cerebellar ataxia, death Bloodwork reveals myelosyppression and CK elevation Supportive care, IHD High mortality rate
81
Amphetamines
Class II binds to dopaminergic, noradrenergic, and adrenergic receptors to cause release of neurotransmitters Lipid soluble, so penetrates BBB Causes hypertension, repetitive movements, hyperthermia, tachycardia, agitation, seizures, mydriasis Hypoglycemia, metarubricytosis, thrombocytopenia, coagulopathy if hyperthermia Supportive care Caution using benzodiazepines, cyproheptadine, phenothiazines Acidification of urine can increase elimination (ascorbic acid or ammonium chloride). Tremors can be managed with methocarb. ILE
82
Baclofen
Skeletal muscle relaxant, works by imhibiting release of excitory NT CNS depression, GI signs, ataxia, vocalizations, hypothermia, bradycardia Treatment of baclofen uses emesis, AC (1x) Cyproheptadine, ILE, mech vent, IHD/HP +/- Noloxone Good survival rate ( 83%)
83
Baclofen acts on
GABA B. Withdrawal of baclofen can lead to a down regulation of gaba receptors leading to excess serotonin Can treat with cyproheptadine
84
Black widow envenomation
Lactrodectus spp Alpha-latrotoxin opens selective cation channels at the presynaptic nerve terminal causing massive release and depletion of ACh and NE -> sustained muscle spasms Can treat with methocarb and diazepam, opioids for pain Fatal in cats without antivenin, uncertain prognosis in dogs, CS can resolve in 48-72 hr
85
86
Botulism
Produces 7 neurotoxins Dogs generally more resistant than horses Inhibits ACh release into NMJ Rapid progression of LMN signs and PSN signs, hypoventilation, ME Tx: SC, abx, mech vent, +/- antitoxin
87
Bromethalin
Uncoupling oxidative phosphorylation in mitochondria, reduces ATP Convulsant, ataxia, CNS depression AC (Multiple), ILE, anti-epileptics, osmotic agents Poor to grave once severe neuro signs seen
88
Bufo toad
Colorado River Toad, Marine Toad Toxin absorbed across mm, causes hyper salivation injected mm, collapses, hyperexcitability, vocalizations, neuro signs bradycardia/tachycardia, arrhythmias Rinse mouth, SC (active cooling, esmolol, anti-epileptics, atropine if not tachycardic) Death uncommon
89
Cholecalciferol diagnostics
Vitamin D panel, low PTH, high iCa2+,
90
Cholecalciferol txs
AC (multiple), cholestyramine, NaCl, phosphate binders If high Ca2+: -furosemide, steroids, bisphosphonates
91
Poor porgnostic indicator of Cholecalciferol
Hematemesis
92
Cocaine
Sympathomimetic, thrombogenic effects Highly lipophilic ILE, Benzos, lidocaines for vtach NaHCO3- improves myocardial dysfunction in experimental models Beta antagonist contraindicated because may exacerbate coronary vasoconstriction
93
Smoke inhalation
CO binds Hg to make COHb, Cyanide inhibits oxidative phosphorylation causing histotoxic hypoxia Hyperemic mm seen with cyanide tox Pulse ox falsely high in smoke inhalation cases No steroids or prophylactic abx
94
Cyanobacteria
Anatoxin-a acts as a colonergic agonist at the nicotinic acetylcholine receptor. It inhibits acetylcholine esterase leading to increased acetylcholine at the synapse. Microcystins result in liver damage or failure. Neuro and GI signs can be seen with Anatoxin-a, potentially can be treated with atropine to help with slud signs. Poor to grave prognosis
95
Etylene glycol
Metabolized by alcohol dehydrogenase to toxic metabolites (oxalic acid) which bind to calcium and form calcium crystals Neuro signs and then AKI Woods lamp on urine or vomit! Tx with IHD, ethano, fomepizaolel, SC NaHCO3- if severe acidosis
96
Ivermectin
Macrocyclic lactone Binds to GABA cl- chanels and inhibits neuronal transmission NO BENZOS DUE TO GABA BINDING ILE,
97
98
Metaldehyde
Found and slug and snail baits Exact mechanism unknown but either increases excitatory neurotransmitters or decreases inhibitory Supportive Care
99
Pyrethrins/pyrethroids
Tyrethrins are derived from chrysanthemum flowers Causes hyper excitability by slowing the closing of sodium channels Highly lipophilic Cats are highly sensitive Causes signs of hyper excitability, tremors ,GI signs ILE/IHD/TPE?
100
MOA of Tetanus
Prevents release of the inhibitory neurotransmitter glycine, getting to overstimulation of motor neurons and muscle rigidity
101
102
When ruling out causes of polyarthritis, it is important to remember the following:
-tick borne diseases -fungal diseases -lishmania (travel dependent) While also ruling out the other bacterial and fungal infections
103
When testing synovial fluid for polyarthritis, you should be testing:
Aerobic bacterial +/- anaerobic if there is a foreign body or bite wounds Based on history, consider mycoplasma
104
Dermis
Composed of a superficial plexus and a middle plexus, where hair and glandular structures arise
105
106
Types of hyperlactatemia
Type 1- hyperlachetemia with no change in pH Type 2-hyperlachetemia with academia Type 2A-hyperlactatemia due to decrease oxygen delivery Type to be includes all causes of lactic acidosis despite adequate oxygen delivery
107