DEFINITION
Weight loss is considered clinically important when it exceeds 10% of the normal body weight and is not associated with fluid loss.
Cachexia is defined as the state of extreme poor health and is associated with anorexia, weight loss, weakness, and mental depression.
PATHOPHYSIOLOGY
Weight loss can result from many different pathophysiologic mechanisms that share a common feature—insufficient caloric intake or availability to meet metabolic needs.
Insufficient caloric intake can be caused by (1) a high energy demand (e.g., that characteristic of a hypermetabolic state); (2) inadequate energy intake, including insufficient quantity or quality of food, or inadequate nutrient assimilation (e.g., with anorexia, dysphagia, regurgitation, or malabsorption–maldigestion disorders); (3) excessive loss of nutrients or fluid, which can occur in patients with gastrointestinal losses, glucosuria, proteinuria, or extensive skin lesions (burns, excoriations, etc.)
Monday, April 18, 2011
Vomiting, Acute
DEFINITION
Forceful, reflex expulsion of gastric contents from the oral cavity
Acute vomiting is defined as vomiting of short duration (<7 days) and variable frequency.
PATHOPHYSIOLOGY
A complex set of reflex activities under central neurologic control involving the coordination of GI, abdominal, and respiratory musculature
Often preceded by prodromal signs of nausea that can include depression, shivering, hiding or seeking comfort, hypersalivation, lip licking, frequent swallowing, and retching
Occurs when the VC in the medulla is stimulated by afferent activity from several sources
Stimulation can occur from stretch receptors, chemoreceptors, and osmoreceptors located throughout the GI tract, hepatobiliary system, genitourinary system, peritoneum, and pancreas.
The CTZ, when stimulated by a variety of drugs and toxins, can also stimulate the VC.
Higher centers can lead to psychogenic vomiting and input from the vestibular apparatus (e.g., motion sickness, vestibular disease) can stimulate the VC.
Forceful, reflex expulsion of gastric contents from the oral cavity
Acute vomiting is defined as vomiting of short duration (<7 days) and variable frequency.
PATHOPHYSIOLOGY
A complex set of reflex activities under central neurologic control involving the coordination of GI, abdominal, and respiratory musculature
Often preceded by prodromal signs of nausea that can include depression, shivering, hiding or seeking comfort, hypersalivation, lip licking, frequent swallowing, and retching
Occurs when the VC in the medulla is stimulated by afferent activity from several sources
Stimulation can occur from stretch receptors, chemoreceptors, and osmoreceptors located throughout the GI tract, hepatobiliary system, genitourinary system, peritoneum, and pancreas.
The CTZ, when stimulated by a variety of drugs and toxins, can also stimulate the VC.
Higher centers can lead to psychogenic vomiting and input from the vestibular apparatus (e.g., motion sickness, vestibular disease) can stimulate the VC.
Vitamin D Toxicity
DEFINITION
Abnormal accumulation of vitamin D in the body, most commonly from ingesting vitamin D–containing rodenticides or other preparation or oversupplementation
PATHOPHYSIOLOGY
Cholecalciferol—fat-soluble vitamin; absorbed through chylomicrons and transported to the liver, where it is metabolized to 25-hydroxycholecalciferol, the major circulating metabolite during vitamin D excess; further metabolism occurs in the kidney, where calcitriol is produced.
Cholecalciferol and 25-hydroxycholecalciferol—limited biological activity
Calcitriol—most potent cholecalciferol metabolite in terms of enhancing calcium resorption from bone and intestinal calcium uptake
Excessive ingestion—increased intestinal absorption of calcium; stimulated bone resorption; increased renal tubular reabsorption of calcium; results in hypercalcemia (serum calcium > 12 mg/dL) and associated dystrophic calcification
Abnormal accumulation of vitamin D in the body, most commonly from ingesting vitamin D–containing rodenticides or other preparation or oversupplementation
PATHOPHYSIOLOGY
Cholecalciferol—fat-soluble vitamin; absorbed through chylomicrons and transported to the liver, where it is metabolized to 25-hydroxycholecalciferol, the major circulating metabolite during vitamin D excess; further metabolism occurs in the kidney, where calcitriol is produced.
Cholecalciferol and 25-hydroxycholecalciferol—limited biological activity
Calcitriol—most potent cholecalciferol metabolite in terms of enhancing calcium resorption from bone and intestinal calcium uptake
Excessive ingestion—increased intestinal absorption of calcium; stimulated bone resorption; increased renal tubular reabsorption of calcium; results in hypercalcemia (serum calcium > 12 mg/dL) and associated dystrophic calcification
Vitamin A Toxicity
OVERVIEW
Skeletal disease that occurs after excessive intake of vitamin A
High concentrations of vitamin A—inhibits intramembranous and endochondral ossification, resulting in dystrophic calcification of the skeleton
SIGNALMENT
Cats aged 2–9 years
No breed or sex predilections recognized
Skeletal disease that occurs after excessive intake of vitamin A
High concentrations of vitamin A—inhibits intramembranous and endochondral ossification, resulting in dystrophic calcification of the skeleton
SIGNALMENT
Cats aged 2–9 years
No breed or sex predilections recognized
Vestibular Disease, Geriatric - Dogs
DEFINITION
Acute nonprogressive disturbance of the peripheral vestibular system in old dogs
PATHOPHYSIOLOGY
Unknown
Suspected abnormal flow of the endolymphatic fluid in the semicircular canals of the inner ear secondary to disturbance in production, circulation, or absorption of the fluid
Possible intoxication of the vestibular receptors or inflammation of the vestibular portion of the vestibulocochlear nerve (cranial nerve VIII)
Often incorrectly referred to as a stroke (disease is neither central in location nor suspected to be vascular or ischemic in origin)
Acute nonprogressive disturbance of the peripheral vestibular system in old dogs
PATHOPHYSIOLOGY
Unknown
Suspected abnormal flow of the endolymphatic fluid in the semicircular canals of the inner ear secondary to disturbance in production, circulation, or absorption of the fluid
Possible intoxication of the vestibular receptors or inflammation of the vestibular portion of the vestibulocochlear nerve (cranial nerve VIII)
Often incorrectly referred to as a stroke (disease is neither central in location nor suspected to be vascular or ischemic in origin)
Ventricular Tachycardia
DEFINITION
ECG Features
Three or more ventricular premature contractions in a row
May be intermittent (paroxysmal) or sustained; heart rate > 150 bpm with a regular rhythm
QRS complexes—typically wide and bizarre.
If P waves—dissociated from the QRS complexes
PATHOPHYSIOLOGY
Potentially life-threatening arrhythmia, usually signifying myocardial disease or metabolic derangement; mechanisms include increased automaticity, reentry, and delayed afterdepolarizations
ECG Features
Three or more ventricular premature contractions in a row
May be intermittent (paroxysmal) or sustained; heart rate > 150 bpm with a regular rhythm
QRS complexes—typically wide and bizarre.
If P waves—dissociated from the QRS complexes
PATHOPHYSIOLOGY
Potentially life-threatening arrhythmia, usually signifying myocardial disease or metabolic derangement; mechanisms include increased automaticity, reentry, and delayed afterdepolarizations
Vasculitis, Cutaneous
OVERVIEW
An inflammation of blood vessels with a neutrophilic (leukocytoclastic/nonleukocytoclastic), lymphocytic, rarely eosinophilic, granulomatous, or mixed cell types
Pathomechanisms—type III (immune complex) and type I (immediate) reactions
An inflammation of blood vessels with a neutrophilic (leukocytoclastic/nonleukocytoclastic), lymphocytic, rarely eosinophilic, granulomatous, or mixed cell types
Pathomechanisms—type III (immune complex) and type I (immediate) reactions
Wednesday, April 6, 2011
Vaccine-Associated Sarcoma
OVERVIEW
Cats—vaccination may induce development of sarcoma (primarily fibrosarcoma) at the injection site, primarily in the muscle, skin, and subcutaneous tissues; malignant fibrous histiocytoma, osteosarcoma, rhabdomyosarcoma, and chondrosarcoma also associated
FeLV and rabies vaccines—most common
Interval from vaccination to tumor development—may be as short as several months
Metastasis common
Fibrosarcoma—prevalence in cats unknown; estimated at 20/100,000 cats
Cats—vaccination may induce development of sarcoma (primarily fibrosarcoma) at the injection site, primarily in the muscle, skin, and subcutaneous tissues; malignant fibrous histiocytoma, osteosarcoma, rhabdomyosarcoma, and chondrosarcoma also associated
FeLV and rabies vaccines—most common
Interval from vaccination to tumor development—may be as short as several months
Metastasis common
Fibrosarcoma—prevalence in cats unknown; estimated at 20/100,000 cats
Uveal Melanoma - Cats
OVERVIEW
The most common primary intraocular tumor in cats
Usually arise from the anterior iridal surface with extension to the ciliary body and choroid
Tend to be flat and diffuse, not nodular (unlike intraocular melanomas in dogs)
Initially has a benign clinical and histologic appearance
Unique feature—may develop metastatic disease up to several years later
Metastasize to regional lymph nodes, numerous visceral organs (especially those in the abdominal cavity), lungs, and less commonly, the skeleton
The most common primary intraocular tumor in cats
Usually arise from the anterior iridal surface with extension to the ciliary body and choroid
Tend to be flat and diffuse, not nodular (unlike intraocular melanomas in dogs)
Initially has a benign clinical and histologic appearance
Unique feature—may develop metastatic disease up to several years later
Metastasize to regional lymph nodes, numerous visceral organs (especially those in the abdominal cavity), lungs, and less commonly, the skeleton
Uterine Tumors
OVERVIEW
Rare tumors, arising from the uterine smooth muscle and epithelial tissues
Compose 0.3%–0.4% of tumors in dogs and 0.2%–1.5% in cats
Dogs—usually benign; leiomyomas, 85%–90%; leiomyosarcoma, 10%; other types (e.g., carcinoma, fibroma, fibrosarcoma, lipoma) rare
Cats—usually malignant (adenocarcinoma); include leiomyoma, leiomyosarcoma, fibrosarcoma, fibroma, and lipoma
Metastasis—may occur with malignant forms
Rare tumors, arising from the uterine smooth muscle and epithelial tissues
Compose 0.3%–0.4% of tumors in dogs and 0.2%–1.5% in cats
Dogs—usually benign; leiomyomas, 85%–90%; leiomyosarcoma, 10%; other types (e.g., carcinoma, fibroma, fibrosarcoma, lipoma) rare
Cats—usually malignant (adenocarcinoma); include leiomyoma, leiomyosarcoma, fibrosarcoma, fibroma, and lipoma
Metastasis—may occur with malignant forms
Urolithiasis, Calcium Oxalate
DEFINITION
Formation of calcium oxalate uroliths within the urinary tract and associated clinical conditions
PATHOPHYSIOLOGY
Presence of hypercalciuria, hyperoxaluria, hypocitraturia, and defective crystal growth inhibitors
Hypercalciuria
In dogs, normocalcemic hypercalciuria is thought to result from either intestinal hyperabsorption of calcium (so-called absorptive hypercalciuria) or reduced renal tubular reabsorption of calcium (so-called renal-leak hypercalciuria). Hypercalcemic hypercalciuria results from excessive glomerular filtration of mobilized calcium, which overwhelms normal renal tubular reabsorptive mechanisms (called resorptive hypercalciuria, since excessive bone resorption is associated with high serum calcium concentrations).
Hyperoxaluria
In humans, hyperoxaluria is associated with inherited abnormalities of excessive oxalate synthesis (i.e., primary hyperoxaluria), excess consumption of foods containing high quantities of oxalate or oxalate precursors, pyridoxine deficiency, and disorders associated with fat malabsorption.
Hypocitraturia
Urine citrate inhibits calcium oxalate urolith formation. By complexing with calcium ions to form the relatively soluble salt calcium citrate, citrate reduces the quantity of calcium available to bind with oxalate. In normal dogs, acidosis is associated with low urinary citrate excretion, whereas alkalosis promotes urinary citrate excretion.
Defective Crystal Growth Inhibitors
In addition to urinary concentration of calculogenic minerals, large-molecular-weight proteins in urine, such as nephrocalcin have a profound ability to enhance solubility of calcium oxalate. Preliminary studies of urine obtained from dogs with calcium oxalate uroliths revealed that nephrocalcin had fewer carboxyglutamic acid residues than nephrocalcin isolated from normal dog urine.
Formation of calcium oxalate uroliths within the urinary tract and associated clinical conditions
PATHOPHYSIOLOGY
Presence of hypercalciuria, hyperoxaluria, hypocitraturia, and defective crystal growth inhibitors
Hypercalciuria
In dogs, normocalcemic hypercalciuria is thought to result from either intestinal hyperabsorption of calcium (so-called absorptive hypercalciuria) or reduced renal tubular reabsorption of calcium (so-called renal-leak hypercalciuria). Hypercalcemic hypercalciuria results from excessive glomerular filtration of mobilized calcium, which overwhelms normal renal tubular reabsorptive mechanisms (called resorptive hypercalciuria, since excessive bone resorption is associated with high serum calcium concentrations).
Hyperoxaluria
In humans, hyperoxaluria is associated with inherited abnormalities of excessive oxalate synthesis (i.e., primary hyperoxaluria), excess consumption of foods containing high quantities of oxalate or oxalate precursors, pyridoxine deficiency, and disorders associated with fat malabsorption.
Hypocitraturia
Urine citrate inhibits calcium oxalate urolith formation. By complexing with calcium ions to form the relatively soluble salt calcium citrate, citrate reduces the quantity of calcium available to bind with oxalate. In normal dogs, acidosis is associated with low urinary citrate excretion, whereas alkalosis promotes urinary citrate excretion.
Defective Crystal Growth Inhibitors
In addition to urinary concentration of calculogenic minerals, large-molecular-weight proteins in urine, such as nephrocalcin have a profound ability to enhance solubility of calcium oxalate. Preliminary studies of urine obtained from dogs with calcium oxalate uroliths revealed that nephrocalcin had fewer carboxyglutamic acid residues than nephrocalcin isolated from normal dog urine.
Tuesday, April 5, 2011
Urine Cortisol: Creatinine Ratio
DEFINITION
To measure a urine cortisol:creatinine ratio (UCCR), a single midstream free-catch urine sample is used; cortisol and creatinine are both measured and the concentrations converted into the same units; the UCCR is simply the ratio of the two values.
A normal UCCR is less than approximately 10–30 × 10-6 depending on the laboratory; this value has no units and is typically reported without the scientific notation, e.g. 10 × 10-6 would be reported as 10.
To measure a urine cortisol:creatinine ratio (UCCR), a single midstream free-catch urine sample is used; cortisol and creatinine are both measured and the concentrations converted into the same units; the UCCR is simply the ratio of the two values.
A normal UCCR is less than approximately 10–30 × 10-6 depending on the laboratory; this value has no units and is typically reported without the scientific notation, e.g. 10 × 10-6 would be reported as 10.
Urine Cortisol: Creatinine Ratio
DEFINITION
To measure a urine cortisol:creatinine ratio (UCCR), a single midstream free-catch urine sample is used; cortisol and creatinine are both measured and the concentrations converted into the same units; the UCCR is simply the ratio of the two values.
A normal UCCR is less than approximately 10–30 × 10-6 depending on the laboratory; this value has no units and is typically reported without the scientific notation, e.g. 10 × 10-6 would be reported as 10.
To measure a urine cortisol:creatinine ratio (UCCR), a single midstream free-catch urine sample is used; cortisol and creatinine are both measured and the concentrations converted into the same units; the UCCR is simply the ratio of the two values.
A normal UCCR is less than approximately 10–30 × 10-6 depending on the laboratory; this value has no units and is typically reported without the scientific notation, e.g. 10 × 10-6 would be reported as 10.
Urinary Tract Obstruction
DEFINITION
Restricted flow of urine from the kidneys through the urinary tract to the external urethral orifice
PATHOPHYSIOLOGY
Excess resistance to urine flow through the urinary tract develops because of lesions affecting the excretory pathway, which cause increased pressure in the urinary space proximal to the obstruction and may cause abnormal distension of this space with urine. Ensuing pathophysiologic consequences depend on the site, degree, and duration of obstruction. Complete obstruction produces a pathophysiologic state equivalent to oliguric acute renal failure.
Perforation of the excretory pathway with extravasation of urine is functionally equivalent.
SYSTEMS AFFECTED
Renal/Urologic
Gastrointestinal, Cardiovascular, Nervous, and Respiratory systems as uremia develops
Restricted flow of urine from the kidneys through the urinary tract to the external urethral orifice
PATHOPHYSIOLOGY
Excess resistance to urine flow through the urinary tract develops because of lesions affecting the excretory pathway, which cause increased pressure in the urinary space proximal to the obstruction and may cause abnormal distension of this space with urine. Ensuing pathophysiologic consequences depend on the site, degree, and duration of obstruction. Complete obstruction produces a pathophysiologic state equivalent to oliguric acute renal failure.
Perforation of the excretory pathway with extravasation of urine is functionally equivalent.
SYSTEMS AFFECTED
Renal/Urologic
Gastrointestinal, Cardiovascular, Nervous, and Respiratory systems as uremia develops
Ureterolithiasis
OVERVIEW
Occurrence of a urolith (calculus) within a ureter; most ureteroliths originate in the renal pelves and so commonly occur in association with nephroliths. Most uroliths that enter the ureter continue to the bladder without impedance, but uroliths may cause partial or complete obstruction of the ureter, resulting in dilation of the proximal ureter and renal pelves and subsequent destruction of renal parenchyma.
SIGNALMENT
Dogs and cats
Breed, age, and sex predispositions vary with type of nephrolith.
See Nephrolithiasis
Occurrence of a urolith (calculus) within a ureter; most ureteroliths originate in the renal pelves and so commonly occur in association with nephroliths. Most uroliths that enter the ureter continue to the bladder without impedance, but uroliths may cause partial or complete obstruction of the ureter, resulting in dilation of the proximal ureter and renal pelves and subsequent destruction of renal parenchyma.
SIGNALMENT
Dogs and cats
Breed, age, and sex predispositions vary with type of nephrolith.
See Nephrolithiasis
Traumatic Myocarditis
OVERVIEW
Traumatic myocarditis is the term applied to the syndrome of arrhythmias that sometimes complicates blunt trauma; it is a misnomer, because myocardial lesions (if present) are more likely to take the form of necrosis than inflammation.
Direct cardiac injury is not required for development of posttraumatic arrhythmia; extracardiac conditions are likely to have equal or greater etiologic importance.
Ventricular tachyarrhythmias occur in most affected patients; supraventricular arrhythmias and bradyarrhythmias are uncommon. Ventricular rhythms that complicate blunt trauma are often relatively slow and detected only during pauses in the sinus rhythm; they are most appropriately referred to as AIVRs. The QRS complexes are wide and bizarre; the rate is > 100 bpm but generally < 160 bpm. Usually, these rhythms are electrically and hemodynamically benign.
Dangerous ventricular tachycardias can also complicate blunt trauma and can also evolve from seemingly benign AIVRs, compromising perfusion and placing the patient at risk for sudden death.
Traumatic myocarditis is the term applied to the syndrome of arrhythmias that sometimes complicates blunt trauma; it is a misnomer, because myocardial lesions (if present) are more likely to take the form of necrosis than inflammation.
Direct cardiac injury is not required for development of posttraumatic arrhythmia; extracardiac conditions are likely to have equal or greater etiologic importance.
Ventricular tachyarrhythmias occur in most affected patients; supraventricular arrhythmias and bradyarrhythmias are uncommon. Ventricular rhythms that complicate blunt trauma are often relatively slow and detected only during pauses in the sinus rhythm; they are most appropriately referred to as AIVRs. The QRS complexes are wide and bizarre; the rate is > 100 bpm but generally < 160 bpm. Usually, these rhythms are electrically and hemodynamically benign.
Dangerous ventricular tachycardias can also complicate blunt trauma and can also evolve from seemingly benign AIVRs, compromising perfusion and placing the patient at risk for sudden death.
Traumatic Myocarditis
OVERVIEW
Traumatic myocarditis is the term applied to the syndrome of arrhythmias that sometimes complicates blunt trauma; it is a misnomer, because myocardial lesions (if present) are more likely to take the form of necrosis than inflammation.
Direct cardiac injury is not required for development of posttraumatic arrhythmia; extracardiac conditions are likely to have equal or greater etiologic importance.
Ventricular tachyarrhythmias occur in most affected patients; supraventricular arrhythmias and bradyarrhythmias are uncommon. Ventricular rhythms that complicate blunt trauma are often relatively slow and detected only during pauses in the sinus rhythm; they are most appropriately referred to as AIVRs. The QRS complexes are wide and bizarre; the rate is > 100 bpm but generally < 160 bpm. Usually, these rhythms are electrically and hemodynamically benign.
Dangerous ventricular tachycardias can also complicate blunt trauma and can also evolve from seemingly benign AIVRs, compromising perfusion and placing the patient at risk for sudden death.
Traumatic myocarditis is the term applied to the syndrome of arrhythmias that sometimes complicates blunt trauma; it is a misnomer, because myocardial lesions (if present) are more likely to take the form of necrosis than inflammation.
Direct cardiac injury is not required for development of posttraumatic arrhythmia; extracardiac conditions are likely to have equal or greater etiologic importance.
Ventricular tachyarrhythmias occur in most affected patients; supraventricular arrhythmias and bradyarrhythmias are uncommon. Ventricular rhythms that complicate blunt trauma are often relatively slow and detected only during pauses in the sinus rhythm; they are most appropriately referred to as AIVRs. The QRS complexes are wide and bizarre; the rate is > 100 bpm but generally < 160 bpm. Usually, these rhythms are electrically and hemodynamically benign.
Dangerous ventricular tachycardias can also complicate blunt trauma and can also evolve from seemingly benign AIVRs, compromising perfusion and placing the patient at risk for sudden death.
Sunday, April 3, 2011
Toxoplasmosis
DEFINITION
Toxoplasma gondii—an obligate intracellular coccidian protozoan parasite that infects nearly all mammals; Felidae the definitive hosts; all other warm-blooded animals are intermediate hosts.
PATHOPHYSIOLOGY
Severity and manifestation—depend on location and degree of tissue injury caused by tissue cysts
Infection—acquired by ingestion of tissue cysts or oocysts; organisms spread to extraintestinal organs via blood or lymph; results in focal necrosis to many organs (heart, eye, CNS)
Acute disseminated infection rarely fatal
Chronic disease—tissue cysts form; low-grade disease; usually not clinically apparent unless immunosuppression or concomitant illness allows organism to proliferate, causing an acute inflammatory response
Clinical disease—often associated with other infections that cause severe immunosuppression (e.g., canine distemper, FIP, and FeLV).
Toxoplasma gondii—an obligate intracellular coccidian protozoan parasite that infects nearly all mammals; Felidae the definitive hosts; all other warm-blooded animals are intermediate hosts.
PATHOPHYSIOLOGY
Severity and manifestation—depend on location and degree of tissue injury caused by tissue cysts
Infection—acquired by ingestion of tissue cysts or oocysts; organisms spread to extraintestinal organs via blood or lymph; results in focal necrosis to many organs (heart, eye, CNS)
Acute disseminated infection rarely fatal
Chronic disease—tissue cysts form; low-grade disease; usually not clinically apparent unless immunosuppression or concomitant illness allows organism to proliferate, causing an acute inflammatory response
Clinical disease—often associated with other infections that cause severe immunosuppression (e.g., canine distemper, FIP, and FeLV).
Thyroid Hormones
DEFINITION
Serum concentrations of T4, T3, free thyroxine, or endogenous canine TSH outside the normal range
PATHOPHYSIOLOGY
The thyroid gland regulates basal metabolism; two molecules, tyrosine and iodine, are important for thyroid hormone synthesis.
The tyrosyl ring can accommodate two iodide molecules; if one iodide attaches, it is called monoiodotyrosine (MIT); if two iodide molecules attach to the tyrosyl ring, it is called diiodotyrosine (DIT).
Two DIT molecules form T4; one MIT coupled with one DIT molecule forms T3.
T4 is the major storage form of thyroid hormone; T3 is the active form of the hormone; most T3 is formed outside the thyroid gland by deiodination of T4.
Another type of T3 is formed when an iodide molecule is removed from the inner phenolic ring of T4; this compound is called reverse T3 and increases in nonthyroidal illness.
Thyrotropin, or TSH, is the most importantregulator of thyroid activity.
TSH secretion is regulated by thyroid hormones via negative feedback inhibition of the synthesis of TRH at the level of the hypothalamus and by inhibition of the activity of TSH at the level of the pituitary.
With thyroid gland failure, the pituitary gland senses decreases in serum free thyroxine (FT4) and TT4, resulting in increased serum endogenous TSH concentration.
The use of endogenous TSH alone is not recommended as a method of assessing thyroid function.
FT4 concentrations are measured by equilibrium dialysis (gold standard) or analogue immunoassays.
Serum concentrations of T4, T3, free thyroxine, or endogenous canine TSH outside the normal range
PATHOPHYSIOLOGY
The thyroid gland regulates basal metabolism; two molecules, tyrosine and iodine, are important for thyroid hormone synthesis.
The tyrosyl ring can accommodate two iodide molecules; if one iodide attaches, it is called monoiodotyrosine (MIT); if two iodide molecules attach to the tyrosyl ring, it is called diiodotyrosine (DIT).
Two DIT molecules form T4; one MIT coupled with one DIT molecule forms T3.
T4 is the major storage form of thyroid hormone; T3 is the active form of the hormone; most T3 is formed outside the thyroid gland by deiodination of T4.
Another type of T3 is formed when an iodide molecule is removed from the inner phenolic ring of T4; this compound is called reverse T3 and increases in nonthyroidal illness.
Thyrotropin, or TSH, is the most importantregulator of thyroid activity.
TSH secretion is regulated by thyroid hormones via negative feedback inhibition of the synthesis of TRH at the level of the hypothalamus and by inhibition of the activity of TSH at the level of the pituitary.
With thyroid gland failure, the pituitary gland senses decreases in serum free thyroxine (FT4) and TT4, resulting in increased serum endogenous TSH concentration.
The use of endogenous TSH alone is not recommended as a method of assessing thyroid function.
FT4 concentrations are measured by equilibrium dialysis (gold standard) or analogue immunoassays.
Thrombocytosis
DEFINITION
A platelet count above the upper end of the reference range
Purdue University Teaching Hospital reference ranges—dogs, 200,000–900,000/mL; cats, 300,000–700,000/mL
PATHOPHYSIOLOGY
Can be caused by overproduction of platelets, decreased clearance of platelets, and decreased sequestration of platelets.
Overproduction occurs secondary to bone marrow stimulation by thrombopoietin and factors such as IL-1, IL-3, IL-6, and IL-11.
For most associated diseases, the exact mechanisms are not well documented.
A platelet count above the upper end of the reference range
Purdue University Teaching Hospital reference ranges—dogs, 200,000–900,000/mL; cats, 300,000–700,000/mL
PATHOPHYSIOLOGY
Can be caused by overproduction of platelets, decreased clearance of platelets, and decreased sequestration of platelets.
Overproduction occurs secondary to bone marrow stimulation by thrombopoietin and factors such as IL-1, IL-3, IL-6, and IL-11.
For most associated diseases, the exact mechanisms are not well documented.
Thrombocytopenia
DEFINITION
Platelet count below the lower limit of the reference range
Purdue University Teaching Hospital reference range—200,000–900,000/mL, dogs; 300,000–700,000/mL, cats
PATHOPHYSIOLOGY
Platelets are produced by megakaryocytes in the bone marrow, released into bloodstream, and circulate for a few to several days.
In the normal state, the platelet count remains stable, because production of platelets is equivalent to the removal of platelets from the circulation and the spleen holds a fairly large reserve.
Caused by decreased production, sequestration, increased destruction, or increased use of platelets.
Platelet count below the lower limit of the reference range
Purdue University Teaching Hospital reference range—200,000–900,000/mL, dogs; 300,000–700,000/mL, cats
PATHOPHYSIOLOGY
Platelets are produced by megakaryocytes in the bone marrow, released into bloodstream, and circulate for a few to several days.
In the normal state, the platelet count remains stable, because production of platelets is equivalent to the removal of platelets from the circulation and the spleen holds a fairly large reserve.
Caused by decreased production, sequestration, increased destruction, or increased use of platelets.
Tetanus
OVERVIEW
Clostridium tetani—an obligate, anaerobic, spore-forming, gram-positive rod found in soil and as part of the normal bacterial flora of the intestinal tract of mammals with a predilection for contaminated, necrotic, anaerobic wounds (puncture, surgery, lacerations, burns, frostbite, open fractures, abrasions)
Germi-nating spores—in wounds produce potent exotoxin tetanospasmin (tetanus toxin); resistant to disinfectants and to the effects of environmental exposure
Found worldwide, especially in the tropics.
Clostridium tetani—an obligate, anaerobic, spore-forming, gram-positive rod found in soil and as part of the normal bacterial flora of the intestinal tract of mammals with a predilection for contaminated, necrotic, anaerobic wounds (puncture, surgery, lacerations, burns, frostbite, open fractures, abrasions)
Germi-nating spores—in wounds produce potent exotoxin tetanospasmin (tetanus toxin); resistant to disinfectants and to the effects of environmental exposure
Found worldwide, especially in the tropics.
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