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SA Medicine > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Does anorexia in adult animals result in significant hypoproteinemia?

A

No

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2
Q

Mechanisms of decreased protein production

A

Hepatic failure

Inflammatory disease

Malnutrition (maldigestion,malabsorption)

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3
Q

Mechanisms of protein loss

A

Renal (PLN)

Intestinal (PLE)

Third spacing

burns/wounds

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4
Q

Common presenting complaints of patients with hypoproteinemia

A

Peripheral limb swelling

Abdominal distention

Coughing/dyspnea

Decreased appetite

Vomiting/diarrhea

None

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5
Q

Causes of hypoglobulinemia

A

PLE

Blood loss

Failure of passive transfer

Combines immunodeficiency

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6
Q

Which values on a chemistry panel are indicators of liver function?

A 
Tbili
Albumin
Glucose
Cholesterol
BUN
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7
Q

Medical concerns associated with hypoproteinemic animals

A

Fluid overload (decreased oncotic pressure, consider colloids or plasma)

Anesthesia (protein bound anesthetic agents)

Wound dehiscence

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8
Q

Why are hypoproteinemic animals prone to thromboembolism?

A

Loss of protein also leads to loss of antithrombin

Consider giving clopidogrel

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9
Q

Congenital causes of hypoproteinemia

A

Hepatic shunt

Failure of passive transfer

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10
Q

Infectious causes of hypoproteinemia

A

Parasites
Viral
Fungal

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11
Q

Inflammatory causes of hypoproteinemia

A

Inflammatory bowel disease

Lymphangectasia

Protein-losing enteropathy

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12
Q

Metabolic causes of hypoproteinemia

A

Hepatic disease
Renal disease (PLN)
EPI

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13
Q

Definition of heat stroke

A

Severe illness characterized by core temperatures of >104 F in humans and >105.8 F in dogs as well as CNS dysfunction

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14
Q

Two classifications of heat stroke

A

Classic/non-exertional

Exertional

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15
Q

Patient predisposing factors for heat stroke

A 
Exercise
Age
Brachycephalic
Obesity
Hypothyroidism
Laryngeal paralysis
Cv disease
CNS disease
Prior heatstroke
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16
Q

What are the protective mechanisms the body uses against heat illness?

A

Thermoregulation

Acclimatization

Acute phase response

Heat shock response proteins

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17
Q

Heat dissipation mechanisms

A

Sensible response (conduction, convection, radiation)

Insensible response (evaporative cooling (panting))

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18
Q

70% of total body heat loss in dogs and cats is due to which mechanisms?

A

Radiation and convection

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19
Q

What is the insensible response to heat?

A

Evaporative cooling via panting

Activation of hypothalamic panting center causes mucosal vasodilation

Partial air system uses unidirectional air flow in through nose and out of mouth to maximize evaporative cooling and heat loss

Salivation further increases evaporative cooling

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20
Q

Physiologic effects of increased body temp

A

Inc. sympathetic tone -> inc. HR and CO -> dec splanchnic circulation -> cutaneous vasodilation -> inc muscle blood supply -> inc cutaneous circulation -> heat loss via radiation, conduction, convection

Evaporative cooling via panting

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21
Q

At what point does evaporative cooling fail?

A

Environmental temp > body temp

OR

Humidity > 80%

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22
Q

How does dehydration affect heat dissipation?

A

Decreases evaporative heat loss because less water is available for respiratory system

Decreases heat dissipation through radiation and convection due to decreased blood flow to periphery

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23
Q

What is acclimatization and how long does this process take in dogs?

A

Adaptive physiologic response to environment and climatic change

Partial acclimatization in 10-20 days

Full acclimatization in 60 days

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24
Q

How does the body acclimatize to a higher environmental temperature? (7 things)

A

Increased ability to resist rhabdomyolysis

Body water conservation via aldosterone and ADH

Activation of RAAS

Salt conservation

Increased GFR

Plasma volume expansion

Enhanced CV performance (inc HR and CO)

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25
Q

What does the acute phase response work (heat stroke)?

A

Stimulation of anti-inflammatory acute phase proteins in liver

Inhibits production of reactive oxygen species

Inhibits release of proteolytic enzymes from activated leukocytes

Promotes wound healing and repair by stimulating endothelial cell adhesion, proliferation, and angiogenesis

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26
Q

What are heat shock proteins (HSP) and what do they do?

A

Protective proteins produced with cell stress (heat, ischemia, endotoxemia, oxidative/nitrosative stress)

Increase levels of HSPs allow a transient state of tolerance to otherwise lethal stage of heat stress allowing cells to survive

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27
Q

Reduced numbers of heat shock protein have been found with

A

Aging

Lack of acclimatization

Certain genetic polymorphisms

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28
Q

What are the physiologic effects of heat shock proteins?

A

Prevents protein breakdown and assists in refolding of denatures proteins into normal configuration

Prevents loss of epithelial barriers and prevents endotoxin leakage

Interferes with oxidative stress and blocks apoptotic cell signaling pathway

Prevents arterial hypotension to decrease cerebral ischemia and neural damage

Offer CV protection by regulating baroreceptor reflex response to abate hypotension and bradycardia

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29
Q

How does heat shock cause cardiovascular collapse?

A

Decreased central venous pressure and CO (circulatory shock)

Decreased plasma volume and hypoperfusion

Indirect myocyte injury

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30
Q

What effects can heat stroke have on the respiratory system?

A

Direct pulmonary epithelial damage

Increased pulmonary vasculature resistance

Can result in non-cardiogenic pulmonary edema, DIC, ARDS

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31
Q

What effect does heat stroke have on the kidneys?

A

Direct thermal injury

Indirect injury - hypoxia, microthombi

Rhabdomyolysis (nephrotoxic myoglobin)

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32
Q

What effects can heat stroke have on the brain?

A

Indirect injury due to edema, hemorrhage, infarcts

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33
Q

What effects does heat stroke have on GI system?

A

Hypovolemia and splanchnic pooling can cause microthrombi -> hypoxia and ischemia

Causes loss of GI integrity (ulceration and sloughing)

Results in bacterial translocation, sepsis, and endotoxemia

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34
Q

How does heat stroke affect the liver?

A

Decreased hepatic blood flow and thermally-altered hepatocyte function leads to decreased blood detoxification

Can cause centrilobular necrosis and cholestatic liver disease

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35
Q

How does heat stroke affect coagulation?

A

Direct:

Direct damage to vascular endothelium -> release of cytokines and inflammatory responses, adherence of leukocytes and platelets to damaged endothelium

Release of tissue factor (activating clotting cascade, producing uncontrolled systemic coagulation)

Depletion of coagulation factors and platelets

Reduced synthesis of coagulation factors from hepatocytes

Development of DIC

Indirect:

Hemoconcentration due to dehydration

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36
Q

Most consistent clinical signs of heat stroke

A

Panting

Dry, hyperemic MM

Tachycardia

Hyperdynamic femoral pulses

Ptyalism

Can by hyper, normo, or hypothermic!

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37
Q

Bloodwork findings with heatstroke

A 
Nucleated RBCs
Thrombocytopenia
Prolonged PT/PTT
Inc ALP/ALT
Axotemia
Inc. muscle enzymes
Hypoglycemia
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38
Q

Treatment for heatstroke

A

Rapid cooling - whole body wetting with water combined with muscle massage and fans, IV fluids

Oxygen supplementation

CV support (control hypotension, arrhythmias)

management of secondary complications (shock, hypoglycemia, DIC, ARDS, renal failure)

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39
Q

When should you stop active cooling techniques in heat stroke patient?

A

103.5-104 F

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40
Q

Should you use alcohol to cool a patient with heat stroke?

A

No

Risk of fire if need to defibrillate

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41
Q

What are exogenous pyrogens?

A

Infectious agents
Immune complexes
Inflammation
Drugs (e.g. tetracyclines)

Do not directly cause an increase in body temp, but cause an increase in endogenous pyrogens

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42
Q

What are endogenous pyrogens?

A

IL-1, IL-6, TNF, INF

Bind to vascular endothelial cells within anterior hypothalamus ->

Cause PGE1 and PEG2 production ->

Alters the set temperature (thermostat) within the hypothalamus

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43
Q

3 most common causes of FUO

A

Infection
Immune-mediated disease
Neoplasia

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44
Q

What are the risks associated with therapeutic trials for patients with FUO?

A

Continued disease progression

Drug toxicity/side effects

Exacerbating underlying diseae

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45
Q

How to treat a fever?

A

Artificial cooling techniques

Fluid therapy

Antipyretic agents

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46
Q

When should you use anti-pyretic agents?

A

Fever > 106F

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47
Q

Which fungi are dimorphic?

A

Blastomyces
Histoplasma
Coccidiodes
Sporothrix

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48
Q

Which fungi have broad-based budding?

A

Blasto

Histo

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49
Q

Even though Blastomyces is present in all soil, why don’t all animals contract this disease?

A

Soil organisms destroy blastomyces in the soil

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50
Q

What environmental conditions precede highest incidence periods of blastomyces infection?

A

Heavy rainfall

Warm temperatures

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51
Q

How is blastomyces transmitted?

A

Inhalation

Contamination of puncture wounds/open sores

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52
Q

Which dogs are prone to getting blastomyces?

A

Males > females

Sporting dogs and hounds

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53
Q

Transformation from blastomyces conidia to yeast occurs where?

A

Lungs

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54
Q

What important virulence factors does blastomyces have?

A

BAD-1 (cell surface glycoprotein tht binds to host cell receptors on macrophages and allows fungus to evade host immune system)

Alpha-1,3-glucan

+/- melanin

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55
Q

Common clinical signs associated with blastomyces infection

A

Respiratory signs (cough, dyspnea, exercise intolerance)

Ocular disease (anterior uveitis, chorioretinitis, endophthalmitis, optic neuritits)

Skin disease (cutaneous/SQ nodules, draining tracts)

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56
Q

Definitive diagnosis of blastomyces infection is based on

A

Cytological, histopathologic, or culture demonstration of organism

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57
Q

Diagnostic tests for blastomyces?

A

Cytology

ELISA Ag assay - may cross react with histoplasma

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58
Q

Thoracic rads are abnormal in what % of blastomyces cases?

A

85%

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59
Q

Treatment for blastomyces infection

A

Intraconazole
Fluconazole
Amphotericin B
Steroids

Treat for at least 60-90 days and continue 1-2 mo past resolution of clinical signs

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60
Q

Prognosis for blastomyces infection

A

~80% cured, 20% relapse

Prognosis poor if CNS involvement

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61
Q

Most common systemic mycoses in the cat

A

Cryptococcosis

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62
Q

Which fungus is narrow-budding?

A

Cryptococcus

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63
Q

Route of transmission of cryptococcus?

A

Inhalation

Hematogenous spread to extra-pulmonary sites

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64
Q

How does cryptococcus evade host immune system?

A

Polysaccharide capsule inhibits phagocytosis, plasma cell function, and leukocyte migration

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65
Q

Most common clinical signs seen with cryptococcosis in cats?

A

Sneezing and nasal discharge (50-8%)

Cutaneous/SQ masses (40-50%)

Ocular lesions (20-25%)

Non-specific signs (lethargy, anorexia)

CNS signs (20%) (blindness, depression, behavior changes, seizures)

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66
Q

Most common clinical signs of cryptococcosis in dogs?

A

Nasal signs

CNS (dull mentation, blindness, hypermetria, cranial nerve deficits)

Eyes

Skin nodules/draining lesions
Non-specific signs

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67
Q

How do you diagnose cryptococcosis?

A

Latex agglutination for Ag in serum, aqueous humor, or CSF

90-100% sensitive

Useful to monitor response to therapy

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68
Q

Treatment for cryptococcosis

A

Itraconazole
Fluconazole (in cats)
Amphotericin B (for systemic or refractory disease or those with ocular or CNS involvement)

Continue for at least 1-2 months past resolution of clinical signs and negative titers

Mean treatment time ~8.5 mo

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69
Q

Primary reservoir for histoplasma

A

Bat (guano and GI tract)

Decaying avian guano (esp. blackbird/starling roosts, chicken coops)

NOT found in fresh feces or shed feces of birds

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70
Q

Pathophysiology of histoplasma infection

A

Inhaled microconidia transform into yeast at body temperature

Yeast binds to CD-11 -18 integrins on alveolar macrophages and are phagocytized

Replicate within and destroy macrophages

Spread via hematogenous or lymphatics

*Most animals’ immune system is able to clear infection

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71
Q

Clinical signsof histoplasma infection in dogs

A

Anorexia/weight loss
Fever
Cough/dyspnea
Large bowel diarrhea

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72
Q

Diagnostic tests used to diagnose histoplasma infection

A

Cytology (rectal scrape, BAL)

ELISA Ag assay (urine)

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73
Q

Treatment for histoplasma infection

A 
Itraconazole
Amphotericin B (cases with CNS involvement or disseminated disease)

Treat for 60-90 days or at least 1-2 mo past resolution of measurable signs

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74
Q

Prognosis of histoplasma infection

A

Excellent with only pulmonary involvement

Guarded to fair with dissemination

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75
Q

Which fungus has a sperule containing multiple endospores?

A

Coccidiodes

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76
Q

Which fungus prefers dry, warm climates and sandy soils at low elevation (Ca, NM, AZ, UT, NV)?

A

Coccidiodes

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77
Q

Infection of coccidiodes follows what type of environmental condition?

A

Moist conditions followed by a dry period, then soil disruption

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78
Q

Clinical signs of coccidiodes infection in dogs?

A

Cough, weakness, lethargy, anorexia, weightloss, fever

Lameness with painful, swollen bone lesions

Localized lymphadenopathy

Ocular lesions

Skin lesions

Diarrhea

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79
Q

Clinical sign of coccidiodes infection in cats?

A

Skin lesions
Fever
Anorexia
Weight loss

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80
Q

Diagnosis of coccidiodes

A

ANTIBODY serology (IgM detectable 2-5 wks, IgG detectable 8-12 wks)

Cytology, histopathology

Bony lesions - may be more proliferative than lytic

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81
Q

Treatment of coccidiodes

A

Treat for 6 months minimum

Itraconazole
Fluconazole (if CNS involvement)
Amphotericin B

Bony lesions -> amputation
Enophthalmitis -> enucleation

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82
Q

What organism causes nasal aspergillosis?

A

Aspergillus fumigatus

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83
Q

What organism causes disseminated aspergillosis?

A

Aspergillus terreus

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84
Q

Why are german shepherds more prone to aspergillosis than other breeds?

A

IgA deficiency

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85
Q

Most consistent clinical findings with disseminated aspergillosis?

A

Vertebral pain, paraparesis, paraplegia, lameness with swelling, draining tracts, kidney disease

Other non-specific signs

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86
Q

Diagnosis of aspergillosis

A

Serological test -aspergillus glactomannan antigen

Cytology/histopathology

PCR for definitive diagnosis

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87
Q

Treatment for systemic aspergillosis?

A

Posaconazole
Itraconazole
Amphotericin B

Static disease rather than cure more common, poor prognosis

88
Q

Transmission of sporothrix

A

Usually cutaneous and SQQ inoculation of organism through puncture wound

Can follow inhalation

89
Q

Clinical signs of sporothrix infection

A

Cats > dogs

Male cats > female cats

Cutaneous lesions on nose and nasal planum

Regional lymphadenopathy

90
Q

Spread of which fungal disease is facilitated through contaminated claw/bite wounds and autoinoculation during grooming?

A

Sporothrix

91
Q

Which fungus is cigar shaped with a double wall?

A

Sporothrix

92
Q

Which fungus is round with a double wall?

A

Histoplasma

93
Q

Treatment of sporothrix

A

Itraconazole

16-8 weeks

Supersaturated KI/NaI (old treatment) for 30 days beyond remission

94
Q

Which fungus is potentially zoonotic?

A

Sporothrix

95
Q

“Large, infrequently septate hyphae with non-parallel walls” describes which organisms?

A

Phythium and lagenidium

96
Q

In what ways are oomycets not like fungus?

A

No chitin or ergosterol in cell wall

Diploid

Non-septate hyphae

97
Q

Pathophysiology of pythiosis

A

Infective, motile flagellate zoospore attracted to damaged tissue

Encysts in damaged skin or GI mucosa

98
Q

What are the two disease spectrums of lagenidium

A

Chronic nodular dermopathy

Fatal dermatologic and disseminated disease

99
Q

Main body systems affected by pythium vs lagenidium

A

Pythuim: cutaneous and GI

Lagenidium: cutaneous and vascular/lymphatic

100
Q

Diagnosis of pythium/lagenidium

101
Q

Why is it important to diagnose the species when dealing with phythium/langenidium?

A

Need to know species to determine

Prognosis
Prediction of behavior
Treatment options

102
Q

Treatment for pythium/lagenidium

A

Aggressive surgical resection

Combination antifungal therapy

Newer generation azoles

Caspofungin, mefenoxam (novel agents)

Hyperbaric therapy

Immunotherapy

Prognosis poor without resection,

103
Q

What are basidiobolus and connidiobolus?

A

Zygomycetes (actual fungi) that can cause skin, nasopharynx, GI lesions and sometimes lower respiratory dz.

104
Q

How do you treat basidiobolus and connidiobolus?

A

Aggressive surgical excision and anti-fungal medication

105
Q

How do you diagnose basidiobolus and connidiobolus?

106
Q

What is phaeohyphomycosis?

A

Cutaneous, SQ, cerebral or disseminated infections caused by cutaneous inoculation with pigmented ( diatiaceous) fungi containing melanin in their cell walls

107
Q

What is hyalohyphomycosis?

A

Non-pigmented (hyaline or transparent) fungal infection in tissue that can cause systemic, disseminated disease

108
Q

How do you diagnose phaeohyphomycosis/hyalohyphomycois?

A

Culture + PCR

109
Q

How do you treat phaeohyphomycosis/hyalohyphomycois?

A

Phaeohyphomycosis: aggressive surgical resection, itraconazole/posaconazole for 3-6 mo after surgery

Hyalohyphomycois: challenging due to systemic disease, poor prognosis

110
Q

Griseofulvin

A

Derived from penicillium

Disrupts mitosis

Used for dermatophytosis

Oral administration (give with fatty meal)

Side effects: GI, BM suppression, teratogenic

111
Q

Amphotericin B

A

Derived from streptomyces

Binds sterols -> inc wall permeability

IV administration

NEPHROTOXIC

Acute toxicity - vomiting, myalgia, fever, anaphylaxis

Poor penetration of bones, brain, eyes

112
Q

How can you reduce nephrotoxicity of amphotericin B?

A

Lipid binding

Cumulative dosing

Monitoring renal values before each treatment

Ensure hydration before administration

113
Q

What fluid type should Amphotericin B be administered with when given IV? Sq?

A

IV: 5% dextrose, Give NaCl or LRS AFTER

SQ: Give in 2.5% dextrose + 4.5% NaCl

114
Q

How does lipid bound amphotericin B work?

A

Taken up by macrophages and taken to site of inflammation

Achieves greatest concentrations in liver, spleen, and lung (spares kidneys)

Still need to monitor renal values!

115
Q

Flucytosine

A

Fluorinated pyrimidine that inhibits DNA/RNA synthesis

Good oral absorption

Penetrates BBB/CSF, use in severe CNS disease

Nephrotoxic

Dogs -> drug eruption

Cats -> thrombocytopenia

116
Q

Mechanism of action of azoles

A

Inhibits cytochrome p-450

FUNGISTATIC

NEED TO TREAT BEYOND CLINICAL SIGNS OF DZ

117
Q

hY should you not use antacids concurrently with azoles?

A

Azoles need acid for absorption

118
Q

Ketoconazole

A

Oral administration (fatty meal)

Poor penetration of brain and eye

Topical administration for candida and malassezia

Side effects: GI, hepatotoxicity, thrombocytopenia, cortisol suppression

119
Q

How are azoles metabolized?

120
Q

Itraconazole

A

Oral administration (capsules -> fatty food, liquid -> fasted)

IV administration

Does not penetrate CNS

Side effects: nausea, vomiting, inappetence, hepatotoxicity, cutaneous drug rxn

121
Q

Which fungal diseases can itraconazole treat?

A 
Histo
Blasto
Crypt
Coccidiodes
Asprgillus
Sporothrix

(Pretty much all of them)

122
Q

Fluconazole

A

Good oral bioavailability

DOES penetrate brain, eye

Renal excretion

123
Q

Which antifungal is the drug of choice for crypto?

A

Fluconazole

124
Q

What fungal diseases can fluconazole treat?

A

Crypto
Candida
Blasto
Histo

125
Q

Voriconazole

A

Good oral bioavailabilty

More potent than itraconazole, fluconazole

Expensive

126
Q

Posaconazole

A

Itra analogue

Expensive

127
Q

Which fungal disease can posaconazole treat?

A 
Candida
Crypto
Systemic asper
Blasto
Histo
128
Q

Main use of topical azoles (clotrimazole, enilconazole)?

A

Primary nasal aspergillus

129
Q

Side effects of topical azoles

A

Irritation
Erythema
Airway obstruction

130
Q

What is clotrimazole used for?

A

Nasal aspergillosis

Non-responsive candida cystitis

Renal pelvis infusions (renal aspergillosis)

131
Q

Iodides as antifungal therapy

A

KI, NaI

Used for sporothrix

Not commonly used

132
Q

Mechanism of action of terbinafine

A

Inhibits ergosterol synthesis

133
Q

Terbinafine

A

Commpnly used for dermatophytosis

Good oral bioavailability

Renal excretion

Side effects: GI, hepatotoxicity, pancytopenia

134
Q

Which drugs are chitin synthesis inhibitors?

A

Lufenuron

Nikkomycin

135
Q

Which drug is a glucan inhibitor?

A

Caspofungin

slow onset of action, expensive

136
Q

What is mefenoxam?

A

Agricultural fungicide

Inhibits RNA polymerase

Effective against plant pathogen oomycets

Has been used to tx pythium

137
Q

What is the MIC?

A

Minimum inhibitory concentration

Lowest concentration of a drug that inhibits growth of the organism cultured

NOT the concentration that kills the organism

138
Q

When do you consider anti-fungal sensitivity testing?

A

Systemic aspergillosis

Non-responsive infection

Minimal $$ constraints

139
Q

Why is nasal discharge not noticed until underlying cause is fairly advanced?

A

Usually the animal will swallow the discharge, so seeing it come out the nose means that the capacity of the mucociliary clearance has been exceeded

140
Q

Differentials for unilateral nasal discharge

A

Foreign bodies
Neoplasia
Tooth root abscess
Fungal rhinitis

141
Q

Differentials for bilateral nasal discharge

A

Bacterial/viral infection
Allergic rhinitis
Fungal rhinitis
Advanced neoplasia

142
Q

Differentials for epistaxis

A 
Fungal disease
Neoplasia
Hypertension
Ricketsial disease
Thromocytopneia/pathia
Coagulopathy
Trauma
143
Q

Are large populations of bacteria seen on nasal cytology concerning?

A

No, can be normal

144
Q

Diagnostic test that is most likely to yield a specific diagnosis if there is primary nasal disease

145
Q

Test that are recommended before performing nasal boipsy

A 
Platelet count
PT/PTT
BMBT
BP
Crossmatch
146
Q

How do you prevent penetrating the calvarium via cribiform plate during nasal biopsies?

A

Measure the distance between the nostril and the medial canthus of the eye with the biopsy instrument and do not advance past that

147
Q

3 primary biopsy techniques used in nasal biopsy

A

Pinch biopsy
Core biopsy
Traumatic nasal flushing

148
Q

Clinical signs of nasal tumors

A

Nasal discharge

Sneezing

Decreased airflow through nostril

Deformation of nasal bones, hard palate, or maxillary dental arcade

Non-specific signs such as weightloss and anorexia

149
Q

Treatment of choice for benign nasal tumors? Malignant tumors?

A

Benign: surgical excision

Malignant: radiation, NSAIDs

150
Q

Survival time for malignant nasal tumors treated with radiation?

A

6-12 months

151
Q

Clinical signs of nasal polyp

A

Stertorous breathing
Nasal discharge
Upper airway obstruction
Signs of otitis externa/media/interna (horner’s, head tilt, nystagmus)

152
Q

Primary pathogens in bacterial rhinitis

A

Bordetella bronchiseptica

Mycoplasma spp

153
Q

How can cardiac disease cause coughing?

A
  1. Chamber enlargement putting pressure on airway

2. Congestion or pulmonary edema

154
Q

T/F: fecal examination should be done on almost all patients presenting for chronic cough

155
Q

Most common complication associated with pulmonary aspirates

A

Pneumothorax

156
Q

Main use of bronchoscopy

A

Facilitate collection of samples from the lower respiratory tract

157
Q

What should you do is your patient experiences transient hypoxemia after tracheal wash or BAL?

A

This is normal

Will respond to oxygen therapy, crackles are normally heard for several hours after and are not of concern if other respiratory parameters are WNL

158
Q

Diseases that present with an acute cough

A

Canine infectious respiratory disease

Pneumonia

PTE

CHF

Non-cardiogenic pulmonary edema

159
Q

How do you definitively diagnose canine infectious respiratory disease?

160
Q

Best antibiotic choices for canine infections respiratory disease?

A

Doxy
TMS
Clavamox

161
Q

When should you use antibiotics with aspiration pneumonitis?

A

No improvement after 2-3 days

Inflammatory leukogram getting worse

Fever develops

Animal has been on H2 blockers or PPIs

162
Q

Causes of chronic cough

A 
Collapsing trachea
Canine chronic bronchitis
Bronchiectasis
Primary ciliary dyskinesis
Parasites
Eosinophilic bronchopneumopathy
163
Q

What radiographic view can you see intrathoracic tracheal collapse? Extrathoracic?

A

Intra: expiratory films

Extra: inspiratory films

164
Q

Emergency management of a patient with tracheal collapse and in respiratory distress should include:

A

Oxygen
Anxiolytic
Anti-inflammatory (short-acting steroids)

Intubation or tracheostomy

165
Q

Medical management of tracheal collapse includes:

A 
Weight reduction
Minimize exercise
Replace collar with harness
Reduction of inhaled irritants
Anti-tussives
Lomotil
Glucocorticoids
Bronchodilators
166
Q

When should surgery be considered for a patient with tracheal collapse?

A

Only in cases where medical management has failed and owners are prepared to accept negative outcomes

167
Q

Most common clinical sign of canine chronic bronchitis

A

A dry cough exacerbated by excitement and exercise

168
Q

Treatment for chronic canine bronchitis includes:

A

Glucocorticoids

Bronchodilators (B agonists or methylxanthines)

Antibiotics

Cough suppressants

169
Q

What is bronchiectasis?

A

Permanent dilation of the bronchi and is commonly a complication of chronic respiratory disease such as chronic bronchitis

170
Q

What is primary ciliary dyskinesis?

A

Congenital defects in the ciliary microtubule structure, resulting in reduced clearance of respiratory secretions, inhaled particles, and infectious agents.

Dogs < 2 yrs, English Pointers and Springer Spaniels

Usually also infertile because cilia on sperm and fallopian tubes are abnormal

Diagnosed with electron microscopy

171
Q

What is eosinophilic bronchopneumopathy?

A

Used to describe a variety of conditions which share the central feature of eosinophilic infiltration of lung and bronchial mucosa

Cause is usually not identified

172
Q

Treatment for eosinophilic bronchopneumopathy?

173
Q

5 mechanisms by which hypoxemia occurs

A
  1. Decreased inspired O2
  2. Hypoventilation
  3. Diffusion abnormalities
  4. Anatomic shunts
  5. V/Q mismatch
174
Q

Clinical signs of laryngeal paralysis

A

Stridor
Bark change
Cyanosis
Syncope

175
Q

Treatment for laryngeal paralysis

A

Oxygen
Anxiolytic
Anti-inflammatory
Intubation/tracheostomy

Surgery

176
Q

Components of brachycephalic airway syndrome

A

Elongated soft palate

Stenotic nares

Everted laryngeal saccules and laryngeal collapse

Hypoplastic trachea

177
Q

Diagnosis of laryngeal collapse

A

Laryngoscopy

178
Q

Surgery can help with which components of brachycephalic airway syndrome?

A

Elongated soft palate

Stenotic nares

Everted laryngeal saccules

179
Q

Primary diseases that have been associated with PTE

A 
Hyperadrenocorticism
Hypothyroidism
PLN
IMHA
HW disease
Sepsis
DIC
Pancreatitis
Neoplasia
180
Q

Clinical signs of PTE

A

Sudden onset of dyspnea in an animal previously not know to have respiratory disease

Acute dyspnea, tachypnea, depression

181
Q

Diagnosis of PTE

A

Angiograpahy
Scintigraphy
CT/MRI angiography

182
Q

Treatment of PTE

A

Anticoagulants (heparin, warfarin)

183
Q

What should you know about the use of heparin for treatment of PTE?

A

Heparin prevents the deposition of fibrin and platelets on the thrombus surface.

For heparin to be effective, adequate concentrations of antithrombin III must be present in the plasma.

High variation between patients.

184
Q

How do you monitor effects of heparin in treatment for PTE?

A

Activated partial thromboplastin time

185
Q

What is the prognosis for PTE?

A

Poor

Usually associated with underlying disease

186
Q

Physical exam findings with feline asthma

A
  1. Increased expiratory effort
  2. Increased expiratory time
  3. Expiratory wheeze
  4. Crackles (+/-)
187
Q

Treatment for feline asthma

A

Long-term corticosteroids

Bronchodilators

188
Q

Causes of non-cardiogenic pulmonary edema

A 
Neurogenic causes
Electrocution
Upper airway obstruction
Vasculitis
ARDS
Allergic reactions
Inhalation of toxins
189
Q

How does near drowning result in severe pulmonary damage?

A

Aspiration pneumonia

Water dilution of pulmonary surfactant leading to alveolar collapse and reduced compliance

190
Q

Clinical signs associated with smoke inhalation

A

Carboxyhemoglobinemia

Tissue hypoxia

Thermal injury to airways (inflammation, edema)

Direct toxic effects with certain chemicals

Suppression of pulmonary mucociliary and macrophage mechanism

DIC

191
Q

How much fluid does it take for clinical signs of pleural effusion to become apparent?

192
Q

Reasons for negative tap (thoracocentesis)

A

No fluid present

Fluid in walled off pocket or on contralateral side of chest

Very thick fluid

Fluid more ventral or deeper than needle

193
Q

What are transudates?

A

Fluids with low protein (< 2.5 - 3 g/dL) and low nucleated cell counts (<500 - 1000/ ul)

194
Q

What are modified transudates?

A

Fluids with protein concentrations up to 3.5 g/dl and cell counts up to 5000/ul

195
Q

What starling forces result in transudates or modified transudates?

A

Increased hydrostatic pressure
Decreased oncotic pressure
Increased vascular permeability

196
Q

What are exudates?

A

Fluids with protein > 3 g/dl and cell count >5000/ul

197
Q

Differentials for non-septic exudate pleural effusion

A 
FIP
Neoplasia
Lung lobe torsion
Chronic diaphragmatic hernia
Resolving septic exudate
198
Q

Differentials for septic exudate pleural effusion

A

Idiopathic
Penetrating wounds
Migrating grass foreign body
Extension of bacterial pneumonia

199
Q

Treatment for pyothorax

A

Antibiotics(IV ampicillin, enrofloxacin initially, then orals)

Chest tubes

+/- lavage

200
Q

Comparing what component of pleural fluid and serum can help identify chyle?

A

Triglycerides

201
Q

Common causes of chylothorax

A

Most are idiopathic

Trauma

Cardiac disease

HW

Lung lobe torsion

Diaphragmatic hernia

202
Q

Treatment for chylothorax

A

Medical treatment - low fat diet, rutin, intermittent chest taps

Surgery

203
Q

Differentials for hemothorax

A

Trauma

Systemic bleeding disorders

Neoplasia

Lung lobe torsion

204
Q

What is the only neoplasia that readily exfoliates into effusions?

205
Q

What is a tension pneumothorax?

A

One-way valve is formed by the tissue at the site of the leak, allowing air to move into pleural space during inspiration but prevents it from moving out during expiration

206
Q

Most common cause of pneumomediastinum?

A

Rupture of airways

207
Q

How is pneumomediastinum diagnosed radiographically?

A

When you are able to see

  1. Dorsal and ventral tracheal walls
  2. Cranial branch of aorta
  3. Longissimus dorsi muscle
208
Q

Treatment of pneumomediastinum?

A

Strict cage rest

Bronchoscopy to locate lesion

Surgery (esophageal laceration)

209
Q

How can mediastinal masses cause respiratory distress?

A

Displacing lung tissue and decreasing lung volume

Displacing tracheal lumen

Causing pleural effusion

210
Q

CT finding most consistent with nasal aspergillosis?

A

Loss of turbinate density

211
Q

Diseases that would benefit from cough suppressants

A

Collapsing trachea

Chronic allergic or sterile bronchitis

Neoplasia

212
Q

What causes crackles?

A

Fluid in the small airways/alveoli

Opening or collapse of small airways/alveoli

Parenchymal fibrosis

213
Q

What does an end-expiratory grunt indicate?

A

Air trapping and/or obstruction of lower airways

214
Q

Disease that cause inspiratory distress?

A

Laryngeal paralysis
Tracheal collapse
Brachycephalic airway syndrome
Pleural space disease

215
Q

Diseases that cause expiratory distress?

A

Asthma
Pneumonia
CHF
PTE

216
Q

Parasitic rhinitis can be cause by which organisms?

A

Pneumonyssoides caninum

Cuterebra

SA Medicine (3 decks)

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