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397 Cards in this Set
- Front
- Back
POA
|
problem oriented approach
|
|
what is the POA
|
a logical way to think about case management based on presenting clinicial signs or findings which are called "problems" in this sytem
|
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POVMR
|
problem oriented veterinary medical record
|
|
the POVMR is designed to
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show the orderly process of the POA- thought process as well as content
|
|
four steps of the POA
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gather a data base, problem ID, plan formulation, assessment and follow up plans
|
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plans in the POA-POVMR contain 3 major components
|
diagnostic plan, therapeutic plan, client education
|
|
differentials
|
possible causes for the problem that need to be ruled out
|
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clinical problem solving: need to know _____ to solve the _____
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normal, to solve the abnormal
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pathophysiology
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understanding the mechanisms that create problems
|
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quality patient care is best achieved by
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managing problems diagnosticaly and therapeutically
|
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most important step in the POA
|
data base collection
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define a problem
|
any abnormality requiring medical or surgical management or one that interferes with the quality of life
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SOAP
|
subjective objective assessment plan
|
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hyperthermia
|
elevated core body temperature
|
|
what is the term hyperthermia generally reserved for
|
heat stroke and malignant hyperthermia
|
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fever
|
a form of hyperthermia provoked by the release of inflammatory proteins called pyrogens. The thermoregulatory center in the hypothalamus is adjusted to a set point above normal body temperature
|
|
how is body temperature regulated in endothermic vertebrates?
|
by controlling production and dissipation of heat via neurological mechanisms mediated in the hypothalams
|
|
normal temperature for dogs/cats
|
101-102
|
|
activation of the sympathetic nervous system ____ body temp
|
increases
|
|
activiation of the parasympathetic nervous sysem ____ body temp
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decreases
|
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body heat is largely generated by
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metabolic activity of skeletal muscles and in the liver
|
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how do dogs and cats largely dissipate heat
|
respiratory tract/panting, and evaporation from mucous membranes
|
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pyrogens have the ability to
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increase the thermoregulatory set point
|
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exogenous pyrogens include
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infections agents, exo and endotoxins, pharmacologic agents
|
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most exogenous pyrogens mostly produce fever by promoting
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the release of cytokines from macrophages and other leukotcytes
|
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chronic fever causes ____ and ____
|
protein catabolism and cachexia
|
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fever is a clinical sign of
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inflammation
|
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four major categories of diseases to consider with fever?
|
infectious, immune mediated, neoplastic, drug induced
|
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FUO
|
fever of unknown origin
|
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define FUO
|
feber of at least three weeks with no cause identified on labs or rads
|
|
some of the more common causes of FUO in cats
|
FELV, FIV, FIP
|
|
some of the more common causes of FUO in dogs
|
endocarditis, prostatis, deep abscess, rickettsial infections, deep mycotic infections
|
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heat stroke
|
reults from inadequate heat dissipation in animals in high ambient temps
|
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exercise induced collapse and hyperthermia
|
most likely a functional myopthaty with concurrent hyperthermia. Likely inherited.
|
|
malignant hyperthermia
|
inherited functional myopathy, causes severe muscle necrosis and hyperthermia, especially in horses/pigs
|
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fevers in which rainge usually do not require treatment unless chronic
|
103-105degrees
|
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temps above ___ do require treatment
|
105
|
|
natures way of signalling that something is wrong
|
fever
|
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classification of true fever: can be
|
intermittent, remittent, relapsing, septic or FUO
|
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where is the thermoregulatory center located
|
anterior hypothalamus- diencephalon
|
|
regulation of body temp:
|
vasoconstriction/vasodilation, symp control/parasymp control
|
|
what are the actual mediators of fever
|
endogens pyrogens
|
|
name three endogenous mediators
|
IL1, IL6 and TNFa
|
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which of the endogenous mediators is most important?
|
IL1
|
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what does IL1 stimulate?
|
release of IL6
|
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potential benefits of fever
|
increased t-cell proliferation, augments the alternate complement pathway, increase neutrophile and macrophage activity, may inhibit growth of bacteria/viruses, makes iron less available for bacterial metabolism
|
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harmful effects of fever
|
over 106 is harmful to cell metabolism. Potential for cerebral edema and neuronal death. Protein catabolism and cachexia, depression and anorexia
|
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which is generally more difficult to determine from the PE: chronic or acute inflammation
|
chronic
|
|
most antipyretic agents are
|
antiprostaglandins
|
|
does heat stroke respond to antipyretics?
|
no
|
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treatment for heat stroke?
|
total body cooling, IV crystalloids and glucocorticoids
|
|
common complication of heat stroke
|
DIC
|
|
hypothermia can occur for three reasons
|
accidental, pathological, purposeful
|
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PU/PD
|
polyurea/polydipsia
|
|
general characteristics of PU/PD?
|
PU = urine output > 25ml/lb. PD = water intake > 50ml/lb
|
|
what is the most common disease in dogs with PU/PD?
|
renal disease
|
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what are the top three causes of disease in cats with PU/PD?
|
renal disease, diabetes mellitus, hyperthyroidism
|
|
glomerular function
|
selective filtration- excludes particles with molecular weight greater than 5000. Excludes protein and cells. Freely permeable to water, glucose, aminoacids and electrolytes. Approximately 1% of glomerular filtrate is excreted as urine.
|
|
what is the specific gravity of glomerular filtrate?
|
1.008 - 1.012 (isothenuria)
|
|
what happens to glomerular filtrate In the proximal tubule
|
solutes are actively transported out and water follows. Volume is decreased 60-70% and specific gravity stays about 1.010
|
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what important actions occur in the ascending limb of Henle's loop
|
sodium, chloride and urea are actively transported into the renal medulla. The tubule is impermeable to water. Urine specific gravity is reduced below 1.008. This is how the renal medulla maintains its high concentration of solute
|
|
what happens in the distal tubule?
|
aldosterone stimulates the excretion of potassium and the retention of sodium. Acid/base mechanisms-bicarb exchange. Specific gravity increases a small amount.
|
|
what stimluates the release of aldosterone?
|
renin/angiotensin
|
|
what happens in the collecting ducts?
|
ADH regulates pore size in the tubule membrane. Water is passively reabsorbed by the osmotic gradient of the renal medulla.
|
|
what regulates the release of ADH?
|
plasma osmolality
|
|
what is the countercurrent system?
|
association of vasa recta and loop of henle. Allows sodium and urea to be concentrated in renal medulla
|
|
medullary washout
|
decreased medullary hypertonicity- failure of NaCl pump in LH., liver failure (decrease urea), prolonged PU/PD (increased fluid flow in LH and vasa recta)
|
|
thirst
|
the conscious desire for water
|
|
where is the thirst center
|
hypothalamus near ADH controlled centers
|
|
what is thirst controlled by?
|
extracellular fluid osmolality
|
|
primary thirst
|
results from increase in sodium or decrease in blood volume
|
|
secondary thirst
|
anticipation of needs before deficiencies occur- oropharyngeal cues and circadian rhythm of eating
|
|
5 causes of pathologic thirst
|
neuronal irritation, compulsive water drinking, increased plasma renin, hypercalcemia, constriction of thoracic vena cava
|
|
cat has extreme PU/PD, and a specific gravity of 1.028. Localize the abnormality
|
consistent with osmotoc diuresis such as diabetes mellitus. Proximal tubular threshold for glucose absorption has been exceeded
|
|
7 year old dog, PU/PD, specific gravity of 1.003. Localize the problem. What diseases come to mind
|
collecting duct/renal medulla. Diabetes insipidus, hyperadrenocorticism, hypercalcemic syndromes, psychogenic polydipsia
|
|
7 year old dog, PU/PD, but specific gravity is 1.009.
|
dog is neither contrating nor diluting, therefore we should be suspicious of renal failure
|
|
dog has PU/PD with dehydration. Rule outs?
|
renal dz, diabetes mellitus, diabetes insipidus, hyperadrenocorticism, hypercalcemia, primary polydipsia, liver disease
|
|
dog has PU/PD with dehydration. Sp. Gr. Is 1.002, all other labs normal. What can we comclude?
|
the dog can dilute its urine but cannot concentrate it
|
|
would you perform a water deprivation test on a dog that is already dehydrated?
|
no
|
|
is diabetes insipidus common?
|
no
|
|
a dehydrated brain followed by an overhydrated brain is a
|
dead brain
|
|
do not perform water deprivation tests on ____, _____ or ____ animals
|
azotemic, dehydrated or hypercalemic
|
|
which can concentrate urine to a greater extent- dogs or cats
|
cats
|
|
normal sp. Gr for cats
|
greater than 1.035
|
|
normal sp. Gr for dogs
|
greater than 1.030
|
|
most polydispsic dogs will have:
|
dilute urine, inability to maximally concentrate urine or glucosurea
|
|
which is usually the primary- the PU or the PD?
|
the polyuria
|
|
glomerulus
|
selectively filters blood retaining proteins and cells, but permits fluid and solutes to enter the renal tubules
|
|
compare the sp. Gr of glomerulus to plasma
|
identical
|
|
how much of the glomerular filtrate is reabsorbed In the PCT?
|
80-90%
|
|
what does the PCT readsorb?
|
sodium, glucose, amino acids, water
|
|
DCT function
|
regulated excretion of potassium into urine and the further reabsorption of sodium
|
|
what regulates the DCT function
|
aldosterone
|
|
what are the collecting ducts responsible for? Hormone?
|
final urine concentration. ADH
|
|
where is adh produced and stored?
|
hypothalamus, stored in the pars nervosa of the pituitary gland
|
|
diagnostic approach to PU/PD: first step
|
determine that problem actually exists
|
|
diagnostic approach to PU/PD: second step
|
CBC/Chem- check for dehydration, electrolyte concentrations, kidney/liver values etc
|
|
what is the most common cause of PUPD in dogs and cats, and what percentages of cases in each?
|
CRF- 80% in dogs, 50% in cats
|
|
what can an ADH response test be used to differentiate?
|
DI from renal dz
|
|
vomiting
|
the forceful ejection of blood and fluids from the stomach or proximal duodenum.. Active reflex mediated process
|
|
regurgitation
|
expuslion of food and fluids from the esophagus. Passive, not reflex mediated. Sign of esophageal dysfunction, obstruction or dz
|
|
dysphagia
|
difficulting swallowing liquids or foods. Clinical sign of pharyngeal dysfunction, obstruction or dz
|
|
what regulates motility in the stomach and intestinal tract
|
autonomic nervous system
|
|
what does the parasymp component stimulate?
|
motiliity, decreases contraction of sphincters, and increases GI secretions
|
|
parasymp nerve innervating GI?
|
vagus
|
|
where is the vomiting center located?
|
in the medulla/ caudal brainstem
|
|
ways to activate vomiting center
|
receptors in ab viscera stimulated by inflammation/distension/hypertonicity
|
|
once activated, the vomiting center cuases
|
nausea, drooling and anorexia. Push/pull rxn in abdomen
|
|
push-pull rxn
|
push= abdominal pressin in which the stomach is squeezed between diaphradm and other viscera. Esophageal sphincters open and contractions of the stomach plus the abdominal press expels food/fluid into esophagus. Pull = negative pressure in the thorax and intra thorax esophagus. epiglottis is closed (prevents aspiration)
|
|
efferent pathway
|
vagus, phrenic and general somatic eferent nerves to skeletal muscles of the abdominal wall and thorax
|
|
reflex is largely mediated by
|
acetylcholine receptors
|
|
how else can the reflex be mediated?
|
by acetylcholie receptors
|
|
vomiting reflex can also be activated by
|
chemoreceptor trigger zone
|
|
where is CTZ located?
|
near vomiting center in the caudal brainstem
|
|
primary NT involved in the CTZ
|
dopamine
|
|
can the CTZ directly activate the vomiting center?
|
yes
|
|
metabolic consequences of vomiting
|
loss of fluids, food, electrolytes, and acid-base compounds
|
|
vomiting resulting in loss of stomach fluids causes
|
metabolic alkalosis and dehydration
|
|
loss of both stomach and duodenal fluid
|
blood pH remains normal or metabolic acidosis
|
|
vomiting results in
|
dehydration, hypokalemia, hypochloremia, hyponatremia
|
|
in which animals is aspiratoin pneumonia most likely to occur?
|
those that are severely depressed
|
|
what can a pure metabolic alkalosis due to vomiting result in?
|
renal retention of bicarb
|
|
regurgitation results in
|
weight loss, dehydration, and aspiration pneumonia
|
|
what increases the risk of aspiration?
|
the epiglottis not closing
|
|
what is the usual acid-base status in regurgitation?
|
normal
|
|
primary GI ruleouts for vomiting
|
functional disorders, inflammatory dz, obstructive, neoplastic, drug induced
|
|
rulouts for non-GI causes of vomiting
|
renal failure, liver dz, acute pancreatitis, peritonitis, hypoadrenocorticism, toxins, drugs
|
|
primary ruleouts for regurg include
|
mechanical or obstructive disorders such as esophageal foreigh body, vascular ring anomalies, strictures, esophagitis, neoplasia, and functional disorders such as- megaesphagus, myasthenia gravis, polymyositis, hypothyroid, hypoadrenocorticism
|
|
what should not be given to dehydrated dogs that may be hypotensive?
|
phenothiaze tranqs to antagonize the action of the NTs that mediate the vomiting reflex
|
|
metaclopramide
|
prokinetic that antagonizes dopamine, promotes gastric motility and emptying
|
|
symptomatic treatment of rugurg
|
elevated feeding platform
|
|
where is the CTZ located
|
on the floor of the fourth ventricle
|
|
what is the CTZ sensitive to
|
blood borne toxins and drugs
|
|
what connects to the CTZ and is involved with motion sickness?
|
the vestibular system
|
|
three types of antiemetics
|
local, anticholinergics, central
|
|
three types of antiacids
|
oral, H2 rc antagonists, proton pump inhibitors
|
|
anorexia
|
lak of or disintrest in the ingestion of food
|
|
three categories of anorexia
|
primary, secondary, pseudo
|
|
primary anorexia
|
direct involvement of the appetite centers of the hypothalamus
|
|
where is the hunger center located
|
lateral hypothalamus
|
|
what does stimulation of the hunger center cause
|
psychc drive to search for ingest food
|
|
where is the satiety center located
|
ventro-medial hypothalamus
|
|
what is located in the satiety center that is not present anywhere else in the CNS
|
insulin receptors for the transport of glucose
|
|
what are two other symptoms that can result from primary anorexia
|
psychologic, loss of smell
|
|
causes of secondary anorexia
|
pain, distension/inflammation of abdominal organs, toxic agents (endogenous waste, bacterial toxins, pyrogens), endocrine, neoplastic
|
|
how can neoplasia result in secondary anorexia?
|
may produce substances that inhibit appetite center, or may be the caues of organ failure or abdominal organ inflammation
|
|
pseudoanorexia
|
there is a desire to eat, but physically unable to. Can be associated with pain, neurologic dysfunction or inflammation of the oral cavity
|
|
define pathologic weight loss
|
unexplained loss of 10%
|
|
cachexia
|
20% weight loss, loss of muscle/fat stores
|
|
classifying decreased food intake
|
anorexia vs starvation/malnutrition
|
|
3 yr old GSD, never has gained weight, cow patty stool- 2 possible causes?
|
EPI, protein losing enteropathy
|
|
define obesity
|
excess body fat in relation to body mass
|
|
what percent obesity requires therapy
|
15% excess in body weight
|
|
what is the most common malnutrition disease?
|
obesity
|
|
obesity is the number 2 disease of:
|
"healthy" pets
|
|
types of obesity:
|
simple, dystrophic, hyperplastic, hypertrophic
|
|
simple obesity
|
normal fat distribution
|
|
dystrophic obesity
|
abnormal fat distribution
|
|
hyperplastic obesity
|
primarily in younger animals, number of adipocytes increases.
|
|
hypertrophic obesity
|
primarily in older animals, increased size of existing adipocytes
|
|
pathogenesis of obesity
|
prolonged caloric intake in relation to caloric requirement (over eating / under exercising)
|
|
two stages of obesity
|
dynamic (body fat accumulates, caloric intake high) and static (body fat stable, low caloric intake)
|
|
what is food intake under the control of
|
the satiety center of the hypothalamus
|
|
what does gastrointestinal filling stimulate?
|
vagal stimulation to inhibit feeding center
|
|
hormonal regulation of food intake
|
CCK, glucagon, insulin
|
|
what are oral receptors?
|
a metering process for food intake
|
|
glucostatic theory
|
glucoreceptor neurons in satiety center. Possibly insulin dependent. Decreased glucose levels increase firing and increased glucose levels decrease firing of neurons
|
|
aminostatic theory
|
certain amino acids decrease appetite
|
|
lipostatic theory
|
breakdown products of fat metabolism, ketoacids, and fatty acids, decrease feeding.
|
|
leptin
|
a peptide hormone produced by adipocytes. A way of signalling brain about energey stores. Leptin levels increase with obesity
|
|
disease that cause obesity
|
hypothyroidism, hypercorisolism, cortisol/hypothalamic lesion, +/- insulinoma
|
|
factors that can contribute to obesity
|
genetic, castration/OHE, age
|
|
disease associated with or exacerbated by obesity
|
diabetes, hyperlipidemia, hepatic lipidosis, musculoskeletal disorders, cardiovascular disorders, respiratory disorders, dermatologic, cancer
|
|
obesity may play a role in the development of:
|
diabetes
|
|
chronic hyperinsulinemia leads to
|
beta cell exhaustion
|
|
hypersecretion of insulin is associated with increased levels of:
|
amyloid deposition
|
|
obesity induces insulin ____
|
resistance
|
|
obesity and hepatic lipidosis:
|
protein deficiency leading to an inability to synthesize VLDLs
|
|
how do you evaluate obesity?
|
body scale charts
|
|
treatment of obesity:
|
calorie restriction AND exercise.
|
|
high fiber vs high protein diets
|
fiber increases gastric fill, protein induces ketosis and utilization of fat stores for energy
|
|
calculating basal energy requirement
|
30(ideal BW in KG) + 70
|
|
calculating maintenance energy requirement factor
|
k9: 1.6(BER), fel: 1.2(BER)
|
|
calculating calorie restricition
|
K9: 60% of MER, fel 70% of MER
|
|
behavioral modification of obesity
|
food does not equal love, need to enhance motivation and commitment, decrease begging
|
|
ascites
|
abnormal accumulation of fluid in the peritoneal cavity
|
|
presenting symptom for ascites:
|
abdominal distention
|
|
other rule outs for abdominal distention?
|
mass, air, organ, muscle weakness, fluid
|
|
pathophysiology of ascites:
|
increased hydrostatic pressure, decreased oncotic pressure, lymphatic, increased capillary permeability
|
|
causes of increased hydrostatic pressure
|
right heart failure, obstruction, overhydration
|
|
causes of decreased oncotic pressure
|
hypoalbuminemia, increased loss (glomerulus, intestine, wounds), decreased production by liver
|
|
causes of ascites due to the lymphatic system
|
obstruction or hypertension
|
|
causes of increase capillary permeability
|
inflammation, sepsis, endotoxemia, trauma
|
|
how does venous obstruction change the protein content of the effusion?
|
depends on anatomic location
|
|
obstruction of the hepatic sinusoids results in _____ effusion
|
high protein
|
|
obstruction of the intestinal lympathics results in _____ effusion
|
low protein
|
|
transudate
|
< 2.5 g/dl protein, < 1000 nucleated cells per ml
|
|
modified transudate
|
2.5-6 g/dl protein, 250-20000 nucleated cells per ml
|
|
exudate
|
>3.5 g/dl protein, >30000 nucleated cells per ml
|
|
what can result in pure transudate
|
hypoalbuminea, long standing portal hypertension
|
|
what can result in modified transudate?
|
right heart failure/congestion, vena cava obstruction, chyle, FIP, neoplasia
|
|
exudate can be caused by _____ or _____ reasons
|
septic or non-septic
|
|
septic causes of exudates include
|
rupture of GI tract, abcess, pyometra, septicemia
|
|
non septic causes of exudates include
|
chemical, inflammation, neoplastic, FIP
|
|
if abdominal effusions result in hypotension
|
activate RAAS system, exacerbate some causes of ascites (increase hydrostatic/decrease oncotic)
|
|
if abdominal effusions result in peritoneal cavity pressure increases:
|
respiration and venous return can be compromised
|
|
what tests are needed to diagnose ascites
|
abdominocentesis, ultrasound, radiograph, cardiac eval, exploratory sx, cbc/chem/ua
|
|
where do you perform abdominocentesis
|
right cranial quadrant- to avoid spleen
|
|
when should you drain fluid in the abdomen?
|
only if causing resporatory distress
|
|
abdominocentesis fluid is clear, red tinged and foamy, with 4.1g/dl protein and 1000 nucleated cells. It is:
|
modified transudate
|
|
abdominocentesis fluid is clear like tap water, .9g/dl protein and 100 nucleated cells
|
pure transudate
|
|
pathogenesis of edema
|
increased vascular permeability, decreased oncotic pressure, increased hydrostatic pressure, decreased lymph drainage
|
|
localized edema
|
decreased lymphatic drainage, vasculitis/increased vascular permeability
|
|
generalized edema
|
hypoalbuminemia --> decreased oncotic pressure
|
|
calculate net filtration pression (arteriolar)
|
(plasma hydrostatic - tissue hydrostatic) -- (plasma oncotic - tissue oncotic)
|
|
calculate net absorption pressure (venular)
|
(plasma hydrostatic - tissue hydrostatic) -- (plasma oncotic - tissue oncotic)
|
|
mediatiors of inflammation include
|
histamine, serotonin, and kinins
|
|
what/when are histamine and serotonin secreted from?
|
from mast cells and platelets in response to a variety of stimuli
|
|
what are kinins
|
potent vasodilators or vasoconstrictions. They increase vascular permeability. They are activated by exposed endothelium and proteases released from neutrophils
|
|
ow are arachidonic acid metabolites form
|
cleaved from cell membrane phospholipids, further degraded to COX and LOX pathways to produce prostaglandins, thromboxanes, leukotrienes
|
|
what can these autocoids cause
|
a variey of effects including vasodilation, vasoconstriction and increased vascular permeability
|
|
nitric oxide
|
released from endothelial cells, causes vasodilation, forms free radicals
|
|
inflammatoin leads to
|
changes in vascular tone and permeability
|
|
system inflammatory response syndrome
|
a common pathologic process behind progression and deterioration of patients
|
|
causes of localized, pitting edema
|
venous or lymphatic problem
|
|
tenesmus
|
straining to defecate and frequent defecation
|
|
hematochezia
|
presence of blood in the stool
|
|
rule outs for diarrhea
|
acute small bowel, chronic small bowel, acute large bowel, and chronic large bowel
|
|
rule outs for chronic mucoid bloody diarrhea
|
parasites/whips, colitis, neoplasia, systemic fungal infection, food interolarance
|
|
define diarrhea
|
increased frequency, fluidity or volume of feces
|
|
pathophysiology of diarrhea
|
increased concentration of fecal water - (hypersecretion, altered mucosal permeability, maldigestion/malabsorption, altered motility, combination
|
|
small bowel origin of diarrhea
|
colonic overload of water, inhibition of water absorption in colon
|
|
large bowel origin of diarrhea
|
failure to absorb water due to reduced absorptive capacity
|
|
what are the two major types of motility in the GI tract
|
peristalsis, segmental/mixing movements
|
|
effects of parasympathetic on motility
|
stimulates motility, relaxes sphincters, stimulates secretion
|
|
effects of sympathetic on motility
|
inhibits motility, increases sphincter tone, decreases secretion
|
|
what are the phases of digestion
|
oral, swallowing, gastric, SI, LI
|
|
the esophagus in dogs and cats is what muscle type?
|
>50% striated
|
|
what stimulates motility and secretion in the stomach
|
gastric distension, gastrin, vagus nerve
|
|
relative to digestion, what chemical proess is generally involved for the major classes of nutrients?
|
hydrolysis
|
|
what controls the release of HCL?
|
gastrin stimulates release from parietal cells, but vagus also increases HCL production. (proton pump/H2 rc)
|
|
where is protein digested and absorbed?
|
gastric, small intestine, absorbed in brush border
|
|
where are carbs digested?
|
in the oral phase and the intestinal phase
|
|
where does fat digestion occur?
|
small intestine
|
|
hypersecretion
|
secretion exceeds absorption
|
|
what type of intestinal movement is often reduced in diarrheal states?
|
rhythmic contractions
|
|
is the gut hyper or hypo motile in diarrhea?
|
hypo
|
|
maldigest can result from
|
deficiences of enzymes, deficiencies of grinding/mixing, and deficiencies of bile
|
|
what can be involved with malabsorption
|
structural and biochemical mechanisms
|
|
what can malabsorption's osmotic effects result in?
|
severe diarrhea
|
|
what can result in malabsorption?
|
villus atrophy/destruction, gluten enteropathy, severe IBD, lympangectesia, diffuse lymphosarcoma of gut
|
|
what part of the spinal cord and what nerves are involved in defecation reflex?
|
sacral, pelvic/pudendal nerves
|
|
metabolic consequences of SI diarrhea
|
metabolic acidosis, hypotension, edema, ascites, nutritional deficiences, electroylyte imbalances
|
|
diarrhea with decreased volume, greatly increased frequency, tenesmus, hematochezia, and mucus is likely from
|
large bowel
|
|
diarrhea with increased volume, increased frequency, melena, and steatorrhea is likely from
|
small intestine
|
|
what kinds of fecal exams should be done?
|
floatations/sedimentations, direct smears, stained fecal smears, rectal mucosal scraping/cytology
|
|
constipation
|
infrequent or difficult passage of feces
|
|
obstipation
|
intractable constipation resulting in severe fecal impaction throughout the rectum and colon
|
|
coprostasis
|
fecal impaction
|
|
pseudocoprostasis
|
matting of hair over the anus resulting in fecal stasis
|
|
megacolon
|
marked dilatation and hypomotility of rectum and colon
|
|
flatulence
|
intestinal gas
|
|
flatus
|
gas expelled through the anus
|
|
clinical signs of constipation
|
tenesmus with little or no passage of feces. Feces may be excessively hard, firm, sticky or form. Fecal mass can be palpated through the abdomen. In chronic cases, weight loss and vomiting may occur in cats
|
|
internal anal sphincter is under
|
parasympathetic control
|
|
external anal sphincter is under
|
pudendal nerve controls
|
|
colonic functions
|
absorption in proximal half, storage in caudal half, elimination and fermentation
|
|
causes of constipation:
|
dietary, environment, colonic obstruction, neurologic, perirectal pain, metabolic, endocrine, drug induced
|
|
what can constipation result in?
|
weight loss, anorexia, weakness, depression, colonic diverticuli, paradoxical diarrhea
|
|
feline idiopathic megacolon
|
impairment of colonic smooth muscle function, progressive loss of colonic motility, sever constipation and obstipation
|
|
pathophysiology of gas production
|
aerophagia, bacterial fermentation, diffusion from blood to GI tract, neutralization of acids
|
|
contents of flatus
|
nitrogen, CO2, hydrogen, oxygen, methane
|
|
what do hydrogen and CO2 result from
|
bacterial fermentation of nonabsorbable oligosaccharies (ie, soybeans)
|
|
what spinal cord segments control defecation?
|
L4 to S3
|
|
what does the pudendal nerve to relative to defecation?
|
control external anal sphincter
|
|
what is the primary component of flatus?
|
nitrogen
|
|
excess of what nutrient predisposes to flatulence?
|
carbohydrates
|
|
breed of cat that has a congenital neuro condition called spinal dysraphism and sacral nerve agenesis
|
manx
|
|
symptomatic treatment of constipation can include
|
dietary management, laxatives and drugs to stimulate motility
|
|
what will help increase the strength and frequency of colonic contractions and make feces easier to pass?
|
bulk- insolunble and soluble fiber added to the diet
|
|
melena
|
darkening of feces by blood pgiments. Implies digested blood
|
|
steatorrhea
|
presence of undigested fecal fat, implies deficiences of lipase or bile
|
|
the major pathophysiologic event affecting motility in diarrheas is loss of
|
segmental concentrations
|
|
breed with a familial immuno-proliferative disease that causes serious malabsorption of fat and the loss of serum proteins into intestinal lumen
|
basenjis
|
|
how does malabsorption result in severe diarrhea?
|
due to osmotic effects of malabsorbed particles that remain in the intestinal lumen
|
|
what other clinical signs can be assocated with small bowel diarrhea?
|
vomiting, marked wieght loss, dehydration, nutritional eficiences
|
|
what other clinical signs can be assocated with large bowel diarrhea?
|
weight loss, dehydration
|
|
what is the hallmark of large bowel diarrhea?
|
tenesmus
|
|
icterus
|
hyperbilirubinemia with bile pigments in skin and mucus membranes
|
|
bilirubin comes from
|
hemoglobin
|
|
true or false: bilirubin comes from senescent erythrocytes
|
TRUE
|
|
what part of hemoglobin is metabolized to bilirubin?
|
heme
|
|
what is the major rate limiting step in bilirubin metabolism in dogs and cats
|
the excretion of conjugated bilirubin (Step 4)
|
|
two main causes of icterus
|
hemolytic and hepatobiliary
|
|
hemolysis may cause hepatic
|
hypoxia
|
|
some ____ conditions involve both hemolytic and hepatic mechanisms
|
icteric
|
|
most common cause of unconjugated hyperbilirubinemia-hemolytic icteris
|
hemolysis (increased release of Hb)
|
|
causes of conjugated hyperbilirubinemia - hepatobiliary icterus
|
hepatocellular and biliary disease and/or hemolytic dz
|
|
hemolytic icterus rule outs
|
IMHA, blood parasites, drugs/toxins, bacteremia/septicemia
|
|
hepatobiliary icterus acute rule outs
|
drugs/toxins, ICH, lepto, acute pancreatitis, bacteremia/septicemia.
|
|
hepatobiliary icterus chronic rule outs
|
hepatic lipidosis, cholangitis/cholangiohepatitis, hepatic copper storage dz, chronic active hepatitis, hepatic cirrhosis, anticonvulsants/antibiotics, neoplasia, ruptured gall bladder, FIP
|
|
symptomatic therapy of icterus
|
maintain hydration, promote renal excretion of bilirubin,
|
|
true or false: bilirubin in urine must be conjugated
|
TRUE
|
|
jaundice
|
yellowness of the skin, mucus membranes or sclera due to the accumulation of bilirubin in tissues. Implies an abnormality in bilirubin metabolism or increased production
|
|
which term is preferred in veterinary medicine: jaundice or icteric
|
icteric
|
|
unconjugated bilirubin
|
bilirubin that has not ben processed by hepatocytes. NOT water soluble
|
|
conjugated bilirubin
|
has been processed by hepatocytes for excretion via the biliary system. Water soluble.
|
|
hemolytic icterus
|
icterus that results from the rapid and excessive destruction of RBCs releasing large amounts of hemoglobin
|
|
hepatobiliary icterus
|
icterus that results from decreased liver metabolism of bilirubin or failure to properly excrete bile into the duodenum
|
|
bilirubinemia
|
excess bilirubin in the blood
|
|
bilirubinuria
|
excess bilirubin in the urine
|
|
hemoglobinurea
|
excess hemoglobin in the urine- indicates severe hemolysis
|
|
what are senescent erythrocytes taken up and destryed by?
|
the macrophage-phagocyte system in the liver and spleen
|
|
____ is the only component of the heme molecule that requires excretion
|
bilirubin
|
|
kernicterus
|
unbound unconjugated bilirubin can enter tissues including the brain
|
|
the most common reason in dogs and cats for very large concentration of unbound, unconjugated bilirubin is
|
severe hemolysis
|
|
dogs and cats hepatocytes have a ___ Capacity to take in bilirubin
|
huge
|
|
oncei n the hepatocyte bilirubin is converted to ________ by ______
|
bilirubin glucuronide by glucuronyl transferase
|
|
dogs and cats hepatocytes have a ___ Capacity for conjugation
|
huge
|
|
conjugated bilirubin is transported to the biliary system for
|
excretion
|
|
the ability to take up and conjugate bilirubin _____ the capactiy to excrete conjugated bilirubin
|
exceeds
|
|
if the excretion pathway is compromised by liver or biliary tract disease, it is _____ into the serum
|
regurgitated
|
|
once excreted into the biliary system, conjugated bilirubin is mixed with other excretory products to form
|
bile
|
|
where is bile stored?
|
gall bladder
|
|
what test can confirm that hemolysis is present?
|
PCV
|
|
initial diagnostic plan for icterus:
|
determine hemolysis vs hepatobiliary
|
|
diagnostic tests only tell you what has happened:
|
in the past few hours
|
|
diagnostic tests do not tell the ___ or the ___
|
past or the future
|
|
lab findings of unconjugated hyperbilirubinemia include:
|
anemia (nonregen first, then regen), increase bilirubin, bilirubinuria after 3 days, liver enzymes normal at first but may increase after day 5, hemoglobinemia/uria
|
|
lab findings of conjugated hyperbilirubinemia include:
|
increased bilirubin, bilirubinuria, increased liver enzymes, increased bile acids
|
|
___ can be toxic to renal cells
|
hemoglobin
|
|
animals die from the disease causeing _____ rather than from the direct result of ______
|
icterus, hyperbilirubinemia
|
|
micturition
|
voluntary voiding of urine
|
|
urinary incontinence
|
lack of voluntary control over the passage of urine
|
|
dysuria
|
painful or difficult urination
|
|
stranguria
|
slow, painfully urination (obstruction, spasm of bladder neck and urethra)
|
|
pollakiuria
|
frequent storage attempts to urinate with voiding of small volumes
|
|
reflex dyssynergia
|
sudden interupttion of micturition
|
|
enuresis
|
involuntary passage of urine during sleep
|
|
innervation of the urinary bladder
|
pelvic and hypogastrric n
|
|
innervation of the urethra
|
pudendal n and hypogastric n
|
|
pelvic n
|
contains both afferent and efferent parasympathetic fibers. Primary nerve for both motor and sensory functions
|
|
hypogastric n
|
sympathetic fibers. Primary function is to facilitate detrussor relaxation during filling phase. Also innervates the internal urethral sphincter- faciliates urethral tone
|
|
pudendal n
|
mixed somatic nerve that innervates the external urethral sphincter. Maintains continence during fill phase and relaxes during voiding phase
|
|
what center mediates the micturition reflex
|
pons
|
|
what is the long tract circuit
|
tract from urethra/bladder to cerebral cortex
|
|
detrussor m innvervation
|
pelvic n
|
|
detrusor atony
|
failure of the bladder to contract, may be caused by disruption of tight junctions- chronic urethral obstruction or neurogenic causes
|
|
how is electrical activity conducted from fiber to fiber in the detrussor m?
|
tight junctions
|
|
characteristics of the filling phase of micturition
|
detrusor inhibited, sphincter stimulated
|
|
characteristics of the voiding phase of micturition
|
detrusor stimulated, urethra inhibited
|
|
what is dysuria a sign of?
|
lower urinary tract dz
|
|
dysuria
|
mucosal irritation or inflamation stimulates sensory receptors in bladder and urethra. This initates the micturition reflex.
|
|
causes of dysuria
|
inflammation/infection of bladder, urethra, prostate. Obstructive disorders (calculi, tumors, FLUTD), ofter assoc with hematuria and pyuria
|
|
two things that can be confused with dysuria by owners
|
polyuria, incontinence
|
|
neurogenic incontinence
|
lesions of nervous innervation and control
|
|
nonneurogenic incontinence
|
disease or anatominical defects of the lower urinary bladder
|
|
what effect can a cerebral lesion have on micturition?
|
can void bladder but no voluntary control, loss of house training, bladder is not distended
|
|
what effect can a lesion on the brain stem and spinal cord rostral to sacral segments hve on micturition?
|
no micturition reflex, but urethral and anal tone is maintained. Urethral pressures are increased and detrusor muscle is paralyzed )high resitance detrusor atony). Bladder is more dificul to express and animal may spurt small amounts of urine when the bladder is compresed. called an UMN bladder
|
|
what effect can a lesion on sacral spinal cord, nerve roots and peripheral nerves hve?
|
both micturion reflex and urethral pressures are decreased resulting in low resistance detrusor atony. Called a lmn bldder- more easily expressed and anal tone/reflexes might also be decreased
|
|
nonneurogenic incontinence: differentials for distended bladder
|
urethral obstruction, mass in bladder neck, detrusor-urethral dyssynergia, detrusor dysfunction
|
|
nonneurogenic incontience: differentials for non distended bladder
|
urethral incompetance, ectopic ureters, patent urachus, reduced bladder capacity, vesiculo-vaginal or ureterovaginal fistula
|
|
diagnostic approach for bladder problems
|
1) analyze history 2) observation and physical exam 3) classify problem-- dysuria, incontinence or a combo; neurogenic or nonneurogenic incontinence
|
|
what do you palpate on the physical exam
|
bladder, prostrate, urethra, empty bladder
|
|
after observing micturition wht should you determine?
|
residual volume in the bladder- should be less than 10 ml
|
|
animals that are incontinent are very prone to
|
UTIs
|
|
if bladder is distended:
|
assume obstruction. Attempt to pass catheter and image the abdomen. In males, be sure to palpate prostrate. May need advanced DXIM. Consider neurogenic, but odds are that it is nonneurogenic
|
|
three major causes if bladder not distended
|
urethral sphincter incompetence, urethral sphincter bypass, bladder contracting involuntarily at low volumes-- urger incontincence
|
|
describe the bladder in an UTI
|
usually small, may spasm during palpation, often feels hard
|
|
what can induce urethral sphincter incompetance
|
spay
|
|
urethral incompetance can be associated with
|
spay and neuter- more common in females
|
|
what occurs with urethral incompetence?
|
decreased urethral pressure, hormone receptors exist in urethral muscle- enhance resting urethral tone. When hormone levels are low the tone is decrased.
|
|
how can you treat uretheral incompetence?
|
hormone replacement therapty (females = estrogen), and alpha adrenergic drugs. Severe cases might require surgery
|
|
Phenylpropanolamine
|
a drug used to treat urethral incompetance
|
|
does the timing of OHE affect development of urethral incompetance?
|
it does not appear to
|
|
what dogs tend to be more affected by urethral incompetance
|
large dogs
|
|
fever is a sign of?
1) infection 2) immune meidated disease 3) cancer 4) drug reaction 5) all of the above |
5) all of the above
|
|
which one of the following diseases will cause extreme PUPD but produce modestly concentrated urine (1.020 - 1.028)
1) renal failure 2) diabetes insipidus 3) hyperadrenocorticism 4) diabetes mellitus 5) hypercalcemia |
4) diabetes mellitus
|
|
the largest component of flatus is?
|
nitrogen
|
|
a dog is presented with acute tenesmus, fresh blood (hematochezia) and mucoid diarrhea. Exam is neg for other clinical signs, TPR is normal. Given the clinical signs, where in the GI tract should one ficus diagnostic efforts?
|
large bowel
|
|
in the metabolism of bilirubin, which of the following steps is the most rate limited in dogs and cats?
a) transport of non conjugated bilirubin to liver b) uptake into hepatocytes c) conjugation d) excretion of bile into the biliary system |
d) excretion of bile into the biliary system
|
|
a dog has a bilateral injury of the spinal cord at T13-L1. all of the following are examples of urinary dysfunction that might occur from this injury except
a) detrussor atony b) distended bladder c) reduced urethral resistance d) urinary incontinence |
c) reduced urethral resistance
|
|
regarding anorexia in dogs/cats, which of the following is not correct?
1) the most common cause is primary anorexia 2) abdominal distension can cause anorexia 3) inflammatory cytokines inhibit the appetite center 4) in the presence of insulin, increased blood glucose can activiate the satiety center |
1) the most primary cause is primary anorexia
|
|
all of the folowing are correct regarding obesity in dogs and cats except
a) the most common form is dystrophic obesity b) the most common cause is excess calories relative to metabolic requirements c) conditions that decrease the basal metabolic rate can cause weight gain d) one of the factors to overcome in treating obesity is the body set point for weight and food intake |
a) the most common form is dystrophic obesity
|
|
liver sinusoids differ from regular cappilaries in all of the following ways except
a) very porous b) leak high protein lymph c) have increased venous hydrostatic pressure d) connect eins to veins |
c) have increased venous hydrostatic pressure
|
|
the cause of low protein ascites is usually which of the following?
a) increased arteriole hydrostatic pressure b) increased tissue hydrostatic pressure c) decreased plasma oncotic pressure d) post sinusoidal hypertension |
c) decreased plasma oncotic pressure
|
|
the first step in the POA approach is
|
database collection
|
|
substances that cause fever are called
|
pyrogens
|
|
a dog has a urine specific gravity of 1.002. what area of the kidney is most likely affected?
a) glomerulus b) proximal tubule c) loop of henle d) collecting ducts |
collecting ducts
|
|
is water deprivation test appropriate for a dog that is 5-7% clinically dehydrated?
|
no
|
|
what is the primary difference in vomiting vs regurgitation?
|
vomiting- food from stomach/prox duodenum, reflex mediated
regurgitation- passive, food from esophagus |
|
in chronic diarrhear what characerizes motility of the intestinal tract?
|
often hypomotile (decreased or slowed)
|
|
dogs and cats with lower urinary disease manifest what major clinical sign
|
dysuria
|
|
what is the cardinal sign of colorectal disease in dogs?
|
constipation
|
|
the most common type of anorexia is
|
secondary
|
|
the most common type of obesity is
|
simple
|
|
what is the most likely cause for a dug with generalized ventral edema and a low protein ascites
|
hypoalbunimia
|