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SA Medicine > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Defintion of syncope

A

Sudden, transient loss or depression of consciousness and postural tone resulting from transient and diffuse cerebral malfunction with spontaneous recovery.

Often due to deprivation of energy substrates (glucose or oxygen)

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2
Q

Definition of pre-syncope

A

An incomplete form of syncope

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3
Q

Definition of seizure

A

Abnormal excessive paroxysmal synchronous discharge in a population of neurons

Dysfunction of grey matter, which may be primary in origin or secondary to a metabolic abnormality

Can be tonic clonic or psychomotor

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4
Q

Definition of narcolepsy and cataplexy

A

Narcolepsy - dog collapses into sleep

Cataplexy - sudden onset of muscle paralysis

Can be induced by excitement or eating

Dogs can usually be roused by stimulation

Inherited forms in poodles, labradors, dobermans

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5
Q

Characteristics of fit (seizure)

A 
Pre-ictal phase
Marked limb movement, urination, defecation
Completely unresponsive
Long duration (>3 min)
Gradual recovery
Behavior change
Evidence of other neurological disease
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6
Q

Characteristics of fainting (syncope)

A 
Sudden onset
Provoking event (vomiting, sudden change in level of activity)
Flaccid collapse 
Followed by opistotonus
Completely unresponsive
Short duration (< 1 min)
No limb movement
Generally rapid and complete recovery
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7
Q

Characteristics of “falling over”

A

Elderly dog with musculoskeletal disease

Usually multiple events at exercise prior to presentation

Gradual onset

Variable duration

Dog becomes recumbent but no loss of consciousness

No spontaneous limb movement, urination, or defecation

Quick, complete recovery

Evidence of pain on clinical exam

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8
Q

Physical exam findings associated with syncope

A 
Pale or cyanotic MM
Hypo or hyperkinetic pulses
Distention of jugular pulses
Neurological deficits
Gallop rhythm
Murmur
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9
Q

Cause of syncope in humans

A

46% non-cardiogenic
36% undiagnosed
16% arrhythmias
2.5% obstructive cardiac disease

(Probably similar in animals)

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10
Q

What kind of hematological disorders can cause syncope?

A

Anemia
Polycythemia
Myeloproliferative disease

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11
Q

Which endocrine disorders can result in syncope?

A 
Cushings, Addisons
DM, DKA
Hyperinsulinemia/insulinoma
Pheo
HypoT4
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12
Q

Which muscular disorders should be differentials for a patient presenting for syncope?

A 
Polymyositis
Muscular dystrophy
Myopathy secondary to hypoK+, steroids, myotonia
Labrador and retriever myopathy
Mitochondrial myopathy
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13
Q

Which neurological disorders should be differentials for a patient presenting for syncope?

A 
Thrombi
Hemorrhage
Space-occupying lesions
Atheroscleosis
Seizure
Vestibular or cerebellar disease
Spinal trauma
Narcolepsy/cataplexy
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14
Q

Which musculoskeletal disorders should be differentials for a patient presenting for syncope?

A 
DJD
Polyarthritis
Panosteitis
Hypertrophic osteodystrophy
Bilateral ACL rupture
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15
Q

Which neuromuscular disorders should be differentials for a patient presenting for syncope?

A

Myasthenia
Botulism
Peropheral polyneuopathies

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16
Q

Which drugs can cause iatrogenic syncope?

A

Digoxin

Vasodilators (phenothiazine derivatives, ACE inhibtors, beta blockers, CCB)

Quinidine

Class 3 agents (cisapride, sotalol)

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17
Q

What effects will class 3 agents have on a patient’s ECG?

A

Prolonged QT interval

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18
Q

Which congenital heart diseases can cause syncope?

A

Obstruction to outflow (AS and PS, tumors, endocarditis)

Tetralogy of Fallot

Shunts (VSD, PDA)

Severe AV valve dysplasia

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19
Q

What physical exam finding may indicate that a patient has a R->L PDA?

A

Cranial MM pink

Caudal MM cyanotic

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20
Q

What acquired cardiac disease can cause syncope?

A 
Severe AV valve disease
Systolic dysfunction (e.g. DCM)
Pericardial disease
Pulmonary hypertension
Arrhythmias
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21
Q

Which bradyarrhythmias can cause syncope?

A

Sinue bradycardia
Sick sinus syndrome
AV Block (2rd and 3rd degree)
Atrial standstill

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22
Q

Which tachyarrhytmias can cause syncope?

A

Afib
Atrial flutter
Supraventricular tachycardia
Ventricular tachycardia

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23
Q

Treatment for VPCs?

A

Lidocaine

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24
Q

Treatment of ventricular tachycardias?

A

Lidocaine, K+

Esmolol, sotalol

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25
Q

Classes of anti-arrhythmic drugs

A

1: Na+ channel blockers
2: B blockers
3: K+ channel blockers
4: Ca+ channel blockers

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26
Q

If an animal is presenting with collapse and ECG shows multiple episodes of profound bradycardia, what is a likely diagnosis?

A

Vasovagal (neurally-mediated) syncope

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27
Q

What is the treatment for vasovagal (neurally-mediated syncope)?

A

None if infrequent

If situational, avoid situation

Sympathomimetics

Beta blockers, mineralocorticoid supplementation

Pacemaker

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28
Q

Two types of leads in pacemakers

A

Passive fixation

Active fixation

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29
Q

What ECG characteristics are representative of atrial fibrillation?

A

No P waves
Supraventricular
Irregular
Fast

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30
Q

What are the goals of treatment for atrial fibrillation?

A

Slow HR
Convert to NSR
Provide inotropic support
Control CHF

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31
Q

Treatment for atrial fibrillation?

A 
Ca channel blocker (diltiazem)
beta blockers (EXCEPT IF CHF PRESENT)
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32
Q

Treatment for pericardial effusion

A

Furosemide (high dose IV)
Pimobendan
Drainage
Fluids (high dose IV)

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33
Q

How is blood pressure regulated?

A

Locally - NO and other metabolites mediate vasomotor tone

Systemically - Baroreceptor reflexes/sympathetic nervous system, RAAS, renal blood volume control

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34
Q

What are the three causes of systemic hypertension?

A
  1. White Coat Syndrome
  2. Primary hypertension
  3. Secondary hypertension
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35
Q

What is White Coat Syndrome?

A

Increase in BP due to measurement process or situation

Usually sympathetic stimulation with stress/excitement

Resolves when cause is eliminated

No treatment necessary

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36
Q

What is primary hypertension?

A

“Essential” or “idiopathic”

May be associated with subclinical renal disease

Uncommon in dogs and cats

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37
Q

What can cause secondary hypertension?

A

Renal disease

Adrenocortical disease (hyperadrenocorticism or hyperaldosteronism)

Diabetes mellitus

HyperT4

Pheo

Polycythemia

Acromegaly

Diet

Breed (sight hounds)

Iatrogenic

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38
Q

What is the most common underlying cause of secondary hypertension?

A

renal disease

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39
Q

What percent of cats with renal disease have hypertension?

A

20-30%

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40
Q

What is the correlation between degree of azotemia and BP?

A

No correlation

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41
Q

How does diabetes mellitus cause hypertension?

A

Blood volume expansion with hyperglycemia

Overproduction of renin

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42
Q

What percent of hyperthyroid cats have hypertension?

A

10-30%

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43
Q

How does hyperthyroidism cause hypertension?

A

Increased cardiac output

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44
Q

How does pheochromocytoma cause hypertension?

A

Increased cardiac output

Peripheral vasoconstriction

*May be episodic

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45
Q

How does polycythemia cause hypertension?

A

Increased blood viscosity increases peripheral vascular resistance

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46
Q

How does diet cause hypertension?

A

Salt intake

Little effect on BP in dogs and cats unless massive or pre-existing secondary hypertension

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47
Q

What drugs can cause hypertension?

A 
Corticosteroids
Phenylpropanolamine
Cyclosporin A
Erythropoeiten
NSAIDs
Electrolyte solutions
Adrenergic agonists
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48
Q

Main tissues affected by hypertension?

A

Heart
Kidneys
Eyes
Brain

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49
Q

Effects of hypertension on the CV system

A

Concentric hypertrophy of LV (-> murmurs or gallops, CHF)

Arteriosclerosis

Hemorrhage

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50
Q

What is a prognostic indicator of effects of hypertension on kidneys?

A

Degree of proteinuria

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51
Q

What effects does hypertension have on the eye?

A

Tortuous retinal vessels

Papilledema

Retinal edema, hemorrhage, detachment, degeneration

Secondary glaucoma

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52
Q

Effects of hypertension on CNS

A

Hypertensive encephalopathy
Stroke
Behavior alterations, depression, ataxia, seizures, stupor coma, death

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53
Q

Can hypertension be diagnosed based off of one BP measurement?

A

Rarely

In cases where there are definite clinical signs or evidence of end-organ damage

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54
Q

How can you measure BP?

A

Direct - arterial catheter

Indirect - doppler and oscillometric methods

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55
Q

Advantages and disadvantages of direct BP measurements

A

Advantages: accurate, objective, repeatable, ability to measure systolic/diastolic/mean BP

Disadvantages: invasive, requires technical skills to place and maintain arterial access

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56
Q

Advantages and disadvantages of indirect BP measurement

A

Advantages: technically simple and non-invasive

Disadvantages:less repeatable and inaccurate with movement or inconsistent technique

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57
Q

What is the most accurate and repeatable non-invasive technique to measure BP in cats?

A

Doppler sphygmomanometry

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58
Q

Normal BP

A

> 150/95

>160/100 considered abnormal

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59
Q

At what blood pressure should treatment be initiated?

A

Moderate risk

160-179/100-119

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60
Q

At what blood pressure is there severe risk of end-organ damage?

A

> 180/120

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61
Q

Treatment of BP is based on

A

Clinical signs

Risk of end-organ damage

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62
Q

Treatment of hypertension?

A 
Avoid high salt intake
ACE inhibitors
Ca channel blockers
Adrenergic blockers
Hydralazine
Nitroprusside
Diuretics
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63
Q

How do ACE inhibitors treat hypertension?

A

Block conversion of angiotensin I to angiotensin II

Vasodilation

Reduced secretion of aldosterone and ADH -> inc Na and H20 excretion

Dec sympathetic tone

Reduced cardiac and vascular hypertrophy

Reduces GFR and proteinuria

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64
Q

Adverse effects of ACE inhibitors in treatment of hypertension?

A

Decreased GFR and azotemia

Hyperkalemia

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65
Q

How do calcium channel blockers (amlodipine, diltiazem) work to treat hypertension?

A

Decreased calcium influx into vascular smooth muscle -> vasodilation

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66
Q

How to adrenergic blockers work to treat hypertension?

A

Decrease HR and contractility to dec CO

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67
Q

Treatment of choice for hypertension caused by hyperthyroidism?

A

Beta blockers

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68
Q

Treatment of choice for hypertension caused by pheochromocytomas?

A

alpha blockers

phenoxybenzamine, prazosin

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69
Q

How does hydralazine work to treat hypertension?

A

we don’t know

causes vasodilation

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70
Q

After initiating therapy for hypertension, how long should you wait to recheck BP?

A

7-10 days

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71
Q

When hypertension is controlled, how often should you monitor BP?

A

1-4 months

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72
Q

Normal pulmonary arterial pressure

A

25/10 mmHg

15 mmHg mean

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73
Q

How does hypoxia affect pulmonary vasculature

A

Causes vasoconstriction

Opposite of systemic circulation

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74
Q

What agents cause vasodilation in pulmonary vasculature?

A

NO
PGI2
O2

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75
Q

What agents cause vasoconstriction in pulmonary vasculature?

A

Thromboxane
Endothelin 1
Angiotensin II
Serotonin

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76
Q

Causes of pulmonary hypertension

A

Idiopathic

Increased PVR:
Primary PHT
HW disease
Chronic pulmonary disease
PTE
High altitude 
Hypoventilation

Increased PBF:
Congenital cardiac shunts
Increased CO

Increased PCWP:
PA stenosis
L-sided CHF

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77
Q

What is the most common cause of pulmonary hypertension in FL? Overall?

A

FL: HW disease

Overall: L-sided CHF

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78
Q

Consequences of pulmonary hypertension

A

Reduced CO
Hypoxemia
Cor pulmonale

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79
Q

Clinical signs/physical exam findings associated with pulmonary hypertension

A

Clinical signs similar to other cardiopulmonary diseases

R-sided CHF
Ascites
Syncope
Cyanosis
Murmur
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80
Q

How can you diagnose pulmonary hypertension?

A

Measurement of pulmonary artery pressure

Direct = cardiac catheterization gold standard

Indirect = echo

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81
Q

What ECG findings are associated with pulmonary hypertension?

A

Deep S wave and right axis deviation (RV enlargement)

Tall P waves (RA enlargement)

Arrhythmias

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82
Q

Treatment for pulmonary hypertension

A

Treat underlying cause (EXCEPT R->L shunts)

Oxygen
Diuretics
ACEi
NO
Ca channel blockers
Synthetic prostacyclins (cost prohibitive)

ET-1 receptor antagonists (cost prohibitive)

Phosphodiesterase inhibitors (sildenafil - most common tx)

Antithrombotics

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83
Q

Regulators of endothelial vascular tone

A

Vasodilators: NO and PGI2

Vasoconstrictor: ET-1

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84
Q

What is the pathophysiology of vascular remodeling in PHT?

A

Chronically elevated ET-1 ang Ag-II cause smooth muscle hypertrophy of vascular walls

Eventually is irreversible

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85
Q

What might thoracic radiographs show for a patient with PHT?

A 
Pleural fluid/pulomary edema
Cardiomegaly
Tortuous, blunted pulmonary arteries
Bronchial or alveolar pattern
Bronchiectasis
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86
Q

PAP estimate equation

A

PG = 4 x V^2

Normal = 10-25

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87
Q

Prognosis for PHT

A

Poor-grave

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88
Q

What are the most common types of thyroid tumor?

A

Follicular cell adenoma

Adenomatous hyperplasia

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89
Q

What percent of thyroid tumors are malignant?

A

1-3%

Most of these are carcinomas

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90
Q

Clinical signs of hyperthyroidism

A 
Weightloss
Polyphagia
Hyperactivity
PU/PD
Vomiting
Diarrhea
Anorexia
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91
Q

Common physical exam findings of hyperthyroid patients

A

Palpable thyroid nodule
Tachycardia
Murmur
Muscle wasting

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92
Q

What is the T3 suppression test?

A

Used to dx hyperthyroidism

Blood drawn for T3 and T4
T3 (cytomel) administered x 3 days
Draw sample 2-4 hr post last pill for T3 and T4

Normal cat will have suppressed T4

Hyperthyroid cat ill not suppress

Why measure T3? -> Assess client compliance

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93
Q

Treatment for hyperthyroidism?

A

Methimazole
Diet (Hill’s y/d)
I 131
Surgery

Not really recommended:
Propylthiouracil
Iopanoic acid

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94
Q

Most common type of hypothyroidism?

A

Acquired, primary (decreased T4)

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95
Q

Which breed is prone to secondary hypothyroidism due to pituitary malformation?

A

GSD

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96
Q

Breed predisposition for hypothyroididm?

A

Beagles, dobies, goldens

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97
Q

Clinical signs associated with hypothyroidism?

A 
"Tragic expression"
Corneal lipid deposits/lipemia retinalis
Truncal alopecia
Hyperpigmentation
Hyperkeratosis
Peripheral neuropathy
Myxedema coma
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98
Q

Lab findings associated with hypothyroidism?

A

Hypercholesterolemia
Hypertriglyceridemia
Low T4

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99
Q

Treatment for hypothyrodism

A

Levothyroxine 0.02 mg/kg BID

Re-test in 6-8 weeks

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100
Q

Which breeds have an autosomal recessive gene for hypoadrenocorticism?

A

Standard poodle
Portuguese water dog
Nova Scotia duck tolling retriver

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101
Q

Physical exam findings with hypoadrenocorticism?

A 
Hypothermia
Pale MM, prolonged CRT
Bradycardia
Weak pulses
Melena
Depressed mentation
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102
Q

Lab findings associated with hypoadrenocorticism?

A 
Lack of stress leukogram
Eosinophilia
Mild, non-regen anemia
HyperK+
HypoNa+
HyperCa++
HyperP
Azotemia
Hypocholestrolemia
Hypoalbuminemia
103
Q

What to do for an unstable patient in which you suspect hypoadrenocorticism?

A 
Start ATCH stim
IV catheter
Dex (0.25-0.5 mg/kg IV)
Fluids (NaCl)
Treat hyperK+
104
Q

Treatment for hypoadrenocorticism?

A

Oral pred
DOCP
Florinef

105
Q

What is atypical addison’s?

A

Similar history, presenting complaint, and PE to Addison’s

Normal Na+ and K+

ACTH stim still abnormal

Don’t need mineralocorticoids, just pred

Rarely progresses to mineralocorticoid deficiency

106
Q

Breed predisposition for hyperadrenocorticism

A

Dachshunds
Terriers
Boxers

107
Q

Clinical signs of hyperadrenocorticism

A 
PU/PD
Alopecia
Pendulous abdomen
Polyphagia
Panting
Facial nerve paralysis
108
Q

Physical exam findings with hyperadrenocorticism

A 
Ptosis
Lip droop
Tachypnea
Pendulous abdomen
Hepatomegaly
Muscle wasting
Truncal alopecia
Comedones
Thin skin
Calcinosis cutis
Cushing's myopathy
109
Q

Lab findings associated with hyperadrenocorticism

A 
Stress leukogram
Thrombocytosis
ELE
Hyperglycemia
Hypercholesterolemia
Proteinuria
110
Q

Screening tests for hyperadrenocorticism

A

Urine cortisol:creatinine ratio
ACTH stim
LDDS

111
Q

Discriminating tests for hyperadrenocorticism

A

LDDS
HDDS
Endogenous ACTH

112
Q

Urine cortisol:creatinine test

A

Negative test -> HAC very unlikely

owner needs to collect first AM urine at home

113
Q

ACTH stim

A

Doesn’t discriminate between PDH and AT

114
Q

LDDS

A

If suppresses at 4 hours but “escapes” at 8 hrs -> HAC

20% of patients with PDH won’t suppress at all

115
Q

HDDS

A

Lack of suppression -> AT

Suppression -> PDH

116
Q

Endogenous ACTH test

A

Low -> AT

High -> PDH

117
Q

Treatment of hyperadrenocorticism

A

Mitotane
Trilostane
Surgery (hypophysectomy or adrenalectomy)
Radiation

118
Q

Mitotane

A

Tx HAC
Should not be administered to sick or anorexic animals
Load with 50 mg/kg/day
Repeat ACTH stim in 1 week
Maintain with 50 mg/kg/week
Goal: pre and post values in normal “pre” range

119
Q

Possible side effects of mitotane

A

vomiting

addison’s

120
Q

Side effects of trilostane

A

Blocks 3B hydroxysteroid dehydrogenase which can lead to increases in precursor hormones, which can have similar effects as cortisol

Addison’s

Adrenal enlargement

121
Q

What is Atypical Cushing’s?

A

Similar clinical signs and PE findings as Cushing’s

Normal pre/post cortisol levels

Extended hormone panel to UTenn -> 2-3 hormones increased post-ACTH

Treatment similar to typical Cushing’s

122
Q

Common presenting complaints/clinical signs with DM

A 
PU/PD
Bumping into things
Vomiting
Hyporexia
Lethargy
Hind-end weakness (cats)
Weightloss
123
Q

Lab findings with DM

A

Hyperglycemia
Hypertriglyceridemia
Inc ALP and ALT
Glucosuria

124
Q

Goals of treatment of DM

A

Resolve clinical signs

Avoid hypoglycemia

125
Q

Long-term effects of DM

A

Eyes: cataracts, lens-induced uveitis, corneal ulceration, diabetic retinopathy

Urinary: bacterial or fungal cystitis, proteinuria, diabetic nephropathy

CNS: diabetic neuropathy (cats)

126
Q

Canine dental formula

A

Deciduous: 2 ( I 3/3 C 1/1 P 3/3) = 28
Permanent: 2 (I 3/3 C 1/1 P 4/4 M 2/3) = 42

127
Q

Feline dental formula

A

Deciduous: 2 (I 3/3 C 1/1 P3/2) = 26
Permanent: 2 (I 3/3 C 1/1 P 3/2 M 1/1) = 30

128
Q

Eruption times of canine teeth

A

Deciduous:
Incisors: 2-4 weeks
Canines: 3 weeks
Premolars: 4-12 weeks

Permanent:
Incisors: 3-5 months
Canines: 4-6 months
Premolars: 4-6 months
Molars: 5-7 months
129
Q

Eruption times of feline teeth

A

Deciduous:
Incisors: 2-3 weeks
Canines: 3-4 weeks
Premolars: 3-6 weeks

Permanent:
Incisors: 3-4 months
Canines: 4-5 months
Premolars: 4-6 months
Molars: 4-5 months
130
Q

Characteristics of normal dental occlusion

A

Scissors bite - upper incisors in front of lower incisors

Lower canine fits evenly between upper canine and 3rd incisor

Premolars fit in a shearing fashion (interdigitate)

Upper 4th premolar fits outside (lateral) to lower 1st molar

131
Q

What is true dental prophylaxis?

A

done on mouth FREE OF DISEASE

  1. Complete oral exam
  2. Supragingival scaling
  3. Subgingival curettage/root planing
  4. Polish (with fluoride)
  5. Flush
  6. Repeat oral exam
132
Q

What are dental caries?

A

Bacterial degeneration of the enamel
Not common in pets
Maxillary 1st molar most common due to incomplete enamel closure

133
Q

What causes enamel abrasions?

A

Excessive grooming
Toys
Rocks

134
Q

What is dental attrition?

A

Wear from other teeth
Caused by malocclusion

Causes increased risk of tooth fracture

135
Q

What causes enamel hypoplasia/hypocalcification?

A

Reduced formation of enamel aka enamel dysplasia

Hereditary

Systemic infection causing high fever during tooth formation (e.g. distemper)

Enamel organ damage during early extraction of deciduous teeth

Other trauma during tooth formation

136
Q

What causes enamel staining?

A

Intrinsic - tetracycline use during enamel development

Extrinsic - metal from fence, cage, bowl, other objects

137
Q

What causes discolored teeth?

A

Trauma that results in pulpal hemorrhage +/- tooth death or nonvital tooth

Pink -> purple -> tan

138
Q

What tooth most commonly undergoes resorption?

A

Mandibular 3rd premolar (80% of the time)

Caused by periodontal disease or oral trauma

139
Q

What is ankylosis?

A

Alveolar bone fused to cementum

Can be caused by:
Resorption/inflammation (no periodontal ligament is visible)

Excessive masticatory forces

Tx: crown amputation

140
Q

Classes of dental malocclusion

A

0: normal or breed normal
1: jaw relationship normal, but one or more teeth is out of position
2: mandible is short (mandibular distoclusion) in relation to maxilla - brachygnathia (overbite)
3: Maxilla short in relation to mandible (mandibular mesioclusion)- prognathia (underbite)

141
Q

T/F: class 2 and 3 dental malocclusion are more likely to be hereditary in origin

A

True

142
Q

Cranial mandibular osteodystrophy

A

Inherited condition (West Highland White Terriers )

Non-cancerous bone formation at the TMJ and spreads to the mandible

Results in pain, fever, resistance to eat or open jaw

143
Q

TMJ Locking

A

Trauma leading to luxation of TMJ

Can be secondary to dysplasia causing laxity

Coronoid slips under zygomatic arch, then mouth cannot close

Must reduce arch or coronoid to get mouth to move

144
Q

Gingival enlargement

A

(Gingival hyperplasia)

Boxers

Can be secondary to chronic inflammation

Pseudoenlarged gingival pocket formation

145
Q

Neoplasia of odontogenic structures

A

Ameloblastoma
Odontoma
Acanthomatous or peripheral ameloblastoma
Peripheral odontogenic fibroma

146
Q

Neoplastic tumors of gingiva

A

Malignant melanoma
SCC
Fibrosarcoma
Osteosarcoma

147
Q

Most important single oral cavity problem

A

Periodontal disease

148
Q

Is periodontal disease reversible?

A

No

At the point where bone/supporting structures are lost, the damage is nor reversible.

Gingivitis IS reversible

149
Q

Why are smaller breeds predisposed to periodontal disease?

A

Smaller breeds have closer teeth that reduce the cleaning ability of saliva/teeth and thinner supporting bone

150
Q

Stages of periodonatal disease

A

Stage 1: Gingivitis

Stage 2: Early periodontitis (up to 25% attachment loss)

Stage 3: Moderate periodontitis (25-50% attachment loss)

Stage 4: Severe periodontitis (>50% attachment loss)

151
Q

What is the only reversible stage of periodontal disease?

A

Gingivitis

152
Q

Indication for the use of antibiotics to treat periodontal disease

A

Oral ulceration

Severe periodontitis including purulent discharge

Additional surgery being performed

Bone implants

Pulp capping (pulpotomy)

153
Q

Most commonly used antibiotics in the treatment of periodontal disease

A

Clavamox
Clindamycin
Doxycycline

154
Q

Chronic ulcerative stomatitis

A

Canine disease

Halitosis, oral pain, inappetence, anorexia, ptyalism, periodontal disease

Unknown cause, may be associated with fusiform bacilli and spirochetes

Immunodeficient patients

PE findings: Severe gingivitis, ulceration, necrosis of oral MM, chelitis, gingival recession, depression, fever, cachexia

Tx: Anti-inflammaories, extractions, debridement, antibiotics, oxygenated mouth rinses, +/- tube feedings

155
Q

Mycotic stomatitis

A

Caused by overgrowth of Candida albicans

Associated with long-term antibiotic use, immunodeficiency, other diseases

Causes chronic dysphagia, inappetence and/or anorexia, ptyalism, halitosis, white plaque-like lesions in mucocutaneous junction, glossitis

Tx: eliminate underlying condition, anti-fungal medication (ketoconazole)

156
Q

How does leptospirosis cause oral disease?

A

Oral signs associated with uremia and thrombocytopenia

157
Q

Oral clinical signs associated with canine distemper virus

A

Hyperemia
Ulceration of MM
Ptyalism

158
Q

Oral clinical signs associated with canine infectious hepatitis

A

Tonsilar enlargement
Oral hemorrhage or petechiation
Injected or hyperemic MM

159
Q

Clinical sign associated with oral blastomycosis

A

Granulomatous, yellow-white, up to 1.5 cm lesions on tongues or MM

(Little white dogs)

160
Q

Oral clinical signs associated with hypothyroidism and diabetes mellitus

A

Severe generalized marginal gingivitis not associated with expected quantities of calculus

Dysphagia

Periodontal disease

161
Q

Oral clinical signs associated with hypoparathyroidism

A

Oral ulcers
Necrosis associated with oral ulcers
Halitosis
Ptyalism

162
Q

How to differentiate whether bleeding in oral cavity is due to oral disease or coagulopathy?

A

Bleeding will only be in oral cavity if it’s oral disease…

163
Q

Clinical signs associated with thallium toxicity

A

Oral inflammation and ulceration
Malaise
Generalized erythema
Generalized severe pain

164
Q

What causes phytogranulomatosis?

A

Oral trauma from plant awns from the hair coat

165
Q

General oral clinical signs associated with oral trauma

A 
Pawing at mouth
Ineffectual swallowing
Ptyalism
Inappetence
Anorexia
Dysphagia
166
Q

Is tonsillectomy indicated for tonsillitis?

A

No

Does not cure clinical signs

167
Q

Causes of tonsillitis

A

Primary - idiopathic (CKCS, eosinophilic)

Secondary - secondary to diseases causing chronic regurgitation, vomiting, coughing

168
Q

Primary goal of treatment of severe feline stomatitis

A

Reduce inflammation through plaque control

Dental prophylaxis is imperative no matter the etiology

169
Q

Treatment of severe feline stomatitis includes

A 
Antibiotics
Analgesics
Anti-inflammatories
Extractions
At-home care

After all therapies have failed, cyclosporine

170
Q

Clinical signs seen in teething animals

A

Serous nasal discharge
Metallic halitosis
Enlarged mandibular lymph nodes

171
Q

What is tight lip?

A

Condition in which the lip is too attached to the gingiva and can result in tooth impressions/trauma to gums

Shar peis

172
Q

What is a dentigerous cyst?

A

Fluid-filled structure that develops at the separation of the follicle of an unerupted tooth (destructive)

173
Q

What is an odontoma? What are the two types?

A

Odontogenic tumor that contains both epithelial and mesenchymal cells

Young animals during development of permanent teeth (except rats)

Compound: tooth-like structures (denticles) present

Complex: conglomerate of dental tissue

174
Q

Feline Juvenile Gingivitis

A

Cats 8-18 months old

Abysinnians, persians, siamese, maine coons

Required early and aggressive treatment

May be proliferative

With proper therapy, will wane at 24 months

175
Q

What causes tooth resorption?

A

There is no proven cause

176
Q

Stages of tooth resorption

A

Stage 1 – Mild dental hard tissue loss, either cementum alone or cementum and enamel. In this stage of the disease, a defect in the tooth’s enamel is all that is usually noted. There is little to no sensitivity because the resorption has not yet reached the dentin.

Stage 2 – Moderate dental hard tissue loss including cementum or cementum and enamel, and loss of dentin that has not yet reached the pulp cavity.

Stage 3 – Deep dental hard tissue loss including cementum or cementum and enamel, and loss of dentin that extends to the pulp chamber. At this third stage of disease, most of the tooth is still viable.

Stage 4 – Extensive dental hard tissue loss and most of the tooth has lost its integrity. A significant amount of the tooth’s hard structure has been destroyed. Stage 4 has three sub-categories: 4a (crown and root of tooth are equally affected), 4b (crown is more severely affected than the root), and 4c (root is more severely affected than the crown).

Stage 5 – Only remnants of the tooth remain, covered by gum tissue. The majority of the tooth has been resorbed, leaving only a raised area on the gum.

177
Q

3 primary patterns of canine tooth resorption

A
  1. Internal resorption
  2. Idiopathic bony replacement resorption (external)
  3. Osteoclastic resorption (like cats, least common)
178
Q

Initiating causes of canine tooth resorption

A

Trauma
Orthodontic treatment
Malocclusion

179
Q

What percent of discolored teeth are non-vital (dead) or dying?

A

92%

180
Q

Only infectious disease that feline stomatitis is correlated with?

A

calicivirus

181
Q

What is insulin “stacking”?

A

If more insulin is given at the peak effect of the last dose, the effect will “stack” and have more of an effect and last longer than intended

Can cause hypoglycemia

182
Q

Goals of therapy for feline diabetic?

A

Eliminate clinical signs

Maintain good QOL for owner and cat

Potential remission

183
Q

Unlike all other insulins that need to be rolled, which needs to be shaken?

A

Vetsulin

184
Q

How long does it usually take to achieve adequate glycemic control in diabetic patients?

A

1-3 months

185
Q

What is the Somogyi effect?

A

Rebound hyperglycemia secondary to hypersecretion of counter regulatory hormones during hypoglycemia

186
Q

Which insulins are short-acting, intermediate-acting, and long-acting?

A

Short: HUmulin R, Novolin R

Intermediate: NPH (Humulin N, Novolin N), Lente, PZI

Long: Glargine, Detemir

187
Q

What is the max starting dose for insulin therapy for a cat?

A

2U/cat

188
Q

What should the diet of a feline diabetic consist of?

A

Low card, high protein to minimize postpradial hyperglycemia

189
Q

What is an appropriate amount of weight loss per week for a diabetic patient?

A

1-2% of body weight per week

190
Q

Which concurrent illnesses or medications can contribute to insulin resistance?

A

Stomatitis
UTI

Glucocoritcoids

191
Q

Advantages and disadvantages of BGCs

A

Advantages:
Nadir and peak time of effect
Duration of effect
Evaluate for Somogyi effect

Disadvantages:
Stress hyperglycemia
Laborious
Cost

192
Q

Why are fructosamine levels used to assess glycemic control?

A

Represent BG of previous 1-2 weeks

Can be artifactually lowered by hyoproteinemia, hyperthyroidism, lean cats, newly diagnosed or mild DM

193
Q

Renal glucose threshold

A

300 mg/dL

194
Q

Why do patients with diabetes develop cataracts?

A

High levels of glucose overwhelm lead to higher levels of sorbitol and fructose in the eye

(Aldose reductase activity decreases with age)

195
Q

Is plantargrade stance in diabetic cats reversible?

A

rarely

196
Q

Pathophysiology of ketosis

A

Decreased amounts of insulin (diabetic patient) lead to decreased inhibition of lipolysis/FFA production result in ketogenesis

197
Q

DKA almost always occurs as a result of

A

DM + a concurrent problem (commonly UTI or pancreatitis)

198
Q

Physical exam findings of patient in DKA

A 
Hypothermic
Tachycardic
Tachypnea
Tacky MM, inc CRT
Weak pulses
Muscle wasting
Depressed/obtunded mentation
199
Q

How to treat hyponatremia in patient in DKA

A

for every 100 mg/dl BG increase above 100, add 1.6 mEq/L of Na

200
Q

Osmolality equation

A

[2 (Na + K) + 0.05 (BG) + 0.33 (BUN)] = osmolality

201
Q

What are the most important things to avoid during treatment of patient with DKA

A

Fluid overload
Rapid changes in osmolarity
Hypokalemia
Hypophosphatemia

202
Q

Pathophysiology of hypokalemia in DKA patient

A

K+ move from cells in to blood with decreased blood pH and insulin levels

Lost through urine

When fluid is replace and acidemia is fixed, K will move back intracellulary

Results in hypokalemia

203
Q

Best insulin choice for treatment of patient in DKA?

A

Regular insulin 0.2U/kg IM

204
Q

Primary goals of treatment of patient in DKA

A

Stop ketogeneisis
Rehydrate
Correct electrolyte imbalances
Avoid hypoglycemia

(NOT regulation of BG)

205
Q

Most common complication associated with treating DKA

A

Hypoglycemia

206
Q

What is hyperosmolar nonketotic DM?

A

Severe hyperglycemia (BG > 600)

Hyperosmolarity (> 350 mOsm/kg)

Dehydration

Absence of ketonuria

207
Q

Pathophysiology of hyperosmolar nonketotic DM

A

Glucosuria -> osmotic diuresis -> water loss

Underlying disease -> dec fluid intake -> dehydration

Dehydration -> dec GFR -> dec renal glucose excretion

208
Q

Why is there no ketonuria in patients with hyperosmolar nonketotic DM?

A

May produce a small amount of insulin

B-hydroxybutyrate not dectecatbe on urine dipstick

209
Q

Physical exam findings for patient with hyperosmolar nonketotic DM?

A

Profound dehydration
Obtunded
Hypotermia
Prolonged CRT

210
Q

Lab findings for patieht with hyperosmolar nonketotic DM

A

Hyperglycemia
HypoK
Hyperosmolality
Azotemia

211
Q

Treatment goals for patient with hyperosmolar nonketotic DM

A

Correct dehydration
Restore electrolyte balance
Correct osmolality

GO SLOWLY

212
Q

Pathophysiology of idiogenic osmol formation

A

Fluid pulled from brain during severe dehydration

Brain produces idiogenic osmols to pull fluid back into brain

When insulin is given, brain glucose and osmolality are increased

Idiogenic osmols cannot leave -> higher osmolality of brain when compared to ECF

Fluid pulled back into brain causing cerebral edema

Need to tx with mannitol +/- corticosteriods

213
Q

Maximum rate of Na decrease when treating hypernatremia

A

Decrease no more than 0.5 mEq/L/hr

214
Q

Diagnosis of DM is based on

A

Clinical signs
Fasting hyperglycemia
Glucosuria

215
Q

Diagnosis of DKA is made by what clinical findings

A

Ketonuria

Metabolic acidosis

216
Q

Extravascular hemolysis

A

Erythrophagocytosis by macrophages

Produced spherocytes

217
Q

Intravascular hemolysis

A

RBCs lysed via complement-mediated destruction

Produced fragmented, ghost cells

218
Q

Hallmarks of intravascular hemolysis

A

Hemoglobinuria

Hemoglobinemia

219
Q

What toxins can cause hemolytic anemia

A

Acetaminophen
Methylene blue
Onions
Zinc

220
Q

What type of hemolysis does microhepatic hemolytic anemia cause?

A

Intravascular (causes physical trauma to cell)

221
Q

How does hypophosphatemia cause hemolysis?

A

Severe hypophosphatemia causes inhibition of RBC ATP production -> oxidative stress -> hemolyis

222
Q

What diseases are associated with hypophosphatemia that may lead to a hemolytic anemia?

A

DM
Hepatic lipidosis
After initiation of enteral feeding

223
Q

Diseases associated with hereditary hemolytic anemia

A

Pyruvate kinase deficiency
Pyruvate phosphofructokinase deficiency
Stomatocytosis

224
Q

What drugs are associated with canine IMHA?

A

Sufla drugs
Cephalosporins
Penicillins

225
Q

What are the two most common infectious diseases to cause hemolysis and regenerative amemia?

A

Babesiosis

Feline Hemoplasmosis

226
Q

What kind of anemia does cytaux cause?

A

Hemolytic, NON-REGENRATIVE anemia

227
Q

What kind of hemolysis does babesia cause?

A

Intravascular

228
Q

Most common neoplasia associated with IMHA?

A

Lymphoma

229
Q

What is the immune response composed of in IMHA?

A

Type II immune reaction: Ab +/- complement-mediated destruction

IgG: macrophage erythrophagocytosis +/- completment-mediated destruction

IgM: complement-mediated destruction only

230
Q

Breeds with hereditary predisposition for IMHA

A 
Cockers
Schnauzer
Bichon
Min Pin
English Springer
Poodle
Collie
OES
Finnish Spitz
231
Q

Lab findings with IMHA

A 
Regen anemia
Leukocytosis
Thrombocytopenia
Spherocytosis
Heinz bodies
Parasites

ELE, Tbili
Azotemia

Bilirubinuria
Hemoglobinuria

232
Q

What three tests help diagnose IMHA?

A

Autoagglutination

Direct Ab test (Coomb’s)

Flow cytometry for anti-RBC Ab

233
Q

What causes autoagglutination?

A

IgM and IgG

234
Q

What is the Coomb’s test?

A

Patient RBCs washed to remove non-bound proteins

Anti-IgG/IgM/complemenet Ab added

Agglutination supportive of IMHA

235
Q

Negative prognostic indicators associated with IMHA

A 
Rapidity of onset
Bilirubin > 10
Intravascular hemolysis
Persisten agglutination
Thromboembolic complications
Marrow-directed disease
236
Q

Complications of IMHA

A

Thromboembolic complications (PTE)

DIC

237
Q

Breed over-represented in feline IMHA

A

Himalayans

238
Q

What is the immune response composed of in ITP?

A

Type II immune reaction

239
Q

Causes of secondary ITP

A

Drugs: cephalosporins and sulfonimides

Infectious: anaplasma, babesia, lepto, leishmania

Neoplasia: lymphoma, hemangiosarc, histiocytic sarc

Inflammation: hepatitis, pancreatitis, SIRS

240
Q

Lab findings with ITP

A

SEVERE thrombocytopenia (<30,000)
Regenrative anemia
Leukocytosis
PT/PTT WNL (unless in DIC)

241
Q

Diagnosis of ITP based on:

A

Exclusion of other disease processes

Presence of severe thrombocytopenia

Normal to increased megakaryopoeisis

Platelet bound Ab

242
Q

How do glucocorticoids work in the treatment of IMHA/ITP?

A

Alter function of macrophage Fc receptor

Inhibit the production of several cytokines

Decrease immunoglobulin affinity

Decrease immunoglobulin production

243
Q

How does cyclosporine work in the treatment of IMHA/ITP?

A

Inhibits T-cell mediated immunity

Inhibits production of IL-2 by activated T cells

244
Q

How does azathioprine work in the treatment of IMHA/ITP?

A

Antimetabolite (purine antagonist) that interferes with DNA and RNA synthesis, mitosis

Inhibits cell-mediated and humoral immunity

245
Q

How does leflumonide work in the treatment of IMHA/ITP?

A

Antimetabolite (inhibits pyrimidine synthesis)

Inhibits cell-mediated and humoral immunity

Reduced B-cell populations

246
Q

What should you warn owners of when treating with leflumonide?

A

teratogenic

247
Q

Which drug is most useful for the treatment of IMHA/ITP during the initial phases during hospitalization?

A

Vincristine

248
Q

Defects of primary hemostasis that produce platelet abnormalities most commonly cause

A

reduced platelet numbers

249
Q

What is glanzmann’s thromboasthenia?

A

Spontaneous bleeding affects Great Pyrenese

250
Q

Most common cause of petechia and ecchymoses in dog?

A

Thrombocytopenia

251
Q

Causes of decreased plately production

A

Drugs (chemo, TMS)

Infection (FIV/FeLV, Rickettsial, fungal)

Myelophthisis

Myelofibrosis

Immune-mediated

Neoplasia

252
Q

What is congential macrothrombocytopenia?

A

Macrothrombcytopenia caused by single nucleotide change in gene encoding beta 1- tubulin, which likely affects microtubule stability resulting in altered platelet formation by megakaryocytes

Affects Cairn, Norfolk terriers, Cavaliers

NO BLEEDING TENDENCIES

253
Q

Most common cause of thrombocytopenia in dogs?

A

ITP

254
Q

Inherited conditions that cause petechia and ecchymoses

A

vWBD

Glanzmann’s thromboasthenia

SA Medicine (3 decks)

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