Case 2 - El Letargo

Front 1

Is the thymus laterally or dorsally compressed?

Back 1

Laterally

Front 2

When does the thymus reach its maximum development?

Back 2

During sexual maturity (during 4th ot 5th month of age in dogs, just before shedding of deciduous teeth)

Front 3

What is the involution of thymus associated with?

Back 3

Changing of the teeth

Front 4

Does the thymus disappear in old age?

Back 4

No, it simply gets smaller and replaced with fat.

Front 5

How far caudally does the thymus extend in the thoracic cavity?

Back 5

5th or 6th costal cartilage

Front 6

What separates the polygonal lobules of the thymus?

Back 6

A delicate but distinct connective tissue capsule

Front 7

Is the thymus divided into lobes?

Back 7

Yes, right and left, but the compressed lobes are difficult to separate from one another (distinct caudally but not cranially)

Front 8

Which lobe of the thymus extends further caudally?

Back 8

The left lobe extends further caudally than the right

Front 9

Which lobe of the thymus is bigger?

Back 9

The right lobe is bigger

Front 10

What supplies the thymus with its blood supply?

Back 10

The thymus receives its chief blood supply from one or two thymic branches that go to each lobe from the ipsilateral internal thoracic artery

Front 11

Where do the lymphatics of the thymus empty into?

Back 11

The lymphatics from the thymus form 4-6 vessels that empty into the cranial mediastinal and sternal lymph nodes

Front 12

What innervates the thymus?

Back 12

Both parasympathetic (vagal) and sympathetic nerve fibers supply the organ and are probably vasomotor

Front 13

What is the basic cell unit of the thymus?

Back 13

Small lymphoctyte (thymocyte)

Front 14

Where are the Hassal's bodies (thymic corpuscles) found in the thymus?

Back 14

In the medulla of the gland

Front 15

More than a dozen blood group systems have been described in dogs. The various systems are referred to as DEA followed by a #? What does DEA stand for?

Back 15

Dog Erythrocyte Antigens

Front 16

Change in behavior of an animal (i.e. lethargy, stupor, coma, etc.) usually indicates a lesion....where?

Back 16

Diencephalon

Front 17

What does the diencephalon consist of?

Back 17

Thalamus and hypothalamus

Front 18

How can you differentiate LMN paresis from UMN paresis?

Back 18

LMN: inability to support wt. with short-strided walk. Tendency to collapse, tremble, bunny hop, and neck flexion.
UMN: delay in onset of protraction & longer stride with variable degree of stiffness - spasticity to the stride. Often paired w/loss of general proproceptive.

Front 19

What is the difference b/w general proprioceptive ataxia, vestibular ataxia, and cerebellar ataxia?

Back 19

Gen. proprioceptive ataxia is loss of awareness of where the limbs are. Vestibular ataxia is loss of balance reflected in a head tilt & tendency to lean, fall, or roll to one side. Cerebellar ataxia is inability to modulate the gait generating systems in brainstem resulting in abnormal uncontrolled, excessive limb movements (hypermetria)

Front 20

What are spinal reflexes based on?

Back 20

Nociception

Front 21

What things should you do to test spinal reflexes?

Back 21

Flex/extend limb/shoulders/hips on lateral recumbency to test for pain. Patellar reflex with hammer for response. Withdrawal/flexor reflex - squeeze digit for response. Perineal reflex - mild pressure on anus.

Front 22

What cranial nerves does the menace response test? And how?

Back 22

CN II (central visual pathway to occipital lobe) & CN VII (closure of palpebral fissure)

Front 23

What cranial nerves does pupil size and light response test?

Back 23

CN II (brainstem) and CN III (parasympathetic - ciliary ganglion - nerves = pupil constriction direct and indirect)

Front 24

What CN test for eye position?

Back 24

CN III (ventrolateral strabismus) and CN VI (medial strabismus)

Front 25

What CN tests for eye movement?

Back 25

CN VIII (brainstem) and CN III (adduction) and CN VI (abduction)

Front 26

Which CN tests for vestibular?

Back 26

CN VIII (strabismus in some eye positions and abnormal nystagmus while head is still)

Front 27

Which CN tests for facial muscles?

Back 27

CN VII (position, tone, movement: eyelids, ears, lips, nose)

Front 28

Which CN are you testing with palpebral reflex?

Back 28

CN V and CN VII

Front 29

Which CN is responsible for facial sensation?

Back 29

CN V

Front 30

Which CN tests for nociception?

Back 30

CN V (ophthalmic branch)

Front 31

Which CN tests masticatory muscles?

Back 31

CN V (mandibular branch)

Front 32

Which CN tests gag reflex (jaw tone)?

Back 32

CN V

Front 33

Which CN tests tongue size movement?

Back 33

XII

Front 34

Which CN tests for reflex gagging, swallowing?

Back 34

CN IX and CN X

Front 35

How are suture material sized?

Back 35

From decreasing to increased mm:
10-0 --> 2-0 -->0 --> 7

Front 36

When is whole blood used during a blood transfusion?

Back 36

Most commonly required to restore oxygen-carrying capacity in patients with anemia. Also used when patient needs clotting factors or is hypovolemic.

Front 37

What type of transfusion is done on normovolemic patients with anemia?

Back 37

pRBCs (packaged RBCs)

Front 38

What are the types of Dog Erythrocyte Antigens (DEA)?

Back 38

1.1., 1.2, 3-8

Front 39

Do dogs have naturally occuring antibodies against blood group antigens?

Back 39

No, they acquire them through transfusions or after pregnancy. Transfusion of blood from donor who has not been typed and has never been pregnant or transfused is generally pretty safe.

Front 40

Which DEA's can cause transfusion reactions?

Back 40

DEA 1.1, 1.2, or 7 (donors should be negative for these antigens)

Front 41

Which blood types do cats have?

Back 41

A, B, A/B

Front 42

What blood type are the majority of cats?

Back 42

A

Front 43

Fatal transfusion reactions occur in cats with type __ receiving type ___ blood

Back 43

Type B cats receiving type A blood (always cross-match/type before transfusions in cats)

Front 44

Difference b/w cross-matching and blood typing

Back 44

Cross-matching detects many incompatibilites but does not guarantee compatibility. Blood-typing gives the blood type of the animal.

Front 45

Which terms refer to either benign or malignant growths?

Back 45

Neoplasm and tumor

Front 46

Which term refers to malignant tumor?

Back 46

Cancer

Front 47

What is the main characteristic of neoplasm?

Back 47

It is unresponsive to normal growth controls

Front 48

What type of tumors usually do not invade surrounding tissue or spread to new anatomic locations?

Back 48

Benign

Front 49

Which type of tumors are usually terminal because they metastisize?

Back 49

Malignant

Front 50

What suffix do malignant tumors usually have?

Back 50

-sarcoma

Front 51

Differences b/w malignant and benign tumors

Back 51

Malignant tumors lack differentiation, have erratic growth rate, have mitotic figures, have no capsule, and metastasize. Benign tumors are well-differentiated, slowly expand, have a capsule, and don't invade.

Front 52

Difference b/w primary peripheral nerve tumors and paraneoplastic neuropathy?

Back 52

Primary peripheral nerve tumors arise from cells in the peripheral nervous system. Paraneoplastic neuropathies are neuropathies caused by tumors near the peripheral nervous system.

Front 53

What is Myasthenia Gravis?

Back 53

A disorder characterized by inefficient neuromuscular transmission secondary to a reduction in ACh receptors on the postsynaptic muscle membrane

Front 54

What are the 2 types of myasthenia gravis in dogs and cats?

Back 54

Congenital and acquired

Front 55

What causes the deficiency in ACh receptors in congenital myasthenia gravis?

Back 55

Reduced or imperfect synthesis, probably secondary to genetic defect

Front 56

What causes the reduction in ACh receptors in acquired myasthenia gravis?

Back 56

Antibodies, usually IgG, are generated against ACh receptors. These antibodies block neuromuscular transmission by directly interfering with the actions of ACh on receptors, accelerating the normal turnover rate of receptors or activating complement mediated lysis of the postsynaptic membrane.

Front 57

What other antibodies can be expressed causing myasthenia gravis?

Back 57

Striational antibodies (StrAbs), which are antibodies against striated muscle proteins such as myosin, actin, etc.
Also, antibodies against calcium channel receptor ryanodine (RyR).

Front 58

Thymoma is more likely in: males or females?

Back 58

Females

Front 59

What are the 2 cell types present in the thymus?

Back 59

Epithelial and lymphoid

Front 60

Which of the cells in the thymus are neoplastic in a thymoma?

Back 60

Epithelial cells are neoplastic in the tumor, with benign, well-differentiated, mature lymphoid cells

Front 61

Describe thymoma (growth? encapsulated? metastasizes?)

Back 61

Slow growth. Generally not metastatic. Well encapsulated. Associated with paraneoplastic syndromes, such as myasthenia gravis.

Front 62

Clinical signs of thymoma?

Back 62

Cough, dyspnea, enlarged jugular vein, edema of head & forelimbs, excess salivation, regurgitation or vomiting, heart & lung sounds muffled

Front 63

How is thymoma diagnosed?

Back 63

Radiographs are useful in locating soft tissue mass.

Front 64

What are the different stages of canine thymoma?

Back 64

Stage I - growth completely w/in intact thymic capsule
Stage II - pericapsular growth into mediastinal fat tissue, adjacent pleura &/or pericardium
Stage III - invasion into surrounding organs &/or intrathoracic metastases
Stage IV - Extrathoracic metastases

Front 65

What is the choice of treatment for thymomas in stage I or II?

Back 65

Thymectomy (removal of thymus)

Front 66

What are some other treatment choices?

Back 66

Radiotherapy, which is helpful in reducing the size in order to remove it.

Front 67

What does Myasthenia gravis result in?

Back 67

Flaccid paralysis of skeletal muscles

Front 68

What type of hypersensitivity is acquired myasthenia gravis?

Back 68

Type II hypersensitivity

Front 69

Clinical signs of myasthenia gravis?

Back 69

Paresis will first be seen in the pelvic limbs wtih shortened, crouched strides or positions, followed by thoracic limbs, which leads to a flaccid neck & collapse. Dyspnea, drooling, and paresis of eyelids and lips, regurgitation due to megaesophagus, and dysphagia

Front 70

Which breeds of dogs have been reported as having myasthenia gravis?

Back 70

Springer spaniel, mini dachshund, and genetic links in fox terriers, JRT

Front 71

What is the common treatment for myasthenia gravis?

Back 71

Exercise the dog for paresis to set in, then administer IV short-acting anticholinesterase endrophonium chloride. This blocks the degradation enzyme giving ACh more opportunity to bind to open receptors (not bound by Ab)

Front 72

Inspiration vs. expiration: which is an active process?

Back 72

Inspiration

Front 73

What is involved in inspiration?

Back 73

Diaphragm, external intercostal muscles, accessory inspiratory muscles

Front 74

What are the accessory inspiratory muscles?

Back 74

Sternocleidomastoid and scalenus (in neck)

Front 75

When are the accessory inspiratory muscles used?

Back 75

For deeper inspirations

Front 76

Does expiration require muscles?

Back 76

Not normally. It is a passive process during quiet breathing. It becomes active when more complete emptying of lungs is needed as with exercise.

Front 77

What are the muscles used in expiration?

Back 77

Abdominal muscles and internal intercostal muscles

Front 78

Where is the respiratory center located?

Back 78

Within portions of the brainstem.
Consists of regions within the medulla and pons

Front 79

What part of the medulla is responsible for generating the basic rhythm of breathing? (primarily for inspiration)

Back 79

DRG: dorsal respiratory group in the dorsal medulla

Front 80

How does DRG cause inspiration?

Back 80

Descending fibers of DRG neurons terminate on motor neurons that supply the inspiratory muscles. When these neurons fire, inspiration occurs. Output is relayed via the phrenic nerve to diaphragm.

Front 81

Which part of the medulla is responsible for expiration?

Back 81

VRG - ventral respiratory group in the ventral medulla

Front 82

How does the VRG cause expiration?

Back 82

When expiration is an active process (i.e. exercise), expiratory neurons are active.

Front 83

What inhibits inspiration?

Back 83

The pneumotaxic center (PC) in the rostral portion of the pons.

Front 84

How does the PC inhibit inspiration?

Back 84

It regulates inspiratory volume and respiratory rate. It sends impulses to DRG that switch off inspiratory neurons and limits duration of inspiration.

Front 85

What prevents inspiratory neurons from being switched off?

Back 85

Apneustic center in the caudal pons (it provides extra boost to inspiratory drive)

Front 86

What do the Hering-Breuer reflexes do?

Back 86

They can change the breathing rate & depth of a breath. Triggered to prevent over-inflation of lungs. Receptors located in lungs. Nerve impulses are trasmitted by the vagus nerves to the respiratory ctr.

Front 87

Where else are receptors for breathing located?

Back 87

Peripherally (on skin), in muscles, joints, in upper air passages (inhibitory)

Front 88

How does carbon dioxide influence alveolar ventilation?

Back 88

An increase in CO2 causes alveolar ventilation to increase. Decrease in CO2 causes it to decrease.

Front 89

How does hydrogen influence alveolar ventilation?

Back 89

Increase in H ion concentration causes alveolar ventilation to increase. Decrease causes decrease.

Front 90

How does oxygen influence alveolar ventilation?

Back 90

Decrease in oxygen cause alveolar ventilation to increase. Increase in oxygen causes alveolar ventilation to decrease.

Front 91

Eupnea?

Back 91

Ordinary quiet breathing

Front 92

Apnea?

Back 92

Condition where there is a transient cessation of breathing, whether normal (hibernation) or abnormal (caused by certain drugs)

Front 93

Dyspnea?

Back 93

Difficult or labored breathing

Front 94

Hyperpnea?

Back 94

Condition of breathing in which the frequency, depth, or both are increased

Front 95

Hypopnea?

Back 95

Breathing in which frequency, depth, or both are decreased

Front 96

Tachypnea?

Back 96

Excessive rapidity of breathing

Front 97

Bradypnea?

Back 97

Abnormal slowness of breathing

Front 98

Polypnea?

Back 98

Rapid, shallow, panting type of respiration

Front 99

Costal breathing?

Back 99

Characterized by pronounced rib movements; when breathing becomes difficult, or during painful conditions of the abdomen, this type of breathing becomes pronounced

Front 100

What innervates the external anal sphincter?

Back 100

Caudal rectal branch of the pudendal nerve

Front 101

What type of muscle is the external anal sphincter?

Back 101

Skeletal muscle (voluntary)

Front 102

Where does the caudal rectal branch of the pudendal nerve originate?

Back 102

At the sacral spinal cord (S1-S3)

Front 103

What is the parasympathetic innervation to the descending colon (inhibitory), rectum (inhibitory), and internal anal sphincter (excitatory)?

Back 103

Hypogastric nerve

Front 104

Where does the hypogastric nerve originate?

Back 104

Lumbar region (L1-L4/5)

Front 105

What is the parasympathetic innervation to the descending colon (excitatory), rectum (excitatory), and internal anal sphincter (inhibitory)?

Back 105

Pelvic nerve

Front 106

Where does the pelvic nerve originate?

Back 106

Sacral spinal cord (S2-S4)

Front 107

What is the hypogastric nerve's function?

Back 107

Storage of feces

Front 108

What is the pelvic nerve's function?

Back 108

Transport of feces

Front 109

What is the normal defecation reflex?

Back 109

Internal anal sphincter relaxes. External anal sphincter contracts. Stretch receptors activated when feces vol. increases. Signals sent to pudendal nerve & pelvic nerve to defecation ctr into sacral spinal cord.

Hint 109

Ascending tracts in spinal cord go to reticular formation in the brainstem. From there, signals are sent to midbrain, basal nuclei, and cerebral cortex. External sphincter relaxes and animal defecates.

Front 110

How can you tell if fecal incontinence is an UMN problem?

Back 110

Anal/perineal tone, reflexes, and sensation are usually normal. Also, urinary incontinence is usually present.

Front 111

Where would the lesion be present if the fecal incontinence was an UMN problem?

Back 111

In the cervical or thoracic portions of the vertebral column

Front 112

Where would the lesion be present if the fecal incontinence was a LMN problem?

Back 112

Lumbosacral spine

Front 113

How can you tell if the fecal incontinence is a LMN problem?

Back 113

Decreased anal tone and reflex. Decreased anal sensation. Decreased tail tone and movement.

Front 114

Which part of the thymus is densely made of lymphocytes?

Back 114

The cortex

Front 115

Which part of the thymus contains the Hassall's corpuscles?

Back 115

Medulla

Front 116

What are Hassall's corpuscles?

Back 116

Aka thymic. Round layered bodies containing keratin. Small blood vessel found at ctr. Contain IgA in cattle.

Front 117

What do Hassall's corpuscles do?

Back 117

They stimulate thymocyte proliferation by secreting growth factors (called thymic stromal lymphopoietin)

Front 118

What is the T-cell function in thymus?

Back 118

Must be able to recognize foreign and self antigens. This process is regulated by 2-stage selection.

Front 119

What is the 2-stage selection process for T-cell function?

Back 119

Negative selection and positive selection

Front 120

What is negative selection?

Back 120

Thymocytes w/receptors that bind self-Ag strongly & cause auto-immunity are killed by apoptosis. Thymocytes that have receptors which cannot bind to any MHC class II molecules are also killed b/c they cannot react to any processed Ag.

Front 121

What is positive selection?

Back 121

Thymocytes that survive negative selection (those that can still recognize specific MHC class II Ag complexes) are stimulated to grow & leave thymus as mature T-cells and circulate within bloodstream, eventually colonizing the secondary lymphoid organs.

Front 122

Why is the gene expression of thymic epithelial cells express 400+ Ag?

Back 122

to ensure that the developing T cells are exposed to a diversity of normal tissue Ag (that way, when T cells leave the thymus, it will not respond to normal body components, otherwise they will be killed off by negative selection)

Front 123

What regulates the cell function in thymus?

Back 123

Cytokines, small peptides, and Hassals corpuscles

Front 124

What is T cell tolerance?

Back 124

Immune system does not respond to specific antigen. Results if there are no functional T cells with receptors that bind self-antigen.

Front 125

What are the 2 types of self tolerance?

Back 125

Central T cell tolerance and Peripheral T cell tolerance

Front 126

How long are T cells vs. B cells tolerant?

Back 126

T cells can be made easily and rapidly (within 24 hrs) and remain in that state for more than 100 days. B cells develop tolerance in 10 days and return to normal within 50 days.

Front 127

Which species have NONKERATINIZED stratified squamous epithelium in their esophagus?

Back 127

Dogs and cats

Front 128

What innervates the esophagus?

Back 128

The vagus nerve and associated branches (glossopharyngeal, pharyngeal, and recurrent laryngeal nerves)

Front 129

The esophagus joins the _______ with the ________

Back 129

Laryngopharynx
Stomach

Front 130

What marks the junction of the laryngopharynx and esophagus in carnivores?

Back 130

Pharyngoesophageal limen (internal fold)

Front 131

What are the layers of the esophagus?

Back 131

Mucosa (stratified squamous epithelium, lamina propria, lamina muscularis), submucosa, and tunica muscularis (circular and longitudinal)

Front 132

What is megaesophagus?

Back 132

Dilation of the esophagus due to insufficient or uncoordinated peristalsis in the mid to cervical esophagus

Front 133

What causes megaesophagus?

Back 133

Motility problems related to innervation or denervation disorders and to partial physical obstructions and stenosis, secondary to inflammatory diseases of the muscle or persistance of the aortic arch

Front 134

What is congenital megaesophagus?

Back 134

Partial blockage of the lumen of the esophagus b/c of the persistence of the right fourth aortic arch. Vascular ring forms around esophagus and trachea, which prevents full dilation.

Front 135

Which breeds are predisposed to congenital megaesophagus?

Back 135

German shepherds, irish setters, & grey hounds

Front 136

What are clinical signs of congenital megaesophagus?

Back 136

Regurgitation (seen at weaning), animals are thin and may have respiration pneumonia

Front 137

What causes acquired megaesophagus?

Back 137

Idiopathic. Secondary to polymyositis (inflammation of esophageal muscle), myasthenia gravis, hypothyroidism, congenital myopathy, lead & thallium poisoning, peripheral neuropathies, esophagitis, and recurrent gastric dilation