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Case Study > Q&A - Cases 1-8 > Flashcards

Q&A - Cases 1-8 Flashcards

1
Q

A horse has left laryngeal hemiplegia, what nerve is responsible for this condition?

A

left recurrent laryngeal nerve

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2
Q

Which muscle is responsible for the abduction of the left arytenoid cartilage?

A

cricoarytenoideus dorsalis

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3
Q

Which portion of the arytenoid cartilage is visible by endoscopic examination of the larynx in the horse?

A

corniculate process

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4
Q

What are the cartilaginous structures that make up the larynx?

A

cricoid, thyroid, epiglottic and pair arytenoid cartilages

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5
Q

Which muscles of the larynx are involved in left laryngeal hemiplegia in addition to the cricoarytenoideus dorsalis?

A

crycoarytenoideus lateralis, vocalis, ventricularis, and arytenoideus transverses

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6
Q

What intrinsic muscles of the larynx are innervated by the cranial laryngeal nerve?

A

cricothyroideus

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7
Q

Where does the cranial laryngeal nerve originate?

A

the vagus nerve

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8
Q

Why is the horse an obligate nasal breather?

A

basically the soft palate blocks the horse from breathing through its mouth; the soft palate forms a continuous sheet of tissue that extends from the hard palate to the dorsal caudal pharyngeal wall, completely separating the oral and nasopharynx. The larynx protrudes through the palate in the intrapharyngeal ostium.

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9
Q

In the endoscopic photo of the horse with epiglottic entrapment, what anatomical structure is responsible for entrapping the epiglottis?

A

the aryepiglottic fold

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10
Q

When performing a laryngeal prosthesis procedure to correct left laryngeal hemiplegia, a large diameter non-absorbable suture is used to hold the arytenoid cartilage in abduction, describe the surgical approach to the larynx and the placement of the suture.

A

the surgeon makes an incision on the left lateral side below the lingual facial vein, and the larynx is exposed via blunt dissection. The suture is passed around the caudal edge of the cricoid cartilage and then underneath the cricopharyngeus and thyropharyngeus muscles. It then is passed through the muscular process of the arytenoid cartilage and is tied under tension which mimics the pull of the cricoarytnoideus dorsalis muscle and holds the cartilage in permanent abduction

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11
Q

In general which vessels could be involved as a source of hemorrhage in guttural pouch epistaxis?

A

internal carotid artery, external carotid artery, maxillary artery and vein, possibly the linguofacial, caudal auricular, superficial temporal, and occipital arteries

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12
Q

What does the internal carotid artery pass through in the horse to get to the guttural pouch?

A

the foramen lacerum

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13
Q

What nerves are closely associated with the guttural pouch?

A

facial, glossopharyngeal, vagus, accessory, sympathetic trunk, cranial cervical ganglion, and hypoglossal nerve

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14
Q

What foramina does the facial nerve pass through?

A

the stylomastoid foramen

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15
Q

What foramina does the glossopharyngeal, vagus, accessory, sympathetic trunk, and cranial cervical ganglion pass through?

A

the foramen lacerum

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16
Q

What nerves are associated with dysphagia and pharyngeal paralysis/paresis?

A

the glossppharyngeal and pharyngeal branch of the vagus

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17
Q

What nerves are associated with Horner’s syndrome?

A

sympathetic innervation from the cranial cervical ganglion

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18
Q

What are symptoms of Horner’s syndrome?

A

constricted pupil, enophthalmos, ptosis, protrusion of the third eyelid, vasodilaton

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19
Q

What is the cranioventral border of Viborg’s triangle?

A

the lingofacial vein

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20
Q

What is the caudodorsal border of Viborg’s triangle?

A

the tendinous insertion of the sternocephalicus or sternomandibularis

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21
Q

What is the cranial border of Viborg’s triangle?

A

the caudal border of the ramus of the mandible

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22
Q

What structure divides each guttural pouch into a large medial compartment and a small lateral compartment?

A

stylohyoid bone

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23
Q

Which artery is most likely to be involved with GP mycosis and the source of hemorrhage?

A

internal carotid artery

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24
Q

What is hyperkalemia caused by?

A

a continued intake of potassium in the diet and lack of excretion of potassium in the urine

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25
Q

What is hyponatremia and hypochloremia caused by?

A

volume dilution from water retention

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26
Q

What is increased plasma BUN and creatine caused by?

A

failure to excrete these waste products from the body

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27
Q

Why is the peritoneal fluid creatine higher than the plasma creatine while the BUN in both is more similar in concentration?

A

creatine is a larger molecule and therefore diffuses across membranes more slowly than the smaller urea molecule which equilibrates rapidly

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28
Q

What is persistent patent ductus arteriosis?

A

when the ductus arteriosis, a fetal vessel, does not close after birth leading to a left to right shunt from the aorta to the pulmonary artery

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29
Q

What mechanisms bring about the conversion of the fetal circulation to that of the neonatal foal?

A

the closure of the ductus arteriosus and the closure of the foramen ovale

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30
Q

What is the affect of hyperkalemia on resting membrane potentials?

A

it will decrease the resting membrane potential

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31
Q

What organs or organ systems are most severely affected by hyperkalemia?

A

hyperexcitability and uncontrolled muscular contractions, nerve dysfunction, and arrhythmia in the heart followed by cardiac arrest

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32
Q

How does blood flow through the fetus (right atrium route)?

A 
Umbilical vein (high O2) to either
(a) through the mass of the liver or  
(b) through the ductus venosus
to the caudal vena cava (low O2) to 
 the right atrium, through the oval foramen, between septum 1 and 2, through foramen 2, into the left atrium, to the left ventricle, out of the aorta, to the head, back to the aortic arch to the umbilical artery
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33
Q

If the blood does not go to the right atrium in the fetus, how does the blood flow?

A

to the right ventricle, joined by the blood returning from the cranial vena cava, to the pulmonary trunk to the ductus arteriosus to the aorta to the aortic arch to the umbilical artery

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34
Q

How does oxygenated blood get from the placenta of a mare to the fetal tissues?

A

diffusion

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35
Q

What factors increase the rate at which tubular potassium secretion occurs?

A

aldosterone, tubular flow rate, and plasma potassium concentration

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36
Q

Where is parathyroid hormone produced?

A

in chief cells of the parathyroid gland

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37
Q

What organs/structures does the parathyroid hormone target?

A

bone, kidney, and salivary glands

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38
Q

What is the effect of the parathyroid hormone in bone?

A

stimulates the proliferation of osteoclasts - increased bone resorption

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39
Q

What is the effect of the parathyroid hormone in the kidney?

A

it increases the absorption of calcium in the distal convulated tubules and decreases phosphate re-absorption in the proximal tubules; it also activates vitamin D

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40
Q

What is the effect of the parathyroid hormone in salivary glands?

A

it increases the secretion of phosphorus

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41
Q

What is the overall effect of parathyroid hormone on serum calcium and phosphorus?

A

it effectively raises serum calcium and lowers phosphorus

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42
Q

Where is calcitonin produced?

A

in the parafollicular C cells of the thyroid gland

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43
Q

What organs/structures does calcitonin target?

A

bone, kidney, and the GI tract

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44
Q

What is the effect of calcitonin in bone?

A

it stimulates bone deposition and inhibits resorption

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45
Q

What is the effect of calcitonin on the kidney?

A

it decreases tubular reabsorption of phosphorus

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46
Q

What is the effect of calcitonin on the GI tract?

A

it inhibits gastrin secretion and reduces calcium absorption

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47
Q

What is the overall effect of calcitonin on serum calcium and phosphorus?

A

it decreases serum calcium and phosphorus

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48
Q

Where is vitamin D produced?

A

cholecalciferol is ingested in the diet and can be synthesized in the skin when exposed to UV light, vitamin D is further hydroxylated in the kidney to calcitriol

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49
Q

What organs/structures does vitamin D target?

A

the GI tract, bone, and the kidneys

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50
Q

What is the effect of vitamin D on the GI tract?

A

increases calcium and phosphorus absorption

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51
Q

What is the effect of vitamin D on bone?

A

it is required for normal bone deposition as well as resorption

52
Q

What is the effect of Vitamin D on the kidney?

A

it increases calcium and phosphorus reabsorption; also negative feedback to prevent overproduction of calcitriol

53
Q

What is the overall effect of vitamin D on serum calcium and phosphorus?

A

it increases serum calcium and phosphorus

54
Q

Why do cows have paresis with hypocalcemia and bitches have tetany?

A

the bovine nerve is affected in the same way as the canine nerve, but the neuromuscular junction is more sensitive to hypocalcemia and will stop releasing acetylcholine while the dog continues to

55
Q

What role does phosphorus play in the body?

A

structurally it is an element of phospholipids and hydroxyapatite (bone), it is a component of nucleic acids, used for storage and distribution of energy as ATP, component of the second messenger system and plays a role in the buffering systems of the body

56
Q

Why is feeding a high calcium diet prior to parturition a bad idea in a dairy cow?

A

a high level of dietary calcium will meet daily requirements predominantly via passive absorption, suppressing active absorption and resorption

57
Q

How does skeletal muscle contract?

A

acetylcholine binds to receptors on skeletal muscle, action potential spreads in both directions and interiorly via transverse tubules causing the release of calcium from the sarcoplasmic reticulum which increases intracellular calcium contraction. The initial calcium binds to troponin changing its shape affecting the binding of tropomyosin to actin exposing the myosin head. Myosine cross-bridges with actin and the myosin head contracts and the muscle contracts

58
Q

How is smooth muscle contraction different from that of skeletal muscle?

A

smooth muscle contains no transverse tubules to spread the actions potential internally; it uses gap junctions. It also depends on extracellular calcium to trigger contraction. It is slower, but lasts longer

59
Q

How does cardiac muscle contraction differ from that of skeletal muscle?

A

the action potential is generated from within with special pacemaker cells, the muscle cells are connected through intercalated disks through which the action potential spreads. Extracellular and sarcoplasmic reticulum calcium are needed to triger contraction

60
Q

What would be the effect of administering intravenous calcium too quickly?

A

it will result in a larger driving force pushing more calcium into the cell during contraction leading to a prolonged contraction cycle and eventual bradycardia. Severe hypercalcemia will cause tetany of the heart muscle

61
Q

When animals die, why do they develop rigor mortis?

A

intracellular calcium concentrations gradually increase causing musclular contraction, however ATP is needed to bind to myosin heads to release the cross-bridging of actin and myoson; thus rigor ensues

62
Q

How much water should a 450 kg horse drink on an average day?

A

approximately 20-25 liters/day

63
Q

What hormones are released by the anterior pituitary?

A

growth hormone, thyroid stimulating hormone, adrenocorticotropic hormone, prolactin, follicle stimulating hormone, and luteinizing hormone

64
Q

What hormones are released by the posterior pituitary?

A

ADH (vasopressin) and oxytocin

65
Q

What does growth hormone do?

A

stimulates protein synthesis and overall growth of most cells and tissues

66
Q

What does thyroid stimulating hormone do?

A

stimulates synthesis and secretion of thyroid hormones (T3 and T4)

67
Q

What does adrenocorticotropic hormone do?

A

stimulates the synthesis and secretion of adrenal cortical hormones

68
Q

What does prolactin do?

A

promotes development of breasts and milk

69
Q

What does follicle stimulating hormone do?

A

causes growth of follicles in ovaries and sperm maturation

70
Q

What does luteinizing hormone do?

A

stimulates testosterone synthesis in Leydig cells of testes; stimulates ovulation, formation of CL, and estrogen and progesterone synthesis in ovaries

71
Q

What does ADH do?

A

increases water resorption by the kidneys and causes vasoconstriction and increased blood pressure

72
Q

What does oxytocin do?

A

stimulates milk letdown and uterine contractions

73
Q

Where in the kidney does glucose uptake occur?

A

in the proximal tubules of the kidney via secondary active transport coupled to sodium reabsorption

74
Q

What is the renal threshold for glucose absorption?

A

180-250 mg/dl blood glucose

75
Q

Why does excess glucose cause polyuria?

A

large volumes of urine are formed when excess solutes are present in the glomerular filtrate, the increased filtered load of glucose acts as an osmotic diuretic and causes rapid loss of fluid via the urine

76
Q

What are the two pools of neutrophils in the blood stream?

A

the circulating pool and the marginal pool

77
Q

How is the marginal pool created?

A

selectins bind neutrophils to the endothelium in the post-capillary venules

78
Q

How do neutrophils travel to the site of infection?

A

they exit the blood stream via diapedesis and follow the chemotactic gradient produced by pro-inflammatory cytokines to the site of infection

79
Q

What is the function of neutrophils?

A

phagocytosis and other killing mechanisms, the most potent is the oxidative burst

80
Q

Why are horses with PPID at risk of infection with opportunistic bacterial infections even though they have increased neutrophil counts?

A

the hormonal changes in PPID inhibit selectin-mediated binding of neutrophils to the endothelium so the marginal pool becomes part of the circulating pool which raises the WBC counts, but neutrophils cannot enter the tissues and follow the chemotactic gradient to go to the site of infection; their oxidative burst is also not as effective

81
Q

Why does hypercortisolemia result in hyperglycemia?

A

cortisol causes an insulin resistance in the peripheral tissues

82
Q

Why does hypercortisolemia result in polydispia?

A

polydispia is secondary to polyuria; polyuria is proposed to result from compression of the posterior pituitary and decreased storage and secretion of ADH and glucosuria resulting in osmotic diuresis

83
Q

Why does hypercortisolemia result in leukocytosis?

A

corticosteriod induced neutrophilia caused by decreased migaration of neutrophils from the circulation to the peripheral tissues, increased bone marrow release of neutrophils, and decreased stickiiness

84
Q

Describe the hypothalamic-pituitary-adrenal axis with respect to the hormones involved, their actions on the body, and how it is effected in the case of equine Cushing’s disease.

A

The hypothalamus releases corticotropin releasing hormone (CRH) which stimulates the anterior pituitary gland to secrete adrenocorticotropin hormone (ACTH). ACTH subsequently stimulates the adrenal gland to secrete, among other hormones, cortisol. In equine cushing’s disease, lack of inhibition to the pars intermedia (pituitary) leads to hypertrophy/hyperplasia of the pituitary and increased ACTH secretion. The end result is excessive cortisol secreted by the adrenal gland.

85
Q

How would you expect the cortisol levels to behave in light of dexamethasone administration in a normal horse and a horse affected with PPID?

A

in a normal horse they would decrease
in a horse with equine Cushing’s disease, the cortisol concentration will not decrease despite the exogenous negative feedback placed on the hypothalamus-pituitary axis

86
Q

What are the regions of the adrenal gland?

A

adrenal medulla and cortex

87
Q

What are the regions of the adrenal cortex?

A

zona glomerulosa, zona fasciculate, and zona reticularis

88
Q

What hormone does the zona glomerulosa secrete?

A

aldosterone

89
Q

What hormone does the zona fasciculate secrete?

A

cortisol and corticosterone

90
Q

What hormone does the zona reticularis secrete?

A

androgens dehydroepiandrosterone (DHEA) androstenedione, estrogens, and glucocorticoids

91
Q

How does food move through the GI tract of the horse?

A

Pylorus, duodenum, jejunum, ileum, ileal papilla and orfice, cecum, cecocolic orfice, right ventral colon, sternal or ventral diaphragmatic flexure, left ventral colon, pelvic flexure, left dorsal colon, dorsal diaphragmatic flexure, right dorsal colon, transverse colon, descending or small colon, and finally the rectum.

92
Q

What anatomic structure delineates the ileum from the jejunum?

A

ileocecal fold

93
Q

What is the arterial supply of the equine gastrointestinal tract?

A

structures derived from the foregut is supplied by the celiac, structures derived from the mid-gut is supplied by the cranial mesenteric artery, structures that are supplied by the hindgut are supplied by the caudal mesenteric artery

94
Q

What is the venous drainage of the equine GI tract?

A

the hepatic portal vein

95
Q

What are the major functions of the colon in the horse?

A

absorption of water and electrolytes and fermentation of organic matter that escapes digestion and absorption in the small intestine

96
Q

What is the volume of the stomach in a horse?

A

approximately 3 gallons or 15 liters

97
Q

How long is the small intestine in the horse in feet or meters?

A

approximately 21 meters or 70 feet

98
Q

How does the anatomy of the small intestinal mucosa allow for large surface area?

A

it is covered with finger-like epithelial projections known as villi, villi are cpvered with a brush-like surface membrane known as the brush border, the brush border is composed of submicroscopic microvilli that further enlarge the surface area

99
Q

Describe the blood flow from the aorta to the jejunum and then back to the caudal vena cava.

A

aorta to cranial mesenteric artery to jejunal arteries to jejunum to jejunal veins to cranial mesenteric vein to portal vein to liver to caudal vena cava

100
Q

What is viscerosomatic and viscerovisceral convergence?

A

the reason why subjective discrimination between visceral and somatic pain can be difficult; they both come out of the spinal cord and synapse on the same neuron so the cortex cannot distinguish where the impulse is coming from

101
Q

How does obstruction of the bowel produce pain?

A

pain results from activation of sensory afferent fibers in the splanchic nerves or vagus nerve or both; distension of the mechanoreceptors is probabjly a major source of the pain

102
Q

What muscles are incised during a paralumbar incision into the abdomen?

A

external abdominal oblique, internal abdominal oblique, and transverses abdominus

103
Q

What direction do the fibers of the external abdominal oblique run?

A

caudoventral direction

104
Q

What direction do the fibers of the internal abdominal oblique run?

A

cranioventrally

105
Q

What direction do the fibers of the transversus abdominus run?

A

transversely (dorsal ventral)

106
Q

What is the blood supply to the bovine forestomach, abomasums, and duodenum derived from?

A

the celiac artery

107
Q

Which artery supplies most of the rumen?

A

the right gastric artery

108
Q

What is the normal location of the abomasum?

A

the proximal portion lies along the midline adacent to the xiphoid process, the body continues caudally angling to the right along the cranioventral abdomen, the pylors sits just ventral to the right costal arch

109
Q

What primary mechanisms does the body use to maintain pH?

A

chemical buffers in the extracellular and intracellular fluid, kidney, and respiratory system

110
Q

What prevents the duodenum from traveling along with the abomasum when it is displaced?

A

the mesoduodenum limits but does not prevent the displacement of the duodenum

111
Q

What immediate effects would administration of hypertonic saline have on the circulatory system?

A

it would immediately increase the osmotic pressure of the circulatory system moving fluid from the extracellular space into the vascular system via diffusion. This increases circulatory volume and blood pressure

112
Q

What are the two regions in the horses stomach and what are they separated by?

A

glandular and non-glandular separated by the margo plicatus

113
Q

Why is it impossible for the horse to vomit?

A

they have a very well developed cardiac sphincter and the angle of the esophagus entering the stomach is at an angle that does not allow for vomitting

114
Q

What type of epithelium lines the upper compartment of the equine stomach?

A

non-glandular simple stratified squamous epithelium

115
Q

What type of epithelium lines the lower compartment of the equine stomach?

A

it is squamous mucosa with frequent invaginations and pores that open into gastric glands, and surface epithelial cells and mucous cells

116
Q

How does the parietal cell produce HCl?

A

K and Cl are secreted into the gastric lumen in equal amounts, the parietal cell has receptors for histamine, gastrin and Ach. Activation of these receptors will upregulate the activity of the K-ATPase pump, the adenosine triphosphatase enzyme will pump potassium back into the cell resulting in anionic luminal environment and a decrease in the pH and the production of HCl

117
Q

What is the liminal pH of the equine stomach?

A

between 1 and 2

118
Q

How does the equine stomach protect itself from its low pH?

A

the mucous layer produced by neck and surface mucus cells and forms a flexible gel that coats the glandular mucosa

119
Q

What are the three direct stimuli to the parietal cell for acid production?

A

vagal stimulation, gastrin, and histamine

120
Q

Approximately 80% of equine gastric ulcers occur in the upper compartment of the stomach, why?

A

the gastric squamous mucosa lacks a mucosal layer, making it more susceptible to acid and peptic injury

121
Q

What is special about HCl secretion in the horses stomach?

A

it is constantly occuring

122
Q

When a horse is eating, what happens to its gastric pH?

A

it increases

123
Q

How does omeprazole work to treat equine gastric ulcers?

A

it binds to the proton pump of the parietal cell diasabling the final common step in the pathway of gastric acid secretion

124
Q

How does cimitidine and ranitidine work to protect against ulcers?

A

they are histamine H2 receptor antagonists only and have a short duration of action

125
Q

How does sucralfate work to protect against equine gastric ulcers?

A

it is a protective substance that adheres and protects the ulcer crater but has no effect on gastric pH and has not been shown to heal ulcers

Case Study (4 decks)

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