Signs And Symptoms Midterm

Front 1

POA

Back 1

problem oriented approach

Front 2

what is the POA

Back 2

a logical way to think about case management based on presenting clinicial signs or findings which are called "problems" in this sytem

Front 3

POVMR

Back 3

problem oriented veterinary medical record

Front 4

the POVMR is designed to

Back 4

show the orderly process of the POA- thought process as well as content

Front 5

four steps of the POA

Back 5

gather a data base, problem ID, plan formulation, assessment and follow up plans

Front 6

plans in the POA-POVMR contain 3 major components

Back 6

diagnostic plan, therapeutic plan, client education

Front 7

differentials

Back 7

possible causes for the problem that need to be ruled out

Front 8

clinical problem solving: need to know _____ to solve the _____

Back 8

normal, to solve the abnormal

Front 9

pathophysiology

Back 9

understanding the mechanisms that create problems

Front 10

quality patient care is best achieved by

Back 10

managing problems diagnosticaly and therapeutically

Front 11

most important step in the POA

Back 11

data base collection

Front 12

define a problem

Back 12

any abnormality requiring medical or surgical management or one that interferes with the quality of life

Front 13

SOAP

Back 13

subjective objective assessment plan

Front 14

hyperthermia

Back 14

elevated core body temperature

Front 15

what is the term hyperthermia generally reserved for

Back 15

heat stroke and malignant hyperthermia

Front 16

fever

Back 16

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

Front 17

how is body temperature regulated in endothermic vertebrates?

Back 17

by controlling production and dissipation of heat via neurological mechanisms mediated in the hypothalams

Front 18

normal temperature for dogs/cats

Back 18

101-102

Front 19

activation of the sympathetic nervous system ____ body temp

Back 19

increases

Front 20

activiation of the parasympathetic nervous sysem ____ body temp

Back 20

decreases

Front 21

body heat is largely generated by

Back 21

metabolic activity of skeletal muscles and in the liver

Front 22

how do dogs and cats largely dissipate heat

Back 22

respiratory tract/panting, and evaporation from mucous membranes

Front 23

pyrogens have the ability to

Back 23

increase the thermoregulatory set point

Front 24

exogenous pyrogens include

Back 24

infections agents, exo and endotoxins, pharmacologic agents

Front 25

most exogenous pyrogens mostly produce fever by promoting

Back 25

the release of cytokines from macrophages and other leukotcytes

Front 26

chronic fever causes ____ and ____

Back 26

protein catabolism and cachexia

Front 27

fever is a clinical sign of

Back 27

inflammation

Front 28

four major categories of diseases to consider with fever?

Back 28

infectious, immune mediated, neoplastic, drug induced

Front 29

FUO

Back 29

fever of unknown origin

Front 30

define FUO

Back 30

feber of at least three weeks with no cause identified on labs or rads

Front 31

some of the more common causes of FUO in cats

Back 31

FELV, FIV, FIP

Front 32

some of the more common causes of FUO in dogs

Back 32

endocarditis, prostatis, deep abscess, rickettsial infections, deep mycotic infections

Front 33

heat stroke

Back 33

reults from inadequate heat dissipation in animals in high ambient temps

Front 34

exercise induced collapse and hyperthermia

Back 34

most likely a functional myopthaty with concurrent hyperthermia. Likely inherited.

Front 35

malignant hyperthermia

Back 35

inherited functional myopathy, causes severe muscle necrosis and hyperthermia, especially in horses/pigs

Front 36

fevers in which rainge usually do not require treatment unless chronic

Back 36

103-105degrees

Front 37

temps above ___ do require treatment

Back 37

105

Front 38

natures way of signalling that something is wrong

Back 38

fever

Front 39

classification of true fever: can be

Back 39

intermittent, remittent, relapsing, septic or FUO

Front 40

where is the thermoregulatory center located

Back 40

anterior hypothalamus- diencephalon

Front 41

regulation of body temp:

Back 41

vasoconstriction/vasodilation, symp control/parasymp control

Front 42

what are the actual mediators of fever

Back 42

endogens pyrogens

Front 43

name three endogenous mediators

Back 43

IL1, IL6 and TNFa

Front 44

which of the endogenous mediators is most important?

Back 44

IL1

Front 45

what does IL1 stimulate?

Back 45

release of IL6

Front 46

potential benefits of fever

Back 46

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

Front 47

harmful effects of fever

Back 47

over 106 is harmful to cell metabolism. Potential for cerebral edema and neuronal death. Protein catabolism and cachexia, depression and anorexia

Front 48

which is generally more difficult to determine from the PE: chronic or acute inflammation

Back 48

chronic

Front 49

most antipyretic agents are

Back 49

antiprostaglandins

Front 50

does heat stroke respond to antipyretics?

Back 50

no

Front 51

treatment for heat stroke?

Back 51

total body cooling, IV crystalloids and glucocorticoids

Front 52

common complication of heat stroke

Back 52

DIC

Front 53

hypothermia can occur for three reasons

Back 53

accidental, pathological, purposeful

Front 54

PU/PD

Back 54

polyurea/polydipsia

Front 55

general characteristics of PU/PD?

Back 55

PU = urine output > 25ml/lb. PD = water intake > 50ml/lb

Front 56

what is the most common disease in dogs with PU/PD?

Back 56

renal disease

Front 57

what are the top three causes of disease in cats with PU/PD?

Back 57

renal disease, diabetes mellitus, hyperthyroidism

Front 58

glomerular function

Back 58

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.

Front 59

what is the specific gravity of glomerular filtrate?

Back 59

1.008 - 1.012 (isothenuria)

Front 60

what happens to glomerular filtrate In the proximal tubule

Back 60

solutes are actively transported out and water follows. Volume is decreased 60-70% and specific gravity stays about 1.010

Front 61

what important actions occur in the ascending limb of Henle's loop

Back 61

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

Front 62

what happens in the distal tubule?

Back 62

aldosterone stimulates the excretion of potassium and the retention of sodium. Acid/base mechanisms-bicarb exchange. Specific gravity increases a small amount.

Front 63

what stimluates the release of aldosterone?

Back 63

renin/angiotensin

Front 64

what happens in the collecting ducts?

Back 64

ADH regulates pore size in the tubule membrane. Water is passively reabsorbed by the osmotic gradient of the renal medulla.

Front 65

what regulates the release of ADH?

Back 65

plasma osmolality

Front 66

what is the countercurrent system?

Back 66

association of vasa recta and loop of henle. Allows sodium and urea to be concentrated in renal medulla

Front 67

medullary washout

Back 67

decreased medullary hypertonicity- failure of NaCl pump in LH., liver failure (decrease urea), prolonged PU/PD (increased fluid flow in LH and vasa recta)

Front 68

thirst

Back 68

the conscious desire for water

Front 69

where is the thirst center

Back 69

hypothalamus near ADH controlled centers

Front 70

what is thirst controlled by?

Back 70

extracellular fluid osmolality

Front 71

primary thirst

Back 71

results from increase in sodium or decrease in blood volume

Front 72

secondary thirst

Back 72

anticipation of needs before deficiencies occur- oropharyngeal cues and circadian rhythm of eating

Front 73

5 causes of pathologic thirst

Back 73

neuronal irritation, compulsive water drinking, increased plasma renin, hypercalcemia, constriction of thoracic vena cava

Front 74

cat has extreme PU/PD, and a specific gravity of 1.028. Localize the abnormality

Back 74

consistent with osmotoc diuresis such as diabetes mellitus. Proximal tubular threshold for glucose absorption has been exceeded

Front 75

7 year old dog, PU/PD, specific gravity of 1.003. Localize the problem. What diseases come to mind

Back 75

collecting duct/renal medulla. Diabetes insipidus, hyperadrenocorticism, hypercalcemic syndromes, psychogenic polydipsia

Front 76

7 year old dog, PU/PD, but specific gravity is 1.009.

Back 76

dog is neither contrating nor diluting, therefore we should be suspicious of renal failure

Front 77

dog has PU/PD with dehydration. Rule outs?

Back 77

renal dz, diabetes mellitus, diabetes insipidus, hyperadrenocorticism, hypercalcemia, primary polydipsia, liver disease

Front 78

dog has PU/PD with dehydration. Sp. Gr. Is 1.002, all other labs normal. What can we comclude?

Back 78

the dog can dilute its urine but cannot concentrate it

Front 79

would you perform a water deprivation test on a dog that is already dehydrated?

Back 79

no

Front 80

is diabetes insipidus common?

Back 80

no

Front 81

a dehydrated brain followed by an overhydrated brain is a

Back 81

dead brain

Front 82

do not perform water deprivation tests on ____, _____ or ____ animals

Back 82

azotemic, dehydrated or hypercalemic

Front 83

which can concentrate urine to a greater extent- dogs or cats

Back 83

cats

Front 84

normal sp. Gr for cats

Back 84

greater than 1.035

Front 85

normal sp. Gr for dogs

Back 85

greater than 1.030

Front 86

most polydispsic dogs will have:

Back 86

dilute urine, inability to maximally concentrate urine or glucosurea

Front 87

which is usually the primary- the PU or the PD?

Back 87

the polyuria

Front 88

glomerulus

Back 88

selectively filters blood retaining proteins and cells, but permits fluid and solutes to enter the renal tubules

Front 89

compare the sp. Gr of glomerulus to plasma

Back 89

identical

Front 90

how much of the glomerular filtrate is reabsorbed In the PCT?

Back 90

80-90%

Front 91

what does the PCT readsorb?

Back 91

sodium, glucose, amino acids, water

Front 92

DCT function

Back 92

regulated excretion of potassium into urine and the further reabsorption of sodium

Front 93

what regulates the DCT function

Back 93

aldosterone

Front 94

what are the collecting ducts responsible for? Hormone?

Back 94

final urine concentration. ADH

Front 95

where is adh produced and stored?

Back 95

hypothalamus, stored in the pars nervosa of the pituitary gland

Front 96

diagnostic approach to PU/PD: first step

Back 96

determine that problem actually exists

Front 97

diagnostic approach to PU/PD: second step

Back 97

CBC/Chem- check for dehydration, electrolyte concentrations, kidney/liver values etc

Front 98

what is the most common cause of PUPD in dogs and cats, and what percentages of cases in each?

Back 98

CRF- 80% in dogs, 50% in cats

Front 99

what can an ADH response test be used to differentiate?

Back 99

DI from renal dz

Front 100

vomiting

Back 100

the forceful ejection of blood and fluids from the stomach or proximal duodenum.. Active reflex mediated process

Front 101

regurgitation

Back 101

expuslion of food and fluids from the esophagus. Passive, not reflex mediated. Sign of esophageal dysfunction, obstruction or dz

Front 102

dysphagia

Back 102

difficulting swallowing liquids or foods. Clinical sign of pharyngeal dysfunction, obstruction or dz

Front 103

what regulates motility in the stomach and intestinal tract

Back 103

autonomic nervous system

Front 104

what does the parasymp component stimulate?

Back 104

motiliity, decreases contraction of sphincters, and increases GI secretions

Front 105

parasymp nerve innervating GI?

Back 105

vagus

Front 106

where is the vomiting center located?

Back 106

in the medulla/ caudal brainstem

Front 107

ways to activate vomiting center

Back 107

receptors in ab viscera stimulated by inflammation/distension/hypertonicity

Front 108

once activated, the vomiting center cuases

Back 108

nausea, drooling and anorexia. Push/pull rxn in abdomen

Front 109

push-pull rxn

Back 109

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)

Front 110

efferent pathway

Back 110

vagus, phrenic and general somatic eferent nerves to skeletal muscles of the abdominal wall and thorax

Front 111

reflex is largely mediated by

Back 111

acetylcholine receptors

Front 112

how else can the reflex be mediated?

Back 112

by acetylcholie receptors

Front 113

vomiting reflex can also be activated by

Back 113

chemoreceptor trigger zone

Front 114

where is CTZ located?

Back 114

near vomiting center in the caudal brainstem

Front 115

primary NT involved in the CTZ

Back 115

dopamine

Front 116

can the CTZ directly activate the vomiting center?

Back 116

yes

Front 117

metabolic consequences of vomiting

Back 117

loss of fluids, food, electrolytes, and acid-base compounds

Front 118

vomiting resulting in loss of stomach fluids causes

Back 118

metabolic alkalosis and dehydration

Front 119

loss of both stomach and duodenal fluid

Back 119

blood pH remains normal or metabolic acidosis

Front 120

vomiting results in

Back 120

dehydration, hypokalemia, hypochloremia, hyponatremia

Front 121

in which animals is aspiratoin pneumonia most likely to occur?

Back 121

those that are severely depressed

Front 122

what can a pure metabolic alkalosis due to vomiting result in?

Back 122

renal retention of bicarb

Front 123

regurgitation results in

Back 123

weight loss, dehydration, and aspiration pneumonia

Front 124

what increases the risk of aspiration?

Back 124

the epiglottis not closing

Front 125

what is the usual acid-base status in regurgitation?

Back 125

normal

Front 126

primary GI ruleouts for vomiting

Back 126

functional disorders, inflammatory dz, obstructive, neoplastic, drug induced

Front 127

rulouts for non-GI causes of vomiting

Back 127

renal failure, liver dz, acute pancreatitis, peritonitis, hypoadrenocorticism, toxins, drugs

Front 128

primary ruleouts for regurg include

Back 128

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

Front 129

what should not be given to dehydrated dogs that may be hypotensive?

Back 129

phenothiaze tranqs to antagonize the action of the NTs that mediate the vomiting reflex

Front 130

metaclopramide

Back 130

prokinetic that antagonizes dopamine, promotes gastric motility and emptying

Front 131

symptomatic treatment of rugurg

Back 131

elevated feeding platform

Front 132

where is the CTZ located

Back 132

on the floor of the fourth ventricle

Front 133

what is the CTZ sensitive to

Back 133

blood borne toxins and drugs

Front 134

what connects to the CTZ and is involved with motion sickness?

Back 134

the vestibular system

Front 135

three types of antiemetics

Back 135

local, anticholinergics, central

Front 136

three types of antiacids

Back 136

oral, H2 rc antagonists, proton pump inhibitors

Front 137

anorexia

Back 137

lak of or disintrest in the ingestion of food

Front 138

three categories of anorexia

Back 138

primary, secondary, pseudo

Front 139

primary anorexia

Back 139

direct involvement of the appetite centers of the hypothalamus

Front 140

where is the hunger center located

Back 140

lateral hypothalamus

Front 141

what does stimulation of the hunger center cause

Back 141

psychc drive to search for ingest food

Front 142

where is the satiety center located

Back 142

ventro-medial hypothalamus

Front 143

what is located in the satiety center that is not present anywhere else in the CNS

Back 143

insulin receptors for the transport of glucose

Front 144

what are two other symptoms that can result from primary anorexia

Back 144

psychologic, loss of smell

Front 145

causes of secondary anorexia

Back 145

pain, distension/inflammation of abdominal organs, toxic agents (endogenous waste, bacterial toxins, pyrogens), endocrine, neoplastic

Front 146

how can neoplasia result in secondary anorexia?

Back 146

may produce substances that inhibit appetite center, or may be the caues of organ failure or abdominal organ inflammation

Front 147

pseudoanorexia

Back 147

there is a desire to eat, but physically unable to. Can be associated with pain, neurologic dysfunction or inflammation of the oral cavity

Front 148

define pathologic weight loss

Back 148

unexplained loss of 10%

Front 149

cachexia

Back 149

20% weight loss, loss of muscle/fat stores

Front 150

classifying decreased food intake

Back 150

anorexia vs starvation/malnutrition

Front 151

3 yr old GSD, never has gained weight, cow patty stool- 2 possible causes?

Back 151

EPI, protein losing enteropathy

Front 152

define obesity

Back 152

excess body fat in relation to body mass

Front 153

what percent obesity requires therapy

Back 153

15% excess in body weight

Front 154

what is the most common malnutrition disease?

Back 154

obesity

Front 155

obesity is the number 2 disease of:

Back 155

"healthy" pets

Front 156

types of obesity:

Back 156

simple, dystrophic, hyperplastic, hypertrophic

Front 157

simple obesity

Back 157

normal fat distribution

Front 158

dystrophic obesity

Back 158

abnormal fat distribution

Front 159

hyperplastic obesity

Back 159

primarily in younger animals, number of adipocytes increases.

Front 160

hypertrophic obesity

Back 160

primarily in older animals, increased size of existing adipocytes

Front 161

pathogenesis of obesity

Back 161

prolonged caloric intake in relation to caloric requirement (over eating / under exercising)

Front 162

two stages of obesity

Back 162

dynamic (body fat accumulates, caloric intake high) and static (body fat stable, low caloric intake)

Front 163

what is food intake under the control of

Back 163

the satiety center of the hypothalamus

Front 164

what does gastrointestinal filling stimulate?

Back 164

vagal stimulation to inhibit feeding center

Front 165

hormonal regulation of food intake

Back 165

CCK, glucagon, insulin

Front 166

what are oral receptors?

Back 166

a metering process for food intake

Front 167

glucostatic theory

Back 167

glucoreceptor neurons in satiety center. Possibly insulin dependent. Decreased glucose levels increase firing and increased glucose levels decrease firing of neurons

Front 168

aminostatic theory

Back 168

certain amino acids decrease appetite

Front 169

lipostatic theory

Back 169

breakdown products of fat metabolism, ketoacids, and fatty acids, decrease feeding.

Front 170

leptin

Back 170

a peptide hormone produced by adipocytes. A way of signalling brain about energey stores. Leptin levels increase with obesity

Front 171

disease that cause obesity

Back 171

hypothyroidism, hypercorisolism, cortisol/hypothalamic lesion, +/- insulinoma

Front 172

factors that can contribute to obesity

Back 172

genetic, castration/OHE, age

Front 173

disease associated with or exacerbated by obesity

Back 173

diabetes, hyperlipidemia, hepatic lipidosis, musculoskeletal disorders, cardiovascular disorders, respiratory disorders, dermatologic, cancer

Front 174

obesity may play a role in the development of:

Back 174

diabetes

Front 175

chronic hyperinsulinemia leads to

Back 175

beta cell exhaustion

Front 176

hypersecretion of insulin is associated with increased levels of:

Back 176

amyloid deposition

Front 177

obesity induces insulin ____

Back 177

resistance

Front 178

obesity and hepatic lipidosis:

Back 178

protein deficiency leading to an inability to synthesize VLDLs

Front 179

how do you evaluate obesity?

Back 179

body scale charts

Front 180

treatment of obesity:

Back 180

calorie restriction AND exercise.

Front 181

high fiber vs high protein diets

Back 181

fiber increases gastric fill, protein induces ketosis and utilization of fat stores for energy

Front 182

calculating basal energy requirement

Back 182

30(ideal BW in KG) + 70

Front 183

calculating maintenance energy requirement factor

Back 183

k9: 1.6(BER), fel: 1.2(BER)

Front 184

calculating calorie restricition

Back 184

K9: 60% of MER, fel 70% of MER

Front 185

behavioral modification of obesity

Back 185

food does not equal love, need to enhance motivation and commitment, decrease begging

Front 186

ascites

Back 186

abnormal accumulation of fluid in the peritoneal cavity

Front 187

presenting symptom for ascites:

Back 187

abdominal distention

Front 188

other rule outs for abdominal distention?

Back 188

mass, air, organ, muscle weakness, fluid

Front 189

pathophysiology of ascites:

Back 189

increased hydrostatic pressure, decreased oncotic pressure, lymphatic, increased capillary permeability

Front 190

causes of increased hydrostatic pressure

Back 190

right heart failure, obstruction, overhydration

Front 191

causes of decreased oncotic pressure

Back 191

hypoalbuminemia, increased loss (glomerulus, intestine, wounds), decreased production by liver

Front 192

causes of ascites due to the lymphatic system

Back 192

obstruction or hypertension

Front 193

causes of increase capillary permeability

Back 193

inflammation, sepsis, endotoxemia, trauma

Front 194

how does venous obstruction change the protein content of the effusion?

Back 194

depends on anatomic location

Front 195

obstruction of the hepatic sinusoids results in _____ effusion

Back 195

high protein

Front 196

obstruction of the intestinal lympathics results in _____ effusion

Back 196

low protein

Front 197

transudate

Back 197

< 2.5 g/dl protein, < 1000 nucleated cells per ml

Front 198

modified transudate

Back 198

2.5-6 g/dl protein, 250-20000 nucleated cells per ml

Front 199

exudate

Back 199

>3.5 g/dl protein, >30000 nucleated cells per ml

Front 200

what can result in pure transudate

Back 200

hypoalbuminea, long standing portal hypertension

Front 201

what can result in modified transudate?

Back 201

right heart failure/congestion, vena cava obstruction, chyle, FIP, neoplasia

Front 202

exudate can be caused by _____ or _____ reasons

Back 202

septic or non-septic

Front 203

septic causes of exudates include

Back 203

rupture of GI tract, abcess, pyometra, septicemia

Front 204

non septic causes of exudates include

Back 204

chemical, inflammation, neoplastic, FIP

Front 205

if abdominal effusions result in hypotension

Back 205

activate RAAS system, exacerbate some causes of ascites (increase hydrostatic/decrease oncotic)

Front 206

if abdominal effusions result in peritoneal cavity pressure increases:

Back 206

respiration and venous return can be compromised

Front 207

what tests are needed to diagnose ascites

Back 207

abdominocentesis, ultrasound, radiograph, cardiac eval, exploratory sx, cbc/chem/ua

Front 208

where do you perform abdominocentesis

Back 208

right cranial quadrant- to avoid spleen

Front 209

when should you drain fluid in the abdomen?

Back 209

only if causing resporatory distress

Front 210

abdominocentesis fluid is clear, red tinged and foamy, with 4.1g/dl protein and 1000 nucleated cells. It is:

Back 210

modified transudate

Front 211

abdominocentesis fluid is clear like tap water, .9g/dl protein and 100 nucleated cells

Back 211

pure transudate

Front 212

pathogenesis of edema

Back 212

increased vascular permeability, decreased oncotic pressure, increased hydrostatic pressure, decreased lymph drainage

Front 213

localized edema

Back 213

decreased lymphatic drainage, vasculitis/increased vascular permeability

Front 214

generalized edema

Back 214

hypoalbuminemia --> decreased oncotic pressure

Front 215

calculate net filtration pression (arteriolar)

Back 215

(plasma hydrostatic - tissue hydrostatic) -- (plasma oncotic - tissue oncotic)

Front 216

calculate net absorption pressure (venular)

Back 216

(plasma hydrostatic - tissue hydrostatic) -- (plasma oncotic - tissue oncotic)

Front 217

mediatiors of inflammation include

Back 217

histamine, serotonin, and kinins

Front 218

what/when are histamine and serotonin secreted from?

Back 218

from mast cells and platelets in response to a variety of stimuli

Front 219

what are kinins

Back 219

potent vasodilators or vasoconstrictions. They increase vascular permeability. They are activated by exposed endothelium and proteases released from neutrophils

Front 220

ow are arachidonic acid metabolites form

Back 220

cleaved from cell membrane phospholipids, further degraded to COX and LOX pathways to produce prostaglandins, thromboxanes, leukotrienes

Front 221

what can these autocoids cause

Back 221

a variey of effects including vasodilation, vasoconstriction and increased vascular permeability

Front 222

nitric oxide

Back 222

released from endothelial cells, causes vasodilation, forms free radicals

Front 223

inflammatoin leads to

Back 223

changes in vascular tone and permeability

Front 224

system inflammatory response syndrome

Back 224

a common pathologic process behind progression and deterioration of patients

Front 225

causes of localized, pitting edema

Back 225

venous or lymphatic problem

Front 226

tenesmus

Back 226

straining to defecate and frequent defecation

Front 227

hematochezia

Back 227

presence of blood in the stool

Front 228

rule outs for diarrhea

Back 228

acute small bowel, chronic small bowel, acute large bowel, and chronic large bowel

Front 229

rule outs for chronic mucoid bloody diarrhea

Back 229

parasites/whips, colitis, neoplasia, systemic fungal infection, food interolarance

Front 230

define diarrhea

Back 230

increased frequency, fluidity or volume of feces

Front 231

pathophysiology of diarrhea

Back 231

increased concentration of fecal water - (hypersecretion, altered mucosal permeability, maldigestion/malabsorption, altered motility, combination

Front 232

small bowel origin of diarrhea

Back 232

colonic overload of water, inhibition of water absorption in colon

Front 233

large bowel origin of diarrhea

Back 233

failure to absorb water due to reduced absorptive capacity

Front 234

what are the two major types of motility in the GI tract

Back 234

peristalsis, segmental/mixing movements

Front 235

effects of parasympathetic on motility

Back 235

stimulates motility, relaxes sphincters, stimulates secretion

Front 236

effects of sympathetic on motility

Back 236

inhibits motility, increases sphincter tone, decreases secretion

Front 237

what are the phases of digestion

Back 237

oral, swallowing, gastric, SI, LI

Front 238

the esophagus in dogs and cats is what muscle type?

Back 238

>50% striated

Front 239

what stimulates motility and secretion in the stomach

Back 239

gastric distension, gastrin, vagus nerve

Front 240

relative to digestion, what chemical proess is generally involved for the major classes of nutrients?

Back 240

hydrolysis

Front 241

what controls the release of HCL?

Back 241

gastrin stimulates release from parietal cells, but vagus also increases HCL production. (proton pump/H2 rc)

Front 242

where is protein digested and absorbed?

Back 242

gastric, small intestine, absorbed in brush border

Front 243

where are carbs digested?

Back 243

in the oral phase and the intestinal phase

Front 244

where does fat digestion occur?

Back 244

small intestine

Front 245

hypersecretion

Back 245

secretion exceeds absorption

Front 246

what type of intestinal movement is often reduced in diarrheal states?

Back 246

rhythmic contractions

Front 247

is the gut hyper or hypo motile in diarrhea?

Back 247

hypo

Front 248

maldigest can result from

Back 248

deficiences of enzymes, deficiencies of grinding/mixing, and deficiencies of bile

Front 249

what can be involved with malabsorption

Back 249

structural and biochemical mechanisms

Front 250

what can malabsorption's osmotic effects result in?

Back 250

severe diarrhea

Front 251

what can result in malabsorption?

Back 251

villus atrophy/destruction, gluten enteropathy, severe IBD, lympangectesia, diffuse lymphosarcoma of gut

Front 252

what part of the spinal cord and what nerves are involved in defecation reflex?

Back 252

sacral, pelvic/pudendal nerves

Front 253

metabolic consequences of SI diarrhea

Back 253

metabolic acidosis, hypotension, edema, ascites, nutritional deficiences, electroylyte imbalances

Front 254

diarrhea with decreased volume, greatly increased frequency, tenesmus, hematochezia, and mucus is likely from

Back 254

large bowel

Front 255

diarrhea with increased volume, increased frequency, melena, and steatorrhea is likely from

Back 255

small intestine

Front 256

what kinds of fecal exams should be done?

Back 256

floatations/sedimentations, direct smears, stained fecal smears, rectal mucosal scraping/cytology

Front 257

constipation

Back 257

infrequent or difficult passage of feces

Front 258

obstipation

Back 258

intractable constipation resulting in severe fecal impaction throughout the rectum and colon

Front 259

coprostasis

Back 259

fecal impaction

Front 260

pseudocoprostasis

Back 260

matting of hair over the anus resulting in fecal stasis

Front 261

megacolon

Back 261

marked dilatation and hypomotility of rectum and colon

Front 262

flatulence

Back 262

intestinal gas

Front 263

flatus

Back 263

gas expelled through the anus

Front 264

clinical signs of constipation

Back 264

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

Front 265

internal anal sphincter is under

Back 265

parasympathetic control

Front 266

external anal sphincter is under

Back 266

pudendal nerve controls

Front 267

colonic functions

Back 267

absorption in proximal half, storage in caudal half, elimination and fermentation

Front 268

causes of constipation:

Back 268

dietary, environment, colonic obstruction, neurologic, perirectal pain, metabolic, endocrine, drug induced

Front 269

what can constipation result in?

Back 269

weight loss, anorexia, weakness, depression, colonic diverticuli, paradoxical diarrhea

Front 270

feline idiopathic megacolon

Back 270

impairment of colonic smooth muscle function, progressive loss of colonic motility, sever constipation and obstipation

Front 271

pathophysiology of gas production

Back 271

aerophagia, bacterial fermentation, diffusion from blood to GI tract, neutralization of acids

Front 272

contents of flatus

Back 272

nitrogen, CO2, hydrogen, oxygen, methane

Front 273

what do hydrogen and CO2 result from

Back 273

bacterial fermentation of nonabsorbable oligosaccharies (ie, soybeans)

Front 274

what spinal cord segments control defecation?

Back 274

L4 to S3

Front 275

what does the pudendal nerve to relative to defecation?

Back 275

control external anal sphincter

Front 276

what is the primary component of flatus?

Back 276

nitrogen

Front 277

excess of what nutrient predisposes to flatulence?

Back 277

carbohydrates

Front 278

breed of cat that has a congenital neuro condition called spinal dysraphism and sacral nerve agenesis

Back 278

manx

Front 279

symptomatic treatment of constipation can include

Back 279

dietary management, laxatives and drugs to stimulate motility

Front 280

what will help increase the strength and frequency of colonic contractions and make feces easier to pass?

Back 280

bulk- insolunble and soluble fiber added to the diet

Front 281

melena

Back 281

darkening of feces by blood pgiments. Implies digested blood

Front 282

steatorrhea

Back 282

presence of undigested fecal fat, implies deficiences of lipase or bile

Front 283

the major pathophysiologic event affecting motility in diarrheas is loss of

Back 283

segmental concentrations

Front 284

breed with a familial immuno-proliferative disease that causes serious malabsorption of fat and the loss of serum proteins into intestinal lumen

Back 284

basenjis

Front 285

how does malabsorption result in severe diarrhea?

Back 285

due to osmotic effects of malabsorbed particles that remain in the intestinal lumen

Front 286

what other clinical signs can be assocated with small bowel diarrhea?

Back 286

vomiting, marked wieght loss, dehydration, nutritional eficiences

Front 287

what other clinical signs can be assocated with large bowel diarrhea?

Back 287

weight loss, dehydration

Front 288

what is the hallmark of large bowel diarrhea?

Back 288

tenesmus

Front 289

icterus

Back 289

hyperbilirubinemia with bile pigments in skin and mucus membranes

Front 290

bilirubin comes from

Back 290

hemoglobin

Front 291

true or false: bilirubin comes from senescent erythrocytes

Back 291

TRUE

Front 292

what part of hemoglobin is metabolized to bilirubin?

Back 292

heme

Front 293

what is the major rate limiting step in bilirubin metabolism in dogs and cats

Back 293

the excretion of conjugated bilirubin (Step 4)

Front 294

two main causes of icterus

Back 294

hemolytic and hepatobiliary

Front 295

hemolysis may cause hepatic

Back 295

hypoxia

Front 296

some ____ conditions involve both hemolytic and hepatic mechanisms

Back 296

icteric

Front 297

most common cause of unconjugated hyperbilirubinemia-hemolytic icteris

Back 297

hemolysis (increased release of Hb)

Front 298

causes of conjugated hyperbilirubinemia - hepatobiliary icterus

Back 298

hepatocellular and biliary disease and/or hemolytic dz

Front 299

hemolytic icterus rule outs

Back 299

IMHA, blood parasites, drugs/toxins, bacteremia/septicemia

Front 300

hepatobiliary icterus acute rule outs

Back 300

drugs/toxins, ICH, lepto, acute pancreatitis, bacteremia/septicemia.

Front 301

hepatobiliary icterus chronic rule outs

Back 301

hepatic lipidosis, cholangitis/cholangiohepatitis, hepatic copper storage dz, chronic active hepatitis, hepatic cirrhosis, anticonvulsants/antibiotics, neoplasia, ruptured gall bladder, FIP

Front 302

symptomatic therapy of icterus

Back 302

maintain hydration, promote renal excretion of bilirubin,

Front 303

true or false: bilirubin in urine must be conjugated

Back 303

TRUE

Front 304

jaundice

Back 304

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

Front 305

which term is preferred in veterinary medicine: jaundice or icteric

Back 305

icteric

Front 306

unconjugated bilirubin

Back 306

bilirubin that has not ben processed by hepatocytes. NOT water soluble

Front 307

conjugated bilirubin

Back 307

has been processed by hepatocytes for excretion via the biliary system. Water soluble.

Front 308

hemolytic icterus

Back 308

icterus that results from the rapid and excessive destruction of RBCs releasing large amounts of hemoglobin

Front 309

hepatobiliary icterus

Back 309

icterus that results from decreased liver metabolism of bilirubin or failure to properly excrete bile into the duodenum

Front 310

bilirubinemia

Back 310

excess bilirubin in the blood

Front 311

bilirubinuria

Back 311

excess bilirubin in the urine

Front 312

hemoglobinurea

Back 312

excess hemoglobin in the urine- indicates severe hemolysis

Front 313

what are senescent erythrocytes taken up and destryed by?

Back 313

the macrophage-phagocyte system in the liver and spleen

Front 314

____ is the only component of the heme molecule that requires excretion

Back 314

bilirubin

Front 315

kernicterus

Back 315

unbound unconjugated bilirubin can enter tissues including the brain

Front 316

the most common reason in dogs and cats for very large concentration of unbound, unconjugated bilirubin is

Back 316

severe hemolysis

Front 317

dogs and cats hepatocytes have a ___ Capacity to take in bilirubin

Back 317

huge

Front 318

oncei n the hepatocyte bilirubin is converted to ________ by ______

Back 318

bilirubin glucuronide by glucuronyl transferase

Front 319

dogs and cats hepatocytes have a ___ Capacity for conjugation

Back 319

huge

Front 320

conjugated bilirubin is transported to the biliary system for

Back 320

excretion

Front 321

the ability to take up and conjugate bilirubin _____ the capactiy to excrete conjugated bilirubin

Back 321

exceeds

Front 322

if the excretion pathway is compromised by liver or biliary tract disease, it is _____ into the serum

Back 322

regurgitated

Front 323

once excreted into the biliary system, conjugated bilirubin is mixed with other excretory products to form

Back 323

bile

Front 324

where is bile stored?

Back 324

gall bladder

Front 325

what test can confirm that hemolysis is present?

Back 325

PCV

Front 326

initial diagnostic plan for icterus:

Back 326

determine hemolysis vs hepatobiliary

Front 327

diagnostic tests only tell you what has happened:

Back 327

in the past few hours

Front 328

diagnostic tests do not tell the ___ or the ___

Back 328

past or the future

Front 329

lab findings of unconjugated hyperbilirubinemia include:

Back 329

anemia (nonregen first, then regen), increase bilirubin, bilirubinuria after 3 days, liver enzymes normal at first but may increase after day 5, hemoglobinemia/uria

Front 330

lab findings of conjugated hyperbilirubinemia include:

Back 330

increased bilirubin, bilirubinuria, increased liver enzymes, increased bile acids

Front 331

___ can be toxic to renal cells

Back 331

hemoglobin

Front 332

animals die from the disease causeing _____ rather than from the direct result of ______

Back 332

icterus, hyperbilirubinemia

Front 333

micturition

Back 333

voluntary voiding of urine

Front 334

urinary incontinence

Back 334

lack of voluntary control over the passage of urine

Front 335

dysuria

Back 335

painful or difficult urination

Front 336

stranguria

Back 336

slow, painfully urination (obstruction, spasm of bladder neck and urethra)

Front 337

pollakiuria

Back 337

frequent storage attempts to urinate with voiding of small volumes

Front 338

reflex dyssynergia

Back 338

sudden interupttion of micturition

Front 339

enuresis

Back 339

involuntary passage of urine during sleep

Front 340

innervation of the urinary bladder

Back 340

pelvic and hypogastrric n

Front 341

innervation of the urethra

Back 341

pudendal n and hypogastric n

Front 342

pelvic n

Back 342

contains both afferent and efferent parasympathetic fibers. Primary nerve for both motor and sensory functions

Front 343

hypogastric n

Back 343

sympathetic fibers. Primary function is to facilitate detrussor relaxation during filling phase. Also innervates the internal urethral sphincter- faciliates urethral tone

Front 344

pudendal n

Back 344

mixed somatic nerve that innervates the external urethral sphincter. Maintains continence during fill phase and relaxes during voiding phase

Front 345

what center mediates the micturition reflex

Back 345

pons

Front 346

what is the long tract circuit

Back 346

tract from urethra/bladder to cerebral cortex

Front 347

detrussor m innvervation

Back 347

pelvic n

Front 348

detrusor atony

Back 348

failure of the bladder to contract, may be caused by disruption of tight junctions- chronic urethral obstruction or neurogenic causes

Front 349

how is electrical activity conducted from fiber to fiber in the detrussor m?

Back 349

tight junctions

Front 350

characteristics of the filling phase of micturition

Back 350

detrusor inhibited, sphincter stimulated

Front 351

characteristics of the voiding phase of micturition

Back 351

detrusor stimulated, urethra inhibited

Front 352

what is dysuria a sign of?

Back 352

lower urinary tract dz

Front 353

dysuria

Back 353

mucosal irritation or inflamation stimulates sensory receptors in bladder and urethra. This initates the micturition reflex.

Front 354

causes of dysuria

Back 354

inflammation/infection of bladder, urethra, prostate. Obstructive disorders (calculi, tumors, FLUTD), ofter assoc with hematuria and pyuria

Front 355

two things that can be confused with dysuria by owners

Back 355

polyuria, incontinence

Front 356

neurogenic incontinence

Back 356

lesions of nervous innervation and control

Front 357

nonneurogenic incontinence

Back 357

disease or anatominical defects of the lower urinary bladder

Front 358

what effect can a cerebral lesion have on micturition?

Back 358

can void bladder but no voluntary control, loss of house training, bladder is not distended

Front 359

what effect can a lesion on the brain stem and spinal cord rostral to sacral segments hve on micturition?

Back 359

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

Front 360

what effect can a lesion on sacral spinal cord, nerve roots and peripheral nerves hve?

Back 360

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

Front 361

nonneurogenic incontinence: differentials for distended bladder

Back 361

urethral obstruction, mass in bladder neck, detrusor-urethral dyssynergia, detrusor dysfunction

Front 362

nonneurogenic incontience: differentials for non distended bladder

Back 362

urethral incompetance, ectopic ureters, patent urachus, reduced bladder capacity, vesiculo-vaginal or ureterovaginal fistula

Front 363

diagnostic approach for bladder problems

Back 363

1) analyze history 2) observation and physical exam 3) classify problem-- dysuria, incontinence or a combo; neurogenic or nonneurogenic incontinence

Front 364

what do you palpate on the physical exam

Back 364

bladder, prostrate, urethra, empty bladder

Front 365

after observing micturition wht should you determine?

Back 365

residual volume in the bladder- should be less than 10 ml

Front 366

animals that are incontinent are very prone to

Back 366

UTIs

Front 367

if bladder is distended:

Back 367

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

Front 368

three major causes if bladder not distended

Back 368

urethral sphincter incompetence, urethral sphincter bypass, bladder contracting involuntarily at low volumes-- urger incontincence

Front 369

describe the bladder in an UTI

Back 369

usually small, may spasm during palpation, often feels hard

Front 370

what can induce urethral sphincter incompetance

Back 370

spay

Front 371

urethral incompetance can be associated with

Back 371

spay and neuter- more common in females

Front 372

what occurs with urethral incompetence?

Back 372

decreased urethral pressure, hormone receptors exist in urethral muscle- enhance resting urethral tone. When hormone levels are low the tone is decrased.

Front 373

how can you treat uretheral incompetence?

Back 373

hormone replacement therapty (females = estrogen), and alpha adrenergic drugs. Severe cases might require surgery

Front 374

Phenylpropanolamine

Back 374

a drug used to treat urethral incompetance

Front 375

does the timing of OHE affect development of urethral incompetance?

Back 375

it does not appear to

Front 376

what dogs tend to be more affected by urethral incompetance

Back 376

large dogs

Front 377

fever is a sign of?
1) infection
2) immune meidated disease
3) cancer
4) drug reaction
5) all of the above

Back 377

5) all of the above

Front 378

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

Back 378

4) diabetes mellitus

Front 379

the largest component of flatus is?

Back 379

nitrogen

Front 380

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?

Back 380

large bowel

Front 381

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

Back 381

d) excretion of bile into the biliary system

Front 382

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

Back 382

c) reduced urethral resistance

Front 383

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

Back 383

1) the most primary cause is primary anorexia

Front 384

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

Back 384

a) the most common form is dystrophic obesity

Front 385

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

Back 385

c) have increased venous hydrostatic pressure

Front 386

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

Back 386

c) decreased plasma oncotic pressure

Front 387

the first step in the POA approach is

Back 387

database collection

Front 388

substances that cause fever are called

Back 388

pyrogens

Front 389

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

Back 389

collecting ducts

Front 390

is water deprivation test appropriate for a dog that is 5-7% clinically dehydrated?

Back 390

no

Front 391

what is the primary difference in vomiting vs regurgitation?

Back 391

vomiting- food from stomach/prox duodenum, reflex mediated
regurgitation- passive, food from esophagus

Front 392

in chronic diarrhear what characerizes motility of the intestinal tract?

Back 392

often hypomotile (decreased or slowed)

Front 393

dogs and cats with lower urinary disease manifest what major clinical sign

Back 393

dysuria

Front 394

what is the cardinal sign of colorectal disease in dogs?

Back 394

constipation

Front 395

the most common type of anorexia is

Back 395

secondary

Front 396

the most common type of obesity is

Back 396

simple

Front 397

what is the most likely cause for a dug with generalized ventral edema and a low protein ascites

Back 397

hypoalbunimia