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ACVECC > Other/general > Flashcards

Other/general Flashcards

1
Q

What are the 4 Heat loss mechanisms?

A
  1. Conduction: body surface in direct contact with a solid object - depends on thermal conduction of that object as well as amount of body surface area in contact with the object (EX: dog in metal kennel with no blankets- heat loss)
  2. Convection: heat transfer from body to surrounding air or water- water is more effective medium than air for convective heat transfer (water to cool down dog; peripheral vasodilation can increase convection)
  3. Radiation: electromagnetic energy that is exchanged btw body and surrounding objects - occurs independently of air temp or velocity (heat from sun, objects around patient)
  4. Evaporation: heat loss with moisture when environmental temp is equal to or exceeds skin temp (panting)
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2
Q

What are the different Mechanisms of edema formation?

A
  1. Venous hypertension
  2. Hypoproteinemia
  3. Impaired lymph flow
  4. Increased microvascular permeability
  5. Increased negativity of interstitial fluid pressure
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3
Q

How does the body protect itself from edema formation (antiedema mechanisms)?

A
  1. increasewd interstitial hydrostatic pressure
  2. increased lymph flow
  3. Decreased interstitial colloid osmotic pressure
  4. increased trans-serosal flow in organs with potential spaces
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4
Q

Sensitivity

A

SnNout: A test with a high sensitivity value (Sn) that, when negative (N), helps to rule out a disease (out).

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5
Q

Arterial Chemoreceptors

A

Increased firing with: decreased pH, increased CO2, and decreased O2

In carotid body: join sinus N–> glossopharyngeal (same route as baroreceptors)

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6
Q

SOFA Score

A

Assume every patietn is 0. Score>/= 2 assd with 10% increase mortality (human defines sepsis)

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7
Q

qSOFA

A

-from sepsis3

RR>/=22 bpm
Altered mentation
SBP </=100mmHg

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8
Q

Aldosterone (stimuli, & effects)

A
  • stimulated release by decreased renal blood flow or blood volume –> stimulates RAAS–> increased aldo secretion

Effect of aldo:
- Increased reabsorption of Na in distal tubule–> inc water reabsorption
- Increased K and H excretion
- Pro inflammatory and profibrotic effects which may lead to progression of renal disease, vascular thrombosis and fibrosis
- Peripheral vasoconstriction from Angio II

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9
Q

Proinflamm cytoikines of sepsis

A

**TNFalpha
IL-1
IL-6
IL-8
IFNgamma

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10
Q

CARS

A
  • Compensatory anti-inflammatorty response syndrome

IL-10
TGFbeta
IL-13
IL-4
+/- glucocorticoids

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11
Q

Gram neg sepsis pathogenesis

A

LPS binds LBP (LPS binding protein) –> complex bind to CD14 on macrophage –> initiated signaling via TLR to neucleus for transcription of cytokines (TNFa, IL1, IL6,IL8 &IFNg) & counterinflamma (IL4, IL10, IL13, TGFb, roids)

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12
Q

Gram + sepsis pathogenesis

A

Gram+ exotoxins –> act as superantigens –> stimulate sidespread Tcell activation –> uncontrolled release IFNgamma and TNF alpha

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13
Q

Tumor lysis syndrome

A

-Destruction of tumor cells –> increased K & phosphorus extracellularly
- Purine release from tumor cells –> inc uric acid –> met acidosis & renal impairment
- may occur within hours or days after therapy

CS: lethargy, v/d, shock, decreased HR, hyperkalemia, hyperphosphatemia, hypocalcemia, met acidosis

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14
Q

Ucath materials that dec urethral reactivity & increase biofilm resistance

A

Plastic
Red rubber
Latex
Siliconized elastomer/teflon coated latex
hydrogel coated latex
pure silicone

in order of Most reactive –> least reactive

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15
Q

List of exogenous pyrogen

A
  • Infectious agent (fungal, viral, rickettsial, bacteria, protozoal)
  • Bacterial products (LPS, strepexotoxtin, staph enterotoxin, staph protein)
  • Soluble antigen-aby complexes
  • bile acids
  • Drugs: bleomnycin, colchicine, tetracyclines, levamisole
  • Tissue inflammation/necrosis
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16
Q

Thermoregulation

A
  • Regulated by preoptic area of anterior hypothalamus
  • Inflammation via microamines and cutaneous deep receptors
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17
Q

Heat gain mechanisms

A
  • Increased production: catecholamines, thyroxine, shivering
  • Decreased loss: vasoconstriction, piloerection, postural changes, seek warm environment
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18
Q

Hyperthermia classifications

A
  1. True fever: production endogenous pyrogens
  2. Inadequate heat dissipation: heat stroke or hyperpyrexic syndrome
  3. Exercise induced hyperthermia: normal exercise, hypocalcemic tetany, seizures
  4. Pathologic/pharm origin: lesions in or around anterior hypothalamus, malignant hyperthermia, hypermetabolic disorders, monoamine metabolism disturbances
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19
Q

Endogenous pyrogens & their sources

A
  • Calchetin(TNFa) –> macs
  • Lymphotoxin (TNFbeta) –> B&Tlymphocytes
  • IL-1alpha & beta–> macs
    IFN alpha –> leukocytes
    IFN beta –> fibroblasts
    IFN gamma –> T lymphocytes
    IL-6 –> many cells
    IL-8 –> macs
    Macrophage inflamm protein 1a & 1b –> macs
20
Q

Hyperpyrexia syndrome

A
  • Assd with moderate to severe exercise in hot or humid climates
  • evaporative cooling in humidity is decreased
  • heavy exercise may lead to vasodilation in M and constriction in cutaneous vessels
21
Q

malignant hyperthermia

A

Leads to myopathy & subsequent metabolic heat production secondary to disturbed calcium metabolism that is initiated by pharm agents (halothan & succinylcholine)

  • hops toxicosis, chlorfenapyr
22
Q

Phases wound healing

A
  1. Inflammation (1st 5 days): vasocoonstriction (first) + platelet aggregation –> vasodilation (due to leukotrienes, PGF, histamine, kinins, complement)–> neutrophil migration within 24-48 hrs + mono within 48-96 hrs –> increased fibroblastic act., collagen synthesis & angiogenesis
  2. Debridement phase - occurs simultaneously with inflamm: Increased macrophages remove necrotic tissue, FB, bacteria
  3. Proliferation (D5-30): Angiogenesis, granulation tissue form and epithelialization
  4. Maturation (D20-years) : Remodel until 10% type III collagen & transforms to type I
    **Only 80%b strength of original
23
Q

Adherent dressing

A

Used in debridement phase
- Nonselectively removes necrotic and healthy tissue alike

Ex: wet to dry

24
Q

nonadherent dressing

A

-Alignates, foams, hydrogels, hydrocolloids, & transparent films
-All phases of wound healing

25
Q

Wound classifications

A

Clean: atraumatic, surgically created under asceptic conditions
2. Clean contaminated: minor break in asceptic technique in which contamination minimal and easily removed
3. Contaminated: recent wound with bacterial contamination from street, soil or oral cavity
4. Dirty infected: older wound with exudate and obvious infection
- contains >10^5 org/gram tissue

26
Q

Open fracture grades

A

I: small break in skin by bone penetrating through

II: ST trauma coniguous with fracture often caused by external trauma (bite wound, low velocity gun shot)

III: Extensive ST injury common in addition to high degree comminution of bone

27
Q

Honey vs sugar for wounds

A

Honey: decreased edema, accelerates sloughing of necrotic tissue, rich acellular energy source, antibiotic properties due to increased osmolarity, aciditiy and H2O2 content

Sugar: Bacteriacidal through osmotic action, draw macrophages to wound

28
Q

Cryptococcus

A
  • from pigeon or bird waste + decaying wood bark
  • Reportable!-PNW
  • CS: cats - nasal planum deformity, nasal signs MC
    Dogs neuro changers, ocular changes, cutaneous lesions and resp distress
  • Prognosis guarded for dogs of any kind infection and cats with neuro
    Treatment is nasal debulking, all other forms difficult to treat
29
Q

Blastomycosis

A
  • Mississippi, MO, Ohio river & great lakes
  • Once inhaled, phagocytized by macrophages and transformed into thick walled yeast phase→ may produce local dz or disseminate to distant sites
    CS:
  • Dog: ocular changes (uveitis, retinal detachment, secondary glaucoma), dermal nodules, bone lesions and CNS abnormalities
  • Cat: dyspnea, increased BV signs, weight loss, ocular manifestations, draining skin lesions, CNS disease and dermal abscesses
    Dx
    -visualization of big budding yeast
    treatment orals–> prognosis good if no pulmonary involvement
30
Q

Histoplasmosis

A

-Location: Ohio, MO and mississippi river valleys
- Route of entry typically inhalation, but oral exposure may occur → converted to yeast form at body temps and disseminate via macrophages in bloodstream and lymphatics
- Dogs may have GI signs, ocular, lymph nodes, liver and spleen ( GI and pulmonary mc in one study)
-Cats: lymphadenopathy, primary pulm disease or GI disease
- diagnosis via cytology or urine antigen
- treat with systemic antifungals
- Prognosis good in dogs

31
Q

Coccidiomycosis

A
  • desert regions: south western US, mexico, central and south America
  • CS:Chronic cough (MC CS), fever, weight loss, anorexia, draining skin nodules over bone lesions, Hypertrophic osteopathy, myocardia or pericardial infections with arrhythmias, heart based masses or restrictive pericarditis, CNS signs (seizures, behavior changes or coma), ocular signs less common,
    Cats more resistant thsn dogs: subconjunctival masses or periorbital swelling
  • Bone or CNS involvement carries poor prognisis
  • Can try aby testing; ag testing not helpful
    Treatment systemic
32
Q

Aspergillosis

A

3 clinical forms: sinonasal (SNA) -> dogs
sinoorbital (SOA)->cat
Invassiv (IA)

CS:
SNA: nasal DC, epistaxis, sneezing
SOA: malformation, exophthalmus, pain on opening mouth +/- nasal signs common with SOA

Ag testing may help diagnose in IA when there is a systemic infection, otherwise not helpful

Tx: debulking and topical clotrimazole

Limited for IA as azoles do not work well

33
Q

what arteries can you place an art line in?

A

Dorsal pedal
Femoral
Auricular
Radial
coccygeal

34
Q

important sites for tracheostomy

A
  • Ventral incision from cricoid cartilage caudally
  • annular lig btw 3-4 or 4-5 tracheal rings

** Do not cut >50% curcum
** laterally recurrent laryngeal and vessels of concern

35
Q

Label

A
36
Q

Different types of Shock & examples

A
  1. Hypovolemic
  2. Cardiogenic –> DCM, CHF, arrhythmia
  3. Distributive (decrease or increase in systemic vascular resistance) –> anaphylaxis, catecholamine excess, sepsis
  4. Obstructive (compression main vessel or heart) –> GDV, tamponade, tension pneumo
  5. Hypoxemic –> Anemia, CO, metHgb
  6. Metabolic –> hypoBG, cyanide, mitochondrial dys, cytopathic hypoxia of sepsis
37
Q

Idiogenic osmoles

A
  • Begin being created within a few hours of increased osmolality - full compensation takes 2-7 days
  • increased osmoles made in neuronal cells to allow them to keep normal size/water content

Examples: inositol & glutamate

38
Q

Osmotic Demyelination Syndrome

A
  • occurs with treatment of chronic or subacute hyponatremia
  • During correction of low Na, neurons shrink away from myeline sheath as water moves out of neuron
  • Clinical signs manifest in days after intervention not before (ataxia, paresis, dysphagia, obtunded) –> thalamus commonly effected
  • Only has been seenw ith patients with Na <110 and had Na corections that exceeded recommendations (>8 meq/L/day)
39
Q

What are the detrimental effects of lipid peroxidation

A
  • Increased cell membrane permeability
  • Inhibition of normal cellular processes
  • Damage to proteins, intracellular membranes, capillaries, & alveoli
  • Inactivation lung surfactant

MC due to hydroxyl free radical and peroxynitrite

40
Q

Differentials High BUN: Crea

A
  • Considered elevated if >20
  • GI hemorrhage, fever, glucocorticoids, burns, infections, starvation
41
Q

Oxidative changes to erythrocyte (Methgb and Sulfa hgb)

A

Normal: iron kept in Ferrous (Fe2+) form

MetHgb: Iron molecule oxidized to FerrIC form (Fe3+)
- Increases affinity to O2 - decreased release–> shifting to left

SulfaHgb: Still oxidizes from Ferrous to ferrIC form (Fe3+) , but also sulfur atom irreversibly binds to Hb –> incapable of carrying O2
- Shift curve to R
- Cyanosis without respiratory distress

42
Q

What are heinz bodies?

A

Aggregates of denatured golbin and metabolized metHgb clumped together in RBC cytoplasm

  • Formation of methgb OR sulfahgb required to form Hz bodies
  • Decrease deformability, disrupt anion transport and may act as autoantibodies
43
Q

Why is feline RBC more susceptible to oxidative damage

A
  1. 8 hgb SH groups on globin part of molecule vs dog has 4
  2. Ultrastructure differences in spleen decrease ability to catch and remove oxidized RBCs
44
Q

Delayed neuropsychiatric Syndrome

A

Syndrome that develops 3- 240 days following the toxic CO episode

**CS: ataxia, inability to ambulate, depressed/stuporous mentation, seizures, deafness

  • Some cases response to NAC & vitamin E
45
Q
A

ACVECC (10 decks)

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