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Small animal GI > Final > Flashcards

Final Flashcards

1
Q

Avg max gastric capacity, comfortable capacity

A

80 ml/kg, 40-60 ml/kg

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2
Q

2 components of gastric filling

A

Receptive relaxation, accommodation

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3
Q

Where does accommodation occur

A

fundic region

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4
Q

Causes of dysfunction of filling

A

Inflammatory proces or neoplasia

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5
Q

Consequence of failure to receptively relax, accommodate

A

increase in post-prandial intragastric pressure causing vagal afferents to stimulate emetic center

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6
Q

What protects stomach from autodigestion

A

Gastric mucosal barrier: defense mechanisms- surface mucus, bicarb to neutralize, tight junctions between epithelial cells stopping H+ deep diffusion, mucosal blood flow of nutrition and bicarb to take away H+, tropic factors for growth/health of cells

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7
Q

Describe mucosal barrier damage

A

Back diffusion of H damages epithelial cells and tight junctions, allowing acid to penetrate deeper layers, histamine releases: tissue edema, dilation and leakage of capillaries which can hemorrhage and lead to ulcers/erosions

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8
Q

Erosions/ulcers more common in

A

Dogs

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9
Q

Secretions from: chief cells, endocrine cels, G cells, parietal cells

A

Chief: pepsinogen digestive hormone; endocrine: histamine; G- gastrin; parietal: H+

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10
Q

Activate proton pump in stomach

A

Vagus Ach to receptors for gastrin and H+ which activate H-K-ATPase

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11
Q

Stomach Rx- function of: Atropine

A

Blocks Ach from vagus - no gastrin

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12
Q

Stomach Rx- function of: Cimetidine

A

Blocks endocrine cells- no histamine

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13
Q

Stomach Rx- function of: omeprazole

A

H-K-ATPase to stop H+

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14
Q

When does stomach empty

A

When intragastric pressure exceeds duodenal pressure and pyloric resistance, physical and chemical composition of meal (pH, osmolarity, etc)

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15
Q

Meal composition effects on emptying- carb vs fat/protein

A

Carbs faster than protein/fat

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16
Q

Emetic center- what affects

A

cerebral cortex (anxiety), CRTZ (drugs, toxins, cardiac glycosides), oculo-vestibular system- motion (stimulates CRTZ first in dogs)

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17
Q

Three phases of the vomiting reflex

A

Nausea, retching, V

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18
Q

Define diarrhea

A

Increase in water content of feces changing freq, fluidity, volume

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19
Q

Fecal water sources

A

25% intake, remainder secretions

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20
Q

Water turnover- SI vs colon

A

Colon takes out less quantity, but 90% of what passes it, SI takes 50%- mostly fromJ and I

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21
Q

Where do cells from intestines start

A

Villous crypt cells, migrate upwards towards tips of villi

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22
Q

Crypt cell functions

A

When in crypt- secrete electrolytes/fluids; towards tip- absorptive

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23
Q

Why is there longer recovery time in parvovirus than acute diarrhea like dietary indescretion

A

Parvo and any disease which attacks crypt cells needs more time to repopulate- degree of disease and duration of recovery depends on where villi are attacked

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24
Q

Mechanisms of D; which most common

A

Osmotic, secretory, exudative, disordered motility, mixed; Mixed most common!

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25
Q

Mechanism of osmotic diarrhea

A

Osmotically active particles retained in GI tract from lack of digestion/absorption

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26
Q

Mechanism of secretory diarrhea

A

Stimulation of excess secretion overwhelms ability to absorb- loss of fluid, protein, +/- blood

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27
Q

Mechanism of exudative D

A

increased mucosal permeability from injury to barrier

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28
Q

What are the two most important diagnostics for any condition

A

Hx and PE

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29
Q

Name the 14 signs of GI dz

A

V, regurg, D, abd pain, tenesmus, dyschezia, hematochezia, constipation, flatus, salivation, shock, weight loss, anemia, appetite change

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30
Q

THreshold of normal cat V frequency

A

No more than 1/month

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31
Q

Clinical sources of V

A

GI vs non-GI (endocrine, neuro, metabolic, systemic, abdominal)

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32
Q

Does fasting improve osmotic diarrhea

A

Yes

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33
Q

Time needed for V to be chronic

A

2-3 weeks

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34
Q

Define delayed emptying parameter

A

more than 12 hours after eating

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35
Q

Main causes of acute V

A

single insult to stomach, proximal GI tract, pancreas

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36
Q

Which type of V is rarely self-limiting

A

Chronic

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37
Q

Does fasting improve secretory diarrhea

A

No, stimulation to secrete outpacing absorption is the cause

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38
Q

Regurgitation more common in

A

Dogs, rare in cats

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39
Q

EPI, intestinal dysbiosis, acute viral diseases will all cause what type of diarrhea

A

Osmotic

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40
Q

What differentiates V from retching

A

Retching/abdominal contractions

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41
Q

Premonitory signs of regurg

A

very few- some ptyalism in obstructive/esophageal inflammatory

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42
Q

Premonitory signs of V

A

ptyalism, pacing, swallowing, tachycardia (from nausea)

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43
Q

SI diarrhea- volume

A

normal to increased

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44
Q

SI diarrhea- mucus content

A

Rare, but can happen as disease progresses to include LI

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45
Q

SI diarrhea- blood

A

Melena (digested), rare

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46
Q

Flatulence and halitosis absent in

A

LI D

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47
Q

What kind of D caused by fat malabsorption

A

Osmotic and partially secretory (osmotically active particles, hydroxyl fatty acids converted by bacteria stimulate secretion)

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48
Q

SI diarrhea- frequency

A

Normal-mild inc (2-3x/day)

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49
Q

Dyschezia- type of D

A

LI

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50
Q

Enterotoxic e. coli causes what type of D

A

Secretory- stimulation of cAMP

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51
Q

Weight loss common in which D

A

SI

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52
Q

Increased urgency in what type of D

A

LI

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53
Q

Lymphangiectasia causes what kind of D

A

Exudative

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54
Q

LI diarrhea- volume

A

Normal to decreased

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55
Q

LI diarrhea- frequency

A

increased (>5x)

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56
Q

Tenesmus- type of D

A

LI

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57
Q

LI diarrhea- weight loss

A

Rare

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58
Q

What kind of D commonly has mucus

A

LI

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59
Q

Hematochezia from what kind of D

A

LI

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60
Q

Causes of constipation

A

diet, environment, anorectal dz, obstruction, neuro dz of spine, endocrine, metabolic, iatrogenic (opioids)

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61
Q

Low oncotic pressure (hypoalbuminemia) and high hydrostatic pressure (RHF, portal hypertension) causes what kind of D

A

Exudative

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62
Q

Cause of tenesmus

A

Distal alimentary (colon, rectum, anus) or urogenital system

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63
Q

Cause of flatus

A

Swallowed air or bacterial degradation of unabsorbed carbohydrates

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64
Q

What condition frequently has flatus

A

IBD

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65
Q

What condition in cats can cause ptyalism

A

Portosystemic shunt

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66
Q

Define malassimilation

A

Liver dysfunction- unable to convert food to useful molecules

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67
Q

Mechanism of bacterial translocation

A

Breakdown of GI mucosal barrier allowing bacteria into bloodstream

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68
Q

What causes sepsis

A

Bacterial translocation exceeds liver’s ability to filter them out

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69
Q

Most common causes of anemia in GI dz

A

tumor, ulcer, bleeding disorder, parasites; defective RBC production from malabsorption (B12) or bone marrow suppression

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70
Q

When patient has polyphagia or pica, thought think of

A

Increased utilization or malabsorption

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71
Q

Cat with increased appetite and weight loss- 4 ddx

A

Hyperthyroidism, IBD, GI lymphoma, DM

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72
Q

Dog with increased appetite and weight loss

A

DM, IBD, lymphoma, EPI

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73
Q

Top 7 signs of GI dz- high to low

A

D, V, appetite change, weight loss, tenesmus, abdominal pain, salivation

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74
Q

Common nutrient deficiency in chronic GI dz

A

Cobalamin

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75
Q

Fecal test for PLE

A

alpha proteinase inhibitor test- supposed to be in blood stream, in feces during PLE

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76
Q

Radiographs better for chronic or acute V and D; signs

A

Acute; ileus, effusion, foreign body, mass effect, pneumoperitoneum,

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77
Q

US utility in GI dz

A

non-specific changes, might show other issues or need for only FNA

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78
Q

Mutual interaction of microbiota with host cells is called

A

Intestinal microbiome

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79
Q

What are the normal intestinal microbiota

A

Bacteria, protozoa, archaea, viruses, fungi

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80
Q

Pros of characterizing microbiome with bacterial culture

A

Pro: can tell viability, susceptibility, analyze genotype, metabolism and virulence

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81
Q

Ways of characterizing microbiome via molecular technique

A

PCR, analysis of amplicons, qPCR/FISH quantification

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82
Q

What molecular technique answers “who is there?”

A

Analysis of amplicons- fingerprint, phylogenetic info

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83
Q

What molecular technique answers “What is there?”

A

PCR- specific genes

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84
Q

FISH and qPCR answer what question

A

How much is there

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85
Q

What study tells species, what they are doing, what they are making

A

Metagenomics

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86
Q

What % of gut bacteria is cultureable

A

5%

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87
Q

Where is there a spike in anaerobic, bacteroides, and spore forming anaerobes

A

Ileum to cecum

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88
Q

What starts almost non-existant and increases in number from D-J-I

A

Aerobes and facultative anaerobes

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89
Q

What are gut flora control mechanisms

A

gastric acid, bile salts’ Abx quality, intestinal motility to sweep, intestinal mucus helps motility, immune response, bacterial products stifling pathogenic bacteria

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90
Q

Function of archaea

A

Take H+ from fermentation and convert to methan (instead of HS which damages enterocytes and colonocytes)

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91
Q

Main fungi, main viruses

A

Yeast, bacteriophages

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92
Q

Where are TLRs found

A

Toll-like receptors are found on and in enterocytes luminal and apical borders

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93
Q

Function of TLRs

A

Communication with microbiota

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94
Q

What are the good bacteria and how do they inhibit pathogenic growth

A

Bacteriocins- compete for O2, nutrients and adhesion sites, create a physiologic restrictive barrier

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95
Q

What is the source of 7% of ME in dogs

A

VFAs from fermentation in colon

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96
Q

Most common pathogen colonization when bacteriocins fail

A

Salmonella, c. diff, campylobacter

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97
Q

Term for the overgrowth of commensals, what results from it

A

Intestinal dysbiosis- change of bacteria and communication with immune system leading to inflammation, cytokine and dz

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98
Q

How can EPI cause intestinal dysbiosis

A

True overgrowth from poor digestion of dietary nutrients

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99
Q

Microbiome causes of disease

A

Pathogen colonization, overgrowth of commensals, altered communication

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100
Q

Inflammatory bowel disease is a microbiome disease of what cause

A

Altered communication

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101
Q

Describe the altered communication route of disease, name two outcomes

A

TLRs and changes in T regulatory lymphocytes lead to altered immune response; underfunction leads to persistent inflammatory response (bc t-regs dont retreat once fixed); over-functioning can make T-regs retreat too soon and allow tumor development

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102
Q

What shift in dysbiosis stimulates an inflammatory response

A

Towards gram negative organisms

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103
Q

How should you tx histiocytic ulcerative colitis?

A

Abx (no longer immunosuppressives

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104
Q

What causes histiocytic ulcerative colitis

A

AIEC- adherent and invasive e. coli

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105
Q

Former and current approaches to change gut microbiome

A

Previously Abx (metronidazole and tylan) now using pre/pro/sym- biotics

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106
Q

What makes up prebiotics

A

non-digestible dietary carbs- fructooligosaccharides, bran, psyllium

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107
Q

Mechanism of prebiotics

A

Increase short chain FA

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108
Q

Benefits of probiotics

A

Improved epithelial barrier, modulation of immune system, inhibit pathogenic colonization

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109
Q

Minimum requirements for probiotic packaging

A

Reputable mfgr, list genus and species (+/- strain), 1x10^8 cfu/g

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110
Q

What org is in prostora

A

b. animalis

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111
Q

What org is in Proviable

A

mix of 7

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112
Q

Study outcomes of probiotics (4)

A

Evidence of shorter days to D resolution with some breed difference, improved fecal score, faster days to remission, increased T-regulator markers

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113
Q

What is the ultimate probiotic, what conditions has itbeen shown to help

A

Fecal transplant: IBD, ulcerative colitis, c. diff

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114
Q

Causes of dysphagia

A

Oral, pharyngeal and cricopharyngeal dz

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115
Q

Dysphagia can be secondary to

A

Pharyngitis or tonsilitis- oral cavity inflammation

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116
Q

Dysphagia ddx

A

oral or pharyngeal dz (or tongue), cricopharyngeal achalasia/asyncrhony, neuromuscular dz (myositis, myasthenia, trauma)

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117
Q

First dx of dysphagia, other useful followups

A

Survey rads of head, neck, chest for mass effect, neoplasia; fluoroscopy, EMG

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118
Q

What muscles make up UES

A

thryopharyngeus and cricopharyngeus

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119
Q

Site of achalasia

A

Cricopharyngeus

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120
Q

Dog vs Cat esophagus

A

dog- all skeletal; cat- lower 1/3 smooth muscle

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121
Q

Esophagus- rather than serosal layer beyond muscularis, have what layer

A

Adventitial thin coating

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122
Q

What causes stricture

A

Damage penetrates mucosa and submucosa and exposes muscularis where fibroblasts can make scar tissue

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123
Q

Describe primary peristaltic wave

A

Pharynx contracts as UES relaxes, activates nerve fibers to propagate swallowing reflex down esophagus, moves bolus to stomach via receptive relaxation of LES

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124
Q

Describe secondary peristaltic wave

A

Clearance mechanism- food that didnt make it to stomach with primary- distension of esophagus activates

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125
Q

Ages for congenital and acquired esophageal dz

A

Congenital young, older acquired

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126
Q

Causes of esophageal dz

A

Caustic/abrasive material ingestion, gastric reflux in anesthesia, doxy/clindamycin in cats

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127
Q

Name the four causes of regurgitation

A

Inflammatory disease (usually esophagitis), extraluminal compression, intraluminal obstruction, neuromuscular dz

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128
Q

Best dx for esophagitis

A

Endoscopy is the only definitive; might see stricture with contrast rads

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129
Q

Most common cause of extraluminal compression in regurgitation; name three others

A

PRAA- vascular ring anomaly; thymoma, intrathoracic tumor, hilar lymphadenopathy

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130
Q

Signs of PRAA present when?

A

6-8 weeks, weaning

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131
Q

Causes of intraluminal obstruction causing regurgitation

A

Stricture, foreign body, tumor, diverticulum

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132
Q

Dx stricture

A

Esophagram or endoscopy

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133
Q

Causes of stricture-

A

foreign body, drugs, anesthesia, tumor, esophagitis

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134
Q

Tx stricture

A

Balloon dilation, bougienage blunt dissection, steroids in lesion, mitomycin C chemo agent, +/- gastrotomy tube. PREVENT!! by tx esophagitis

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135
Q

Rx stricture

A

Omeprazole, cisapride, sucralfate liquid

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136
Q

Most common site of foreign body

A

thoracic inlet, heart base, distal esophagus

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137
Q

Causes of congenital megaesophagus

A

unknown, familial, efect in vagal afferents from esophagus

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138
Q

Tx foreign body

A

remove, push, sucralfate, omeprazole, rest with tube

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139
Q

Congenital megaesophagus ddx, differentiate between them

A

R/o vascular ring anomaly- usually focal/segmental dilation; true congenital is generalized

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140
Q

regurgitation, ptyalism, inappetance, nasal d/c, +/- cough and fever- name the condition

A

Esophageal dz

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141
Q

Causes of acquired megaesophagus, name biggest category

A

tox (lead, organophosphates), endocrine (hypoadreno, hypothy), neuromuscular (myasthenia, polyneuritis/myositis); Idiopathic most common

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142
Q

Megaesophagus congenital breeds

A

GSD, irish setter, mini schnauzer, great dane

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143
Q

Dx megaesophagus

A

Survey rads- d not use barium!; CBC for aspiration, serum chem for neuro/addisons, CK for myositis

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144
Q

What tests for myasthenia gravis

A

Ach receptor Ab test

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145
Q

What tests for organophosphate toxicity

A

Cholinesterase activity

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146
Q

Tx megaesophagus

A

fluids, nutrition, elevation, tx aspiration if present

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147
Q

Tx myasthenia gravis and myositis

A

pyridostigmine and prednisone

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148
Q

What is the most common cause of acute vomiting in the dog and cat

A

acute gastritis

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149
Q

Mechanism of acute gastritis

A

Mucosal damage from food/foreign/etc results in increased permeability for acid and inflammatory irritation of vagal afferents for emetic center

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150
Q

What causes hematemesis in acute gastritis

A

Necrosis and erosion of epithelial cells

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151
Q

What is the most common sign of acute gastritis

A

V

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152
Q

Acute gastritis Ddx

A

gastric foreign body, obstruction; acute pancreatitis, infectious dz (parvo, corona), systemic (liver, kidney, toxin)

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153
Q

Most effective tx for acute gastritis

A

Brief fast (12-24 h)

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154
Q

Define chronic gastritis

A

Persistent insult present in GI

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155
Q

Causes of chronic gastritis

A

Inflammatory (lymphoplasma, eosino), FRD, helicobacter gastritis, reflux gastritis (bilious V syndrome)

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156
Q

CS of lymphoplasmacytic chronic gastritis

A

V, hematemesis, appetite change in cats

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157
Q

T/F degree of cellular infiltrate corresponds with degree of CS in chronic gastritis

A

False

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158
Q

Rx- lymphoplasmacytic chronic gastritis

A

Acid reducer (omeprazole or famotidine); prokinetic (cisapride, metoclopramide); prednisone +/- rx to increase

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159
Q

Rx to add to pred for dogs with lymphoplasmacytic chronic gastritis

A

Azathioprine or cyclosporine

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160
Q

Rx to add to pred for cats with lymphoplasmacytic chronic gastritis

A

Chlorambucil

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161
Q

Gross lesions- eosinophilic inflammatory chronic gastritis

A

Nodules filled with eos

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162
Q

eosinophilic inflammatory chronic gastritis breeds

A

Rotties

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163
Q

Tx eosinophilic inflammatory chronic gastritis

A

dietary manipulation +/- corticosteroids

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164
Q

Cause of helicobacter chronic gastritis

A

h. felis

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165
Q

Vomiting, lethargy, polydipsia, hematemesis, mild-moderate cranial abdominal pain- name the condition

A

Acute gastritis

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166
Q

Patient has chronic vomiting and all other causes have been r/o, what should you test for?

A

Helicobacter via warthin-starry stain

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167
Q

Tx helicobacter

A

amoxicillin with clarithromycin +/- metronidazole

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168
Q

Mechanism of bilious vomiting syndrome (reflux gastritis)

A

defect in pyloric sphincter tone allowing reflux or gastric motility allows prolonged contact of bile with mucosa

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169
Q

T/F helicobacter can cause ulceration in dogs and cats

A

False

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170
Q

What kind of substance is bile

A

Detergent

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171
Q

Tx bilious vomiting syndrome

A

BID feeding, prokinetic (cisapride, metoclopramide), acid reducer (omep or ranitidine)

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172
Q

Why is ranitidine indicated for bilious V synd

A

Has some possible prokinetic effect on stomach

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173
Q

Ulcer vs erosion

A

ulcer penetrates to muscularis, erosion only to submucosa

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174
Q

Causes of ulcer/erosion

A

Drugs (steroids and NSAIDs), liver dz (shunts, portal hypertension), tumors, malnutrition, uremia/stress?

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175
Q

Tumors that cause ulcer/erosion

A

mast-histamine release, gastrinoma- gastrin release, LSA

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176
Q

Cause of lymphoid follicular hyperplasia lesions and bx result lymphocytic gastritis

A

Helicobacter gastritis

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177
Q

Dx ulcer

A

Endoscopy! (also contrast rads, biopsy)

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178
Q

Best Tx ulcers

A

Omeprazole PPI- longest/greatest acid reducer, tx underlying dz

179
Q

Causes of gastric outlet obstruction

A

GDV, gastric tumor, foreign body, stenosis

180
Q

Types of stenosis, which more common, breeds predisposed

A

Congenital- boxers, bulldogs, boston, cats- pyloric; Acquired– male small breeds (lhasa, shih, pekingese)- antral

181
Q

Blood findings in advanced gastric outlet obstruction

A

Hypochloremia, hypokalemia, metabolic acidosis

182
Q

Most common gastric tumor in dogs

A

adenocarcinoma in distal stomach at antrum angularis incisra- circumferential

183
Q

Most common gastric tumor in cats

A

LSA

184
Q

What is the cat puke worm

A

Ollulanus

185
Q

Dog vomits first thin in the morning before eating, green yellow with a little bit of blood- waht is this?

A

Bilious vomiting syndrome

186
Q

Tx gastric parasites

A

Pyrantel or fenbendazole

187
Q

Most common gastric parasite, CS

A

Physaloptera from dung beetle; chronic V

188
Q

Life threatening SI diarrhea causes

A

Parvovirus, intussusception

189
Q

Life threatening LI diarrhea causes

A

Pythium, histoplasmosis

190
Q

Causes of infectious acute diarrhea

A

Parasitic (helminths and protozoa), bacterial (clostridium>e.co, salm, campylo), viral (parvo, corona)

191
Q

Name 3 helminths

A

ascarids (round), whips, hooks

192
Q

See beak sign on rads- what is this?

A

Contrast funneling through plyorus= gastric outlet obstruction

193
Q

Coccidia, giardia, cryptospor, tritrich are all what parasite type

A

Protozoa

194
Q

Which parasite causes worst CS

A

hookworms

195
Q

What fecal test is best for motile parasites

A

Direct smear

196
Q

What fecal test is most sensitive for giardia

A

ELISA or PCR

197
Q

Clostridium primarily causes what type of D, how?

A

Large intestine; Undergoing sporulation and releasing enterotoxins

198
Q

Y-U pylorostomy and pyloromyotomy tx for?

A

Gastric outlet obstruction (muscular cutting)

199
Q

Intermittent V becoming projectile, contains food hours after eating, starting to show signs of hypo-Cl, K, metabolic acidosis

A

Aquired stenosis causing gastric outlet obstruction

200
Q

Tx clostridium

A

Metronidazole, amoxicillin

201
Q

Dx coronavirus

A

EM of fresh feces, PCR

202
Q

Which viral D agent will show signs of fever, leukopenia

A

Parvo (not coronavirus)

203
Q

Tx coronavirus

A

Self limiting, resolution in 1.5 weeks

204
Q

Depression, strawberry jam diarrhea, V +/- blood, prolonged CRT, normal MM

A

Hemorrhagic gastroenteritis

205
Q

Hemorrhagic gastroenteritis- labs

A

Increased PCV, normal TP, thrombocytopenia, metabolic acidosis

206
Q

Tx Hemorrhagic gastroenteritis

A

12-24 hr NPO until V stops, antiemetics, fluids, electrolytes (titrate fluids to normal PCV)

207
Q

Name two extra-intestinal causes of D

A

Addison’s and hyperthyroidism

208
Q

Sudden onset of D, vomiting rare, orange smelly feces; resolves in 8-10 days

A

Coronavirus

209
Q

What causes feline panleukopenia

A

Parvovirus

210
Q

Mechanism of parvovirus

A

Fecal-oral transmission, Epitheliotropic enterovirus invading rapidly dividing cells lining intestinal tract

211
Q

Parvovirus breed susceptibility

A

Black and tans

212
Q

Incubation time of parvovirus

A

3-7 days before shedding in feces; can shed 5-6 days before CS; remember subclinical infections in adults-

213
Q

Where does parvo replicate, travel?

A

oro-pharyngeal lymph tissue (LN, tonsils) then circulates to other lymphoid tissue, bone marrow, intestines

214
Q

Parvo- cbc findings

A

lymphopenia with first neutropenia due to bone marrow invasion/necrosis and their short half life

215
Q

What kind of diarrhea is parvo and why

A

Exudative bc epithelial cell loss leads to exposed lamina propria

216
Q

What day will some regrowth of epithlium be seen? What day will they start to look normal

A

7, 8 (when diarrhea resolved)

217
Q

Parvo CS

A

D and V from subclinical to peracute, fever

218
Q

Dx parvo

A

EM fresh feces, intestinal histopath, ELISA

219
Q

If parvo patient is hypoproteinemic- tx

A

Plasma/albumin

220
Q

Parvo abx

A

cephalosporin, amikacin, enrofloxacin

221
Q

Antiemetics- parvo

A

Metaclopramide CRI, cerenia (some dont respond), ondansetron

222
Q

Two alternative parvo tx

A

Feline omega interferon, hyperimmune plasma

223
Q

Best tx for parvo

A

Good nursing

224
Q

Nutrition approach in parvo

A

EEN- early enteral nutrition- prevents further breakdown of gut barrier leading to shock that can be caused by fasting

225
Q

Parvo- monitoring parameters

A

Glucose, PCV/TP, weight, electrolytes, azotemia

226
Q

Major causes of chronic D in dog

A

IBD, ARD, FRD, intestinal parasites, lymphangiectasia, EPI, intestinal neoplasia, fungal

227
Q

Major causes of chronic D in cat

A

IBD, intestinal tumors (diffuse), FRD, ARD, viral, intestinal parasite

228
Q

Age and chronic D

A

Younger- parasites, older- neoplasia, IBD

229
Q

Vomiting indicates what kind of diarrhea location

A

Upper GI, but can be any part

230
Q

What type of D is dehydration most seen in

A

Acute- chronic compensates

231
Q

How does chronic D hypoproteinemia present

A

subcu edema on ventral neck, pitting edema in legs of large breed, ascites in small breed

232
Q

Severe V and D, fever, depression, leukopenia, dehydration

A

Parvovirus

233
Q

Why is Ca decreased in chronic D

A

hypoalbuminemia affects bound portion

234
Q

What part of chronic D causes panhypoprot’a

A

PLE, hemorrhage

235
Q

Dx FRD

A

Diet trial for 2-4 weeks, takes 6-8 weeks to resolve

236
Q

Cause of ARD

A

Altered or increased bacteria from antibiotics, abnormal host response

237
Q

Most important dx in ARD/intestinal dysbiosis

A

Cobalamin- tx not successful if low

238
Q

Mechanism of cobalamin loss

A

cobalamin+R protein in stomach –> IF (intrinsic factor) from parietal cells/stomach/pancreas –> IF needed to bind receptors in ileum for cobalamin uptake

239
Q

Species difference- cat cobalamin

A

IF only comes from pancreas, not stomach, so this is why pancreatitis often linked to enteropathies- lack of production

240
Q

Dx LI chronic D; name best

A

Diet trial, clostridium test, response to deworm or Abx, contrast radiography for intussusception; colonoscopy/bx

241
Q

Rx for chronic D

A

metro, tylan

242
Q

Define IBD

A

Disorder of SI characterized by persistent or recurrent GI signs and histo evidence of inflammation

243
Q

Describe IBD infiltration

A

Lymphocytes and plasmacytes invade lamina propria

244
Q

Pathogenesis of IBD

A

Alteration in TLRs, Epithelial lining, immune system receptors under epithelial layer- genetic loss of tolerance to bacterial or food antigens; environmental; microbiome;

245
Q

Most important TLRs in dogs

A

4 and 5, esp in GSD- altered expression leads to risk

246
Q

What causes the cinical signs of IBD

A

mucosal cell infiltrates and inflammatory mediators (complement, leukotrienes, inflammatory cytokines, etc)

247
Q

IBD breeds

A

Nasenji, lundehund, wheatons, irish setters

248
Q

Most common sign of IBD in cats

A

V clear foam/bile

249
Q

Cats or dogs, more PLE in IBD

A

Dogs, so cats no edema (but more mesenteric LN enlargement)

250
Q

Dx IBD

A

BIOPSY via endoscopy or laparotomy- confirm inflammation, r/o infection/neoplasia

251
Q

IBD-SI endoscopic findings

A

50% normal grossly, erythema, erosions, lymphangiectasia, granular, friable

252
Q

IBD-SI histo

A

Mucosal atrophy, villous atrophy, erosion, eos debris in crypts, lymphangiectasia

253
Q

Tx SI IBD

A

diet –> abx –> steroids

254
Q

Effect of steroids on IBD-SI

A

dec neut migration, dec mac fxn, dec cytokine production, inhibit arachidonic acid pathway of inflammation

255
Q

IBD-SI Rx

A

Pred, dex (more potent, less dosing), budesonide (better for liver, suppresses HPA axis)

256
Q

Taper IBD-SI steroids

A

25% reduction q 2-4 weeks to lowest effective dose

257
Q

Alternative IBD-SI Rx

A

Azathioprine, cyclosporine, chlorambucil

258
Q

Use and benefit of azathioprine in IBD-SI

A

Cheaper, combine with pred, use in PLE/large breed cases

259
Q

Rx IBD-SI with PLE

A

cyclosporine (or pred/aza)

260
Q

Adjunctive tx for IBD- SI

A

plasma/alb, cat cobalamin, nutrition, pancreatic enzymes

261
Q

Tx IBD-LI, mild

A

Diet- hypoallergenic or high fiber; Rx- metronidazole

262
Q

Tx IBD-LI, moderate-severe

A

Sulfasalazine or pred- sulfasalazine wont compromise bx results

263
Q

D, hematochezia, tenesmus- used to be called IBD

A

Histiocytic ulcerative colitis from AIEC (adherent/invasive)- large intestine disease

264
Q

HUC tx

A

NO STEROIDS- enro +/- amoxicillin/metronidazole - some need long term

265
Q

What specific cell type is in HUC

A

PAS+ macrophages

266
Q

FRD diet recommendation

A

Hypoallergenic (no cross linking to Ig); novel protein, bland

267
Q

What type of dz is fiber response colitis

A

Mostly LI

268
Q

Most frequent breed with intestinal dysbiosis

A

GSD

269
Q

Tx intestinal dysbiosis

A

tylan, amox, tetracyc metro/enro, probiotics, fecal transplant

270
Q

Mechanisms of PLE

A

Lymphatic obstruction/rupture, increased mucosal permeability (exudative), mechanical (ulcers)

271
Q

Dz assoc with PLE

A

inflammatory, infectious infiltrative, neoplasia (LSA, mast), lymphangiectasia, addisions

272
Q

Primary vs secondary lymphangiectasia

A

1- congenital, 2- inflammation obstruction

273
Q

Lymphangiectasia- breed most common

A

Yorkie

274
Q

Lymphangiectasia- CS

A

muscle wasting, edema, ascites, pleural effusion- clear transudate- panhypoproteinemic (30-40% are hypoalb only due to increased immune Ig)

275
Q

Define hypoproteinemia in lymphangiectasia

A

Loss of protein-rich lymph

276
Q

2 main causes for panhypoproteinemia

A

GI loss or hemorrhage

277
Q

Other causes of hypoalbuminemia

A

liver dz, kidney loss

278
Q

Loss of protein in Lymphangiectasia leads to a decrease in what minerals

A

Ca–> vitamin D

279
Q

Dx Lymphangiectasia

A

Intestinal biopsy- dilated lymphatics

280
Q

Cause of lymphopenia in Lymphangiectasia

A

Loss of lymphocytes to GI tract

281
Q

Mainstay Tx Lymphangiectasia

A

low fat diet (to reduce chylomicrons in blood to increase flow)- Purina HA (low fat and hydrolyzed)

282
Q

Causes of infectious colitis

A

Clostridium, pythium, prototheca, histoplasma

283
Q

Geography of clostridium

A

Gulf atlantic states

284
Q

Clostridial infection- location, CS

A

LI chronic D

285
Q

Drug response dx for clostridium

A

Metronidazole, amoxicillin

286
Q

Location of pythium

A

ileo-colic junction but can be anywhere dermal or GI- not usually both

287
Q

Dx pythium

A

Abdominal LN enlargement, org in intestinal wall

288
Q

Infectious colitis source from Ohio river valley- rectal scrape, LN aspirate, wall aspirate all dx

A

histoplasma

289
Q

Exocrine panc fxn

A

Digestive enzymes and cofactors into duodenum via acini and ducts with buffer for enzymes

290
Q

Speckled/perpendicular striation pattern of mucosal layer of intestine on U/S- dz

A

Lymphangiectasia

291
Q

Endocrine panc fxn

A

into portal blood- islets with hormones to portal vein

292
Q

Test for histoplasma

A

histo/blasto Ag with GI signs only

293
Q

Panc enzyme synthesis location

A

RER

294
Q

How are digestive enzumes from panc secreted

A

Zymogens

295
Q

Yorkie with ascites, muscle wasting, panhypoprot, hypoCa, hypoMg, low cholesterol, low vitamin D- name the dz

A

Lymphangiectasia

296
Q

Pancreatic enzymes

A

Amylase, lipase, proteolytic, trypsinogen

297
Q

How are proteolytic enzymes secreted

A

In inactive zymogens to have terminal am ac removed to activate

298
Q

What mineral is critical to activation of pancreatic zymogens

A

Calcium

299
Q

Path/actions of trypsinogen

A

T’gn from panc to GI lumen, enterokinase in brush borders of enterocytes of duodenum converts to trypsin by making an active site for further zymogens

300
Q

Inhibitory mechanism of trypsin, source

A

PSTI (panc secretory trypsin inhibitor) filling active site on trypsin- secreted at same time from acinar cells, works in duct areas

301
Q

Mechanisms stopping autodigestion of the pancreas

A

PSTI, intracellular compartmentalization (zymogens separate from lysosomes), proteases formed and secreted inactive and activating factors in duod (enterokinase), maintenance of low intracell-Ca (activation cofactor)

302
Q

Alpha1-proteinase inhibitor function

A

Binds trypsin in blood stream so proteases not activated outside GI

303
Q

Alpha1-macroglobulins

A

Form buffer around trypsin to block active site so proteases not activated outside GI

304
Q

Age groups for cat/dog pancreatitis

A

Dog >4yr, Cat >1yr, usually chronic but can be acute

305
Q

Pathogenesis of pancreatitis

A

Co-localization theory- apical block at ductal level from obstruction, inflammation, edema leads to build up of lysosomes and zymogens, causing intermixing and fusing with each other, activating trypsin intracellularly- PSTI stops some, but is overwhelmed- causes autodigestion–> inflammation, edema –> hemorrhage, necrosis and moves on to peri-pancreatic fat

306
Q

Risk factors of pancreatitis

A

Dietary indescretion, panc ischemia (trauma, anesthetic hypertension), duodenal reflux of bile, drugs (not steroids), duct obstruction, genetics, idiopathic 50%

307
Q

Dog CS pancreatitis (most to least)

A

V, weakness, abdominal pain, dehydration, D (LI, colon in chronic)

308
Q

Cats CS pancreatitis (most to least) +acute signs

A

Lethargy, anorexia, dehydration; acute: hypothermia, subtle abdominal pain

309
Q

Co-diseases for pancreatitis

A

IBD, cholangiohepatitis (triaditis)

310
Q

Cat labs pancreatitis

A

anemia in >1/3, dehydration, +/- leukocytosis

311
Q

Dog labs pancreatitis

A

Neutrophilia with left shift (inflammation), thrombocytopenia

312
Q

Both dog and cat labs- pancreatitis

A

Pre-renal azotemia, hypoalbuminemia (esp in dogs with peritonitis), hyperglycemia, hypoCa, hyperlipidemia, hyperbilirubinemia, increased liver enzymes

313
Q

Dog vs cat pancreatic anatomy

A

Dog bile duct joins with panc duct in wall of duod near papilla, cat joins before entering wall- probable reason for triaditis in cats- IBD stops flow, backs up and liver and panc are affected

314
Q

Dx pancreatitis

A

cPL and fPL 200/400

315
Q

Snap test- cPL, fPL- limitations

A

Good sensitivity (no false neg), poor specificity (foreign body, panc tumor, GI inflamm)

316
Q

Test to confirm pancreatitis Snap

A

Pancreatic lipase test >400

317
Q

U/S changes in pancreatitis

A

hypoechoic pancreas enlarged, hyperecholic fat surrounding- fibrosis might make it look normal if previously dz’d

318
Q

Tx pancreatitis

A

Fluids, electrolytes +/- K supp, analgesics (buprenorphine, oxymorphone, fentanyl), anti-emetics (metaclop, maropitant, ondansetron), parenteral Abx if risk of translocation, early enteral nutrition via E, G, NG, NE- low fat!

319
Q

EEN study results

A

Early enteric nutrition tx in pancreatitis showed less V than parenteral but more post-prandial pain

320
Q

Indications for pancreatitis sx

A

Pancreatic abscesses, prolonged bile duct obstruction

321
Q

When can steroids be used in cats with pancreatitis

A

When biopsy has confirmed diagnosis

322
Q

What is EPI

A

lack of pancreatic enzymes due to defenerative atrophy in dogs- esp GSD and mixes

323
Q

What causes EPI in cats, CS

A

Chronic pancreatitis: polyphagia, weight loss, steatorrhea, voluminous D

324
Q

Dx EPI

A

Trypsin-like immunoreactivity TLI

325
Q

Tx EPI

A

Powdered enzymes, oral Abx, cobalamin

326
Q

Exception of blood from from tributaries of GI organs to liver

A

Rectal vessels straight to venous system

327
Q

Liver function

A

Metabolic filter to remove nutrients (carb metabolism to make/store glucose; lipid and protein metab) vitamin storage/conversion, toxins, GI tract immunity (translocated GI bacteria filtering)

328
Q

Blood flow into and out of liver

A

Portal vein + hepatic artery into liver, branch to venules/arterioles to capillary beds- feed sinusoids, come out hepatic veines to vena cava

329
Q

Cause of ALP, bili and GGT rise in cats with pancreatitis

A

Early merge of bile duct and pancreatic duct makes GI-inflammatory obstruction back up all three systems

330
Q

How does biliary system flow in liver

A

Countercurrent to portal vein and hepatic arteries

331
Q

Biliary vessel tract

A

Biliary vessels join into bile duct, merge into common bile duct, out to pancreas then to GI tract via duodenal papilla

332
Q

Liver lobule arrangement

A

lobule radially arranged around central hepatic venule with portal triads at periphery

333
Q

Lobular terminology- define

A

centered around central vein taking blood out of liver via hepatic veins, portal triad at margins of lobule= lesions described as per-portal (around triads) or centrilobular (around central vein)

334
Q

Increased appetite, decreased weight, large stool volume and frequency, steatorrhea-

A

EPI

335
Q

Alternative terminology for hepatocytes

A

Acinar- portal triad in middle, each point of hexagon a central vein; periportal, intermediary and central vein zones (1-3)

336
Q

Portal triad

A

hepatic a, portal v, biliary duct

337
Q

Sinusoids in liver lined by

A

Hepatocytes

338
Q

Liver immune cells

A

Kupfer cells

339
Q

Location of stellate and dendritic cells in liver

A

Between vascular wall and hepatocytes (space of dis)

340
Q

Detox and excretion functions of the liver

A

hepatic biotransformation of lipophilic compounds to promote excretion, metabolism of steroids, bilirubin, ammonia activate or clear drugs,

341
Q

Ammonia

A

Byproduct of protein metabolism in liver

342
Q

Why are liver dz hard to diagnose early

A

Vague signs due to functional reserve and regeneration

343
Q

% of the liver that can be lost without evidence of dysfunction

A

70

344
Q

Most specific CS of liver dz

A

Jaundice of oral mucosa, skin, sclera- cats soft palate way early!

345
Q

Forms of portal hypertenison

A

Primary- obstruction (cirrhosis fibrosis) or secondary to obstruction further upstream than the liver causing backflow

346
Q

Causes of low protein ascites

A

Portal hypertension, hypoalbuminemia (liver not making enough)

347
Q

Causes of high protein ascites

A

RHF causing CaVC backup into hepatic veins, HWDz caval syndrome, mass lesions, thrombi in vena cava or hep vein

348
Q

Cats- liver disease differences

A

Ascites uncommon, no cirrhosis, RHF congestion to chest

349
Q

ALT increase in cats NOT from primary hepatic dz

A

Hyperthyroid

350
Q

Copper eyed cat

A

Liver shunt

351
Q

Define reactive hepatopathy

A

Dz elsewhere impacts liver- ex IBD, LSA in GI, periodontal dz- cytokines and bacteria from GI

352
Q

Greatest increases in liver enzymes indicates

A

Necrosis

353
Q

Leakage/cellular damage enzymes

A

ALT, AST (think almost always liver leakage and sometimes)

354
Q

T/F liver enzymes are not markers of function

A

True

355
Q

Liver-specific enzyme found in cytoplasm

A

ALT

356
Q

Widespread, acute necrotic damage to liver will cause very high elevation of what

A

AST

357
Q

Liver pseudofunction tests, name and define

A

(pulled from blood by liver, but liver not only source of abnormal level) Bili, albumin, BUN, Gluc, cholesterol

358
Q

Causes of increased bilirubin

A

Pre-hepatic (hemolysis), hepatic (hepatitis, lipidosis, neoplasia, cirrhosis, etc), post-hepatic (panc-, cholang-, cholecyst-itis, liths, biliary neoplasia, GB mucocele, dudoenal dz)

359
Q

First liver enzyme to leak in cell damage

A

ALT

360
Q

AST > ALT

A

Probably muscle, not liver, check CK- if it is from the liver, more irreversible damage done

361
Q

ALP comes from

A

Bone, liver, drugs (+others with short half-lives) (different isoenzymes)

362
Q

Location of cholestatic liver enzymes

A

Membrane bound (ALP, GGT)

363
Q

Liver cholestasis enzymes

A

ALP, GGT

364
Q

Bilirubinuria- form excrete

A

conjugated (water soluble)

365
Q

Dog vs cat bilirubinuria differences

A

dog has low renal threshold for conj bili, common in urine- cat has high so bili in urine is significant

366
Q

Path of bilirubin

A

Mostly unconjugated bili in blood, liver conjugates, dumped into bile, gets unconjugated back to blood

367
Q

Dog vs cat ALP

A

Cat only 6 hr half life (72 in dog)- ALP always significant in cat

368
Q

Ddx of low albumin from liver dz

A

PLE and PLN (anorexia will not cause)

369
Q

Steroids increase what liver enzyme in dogs but not cats

A

ALP (alk phos)

370
Q

BUN in liver dz- high or low? why?

A

Low BUN bc liver converts ammonia to urea

371
Q

Liver true function tests

A

Blood ammonia, serum bile acids, post-prandial bile acids

372
Q

Causes of high blood ammonia

A

Bypass liver in PSS, hepatitis not allowing uptake, cirrhosis acquired shunts

373
Q

Biliary neoplasia is a _____ cause of bilirubinemia

A

post-hepatic

374
Q

Effect of high serum bile acids on liver

A

No contribution to hepatic enceph or anything negative- stable in serum

375
Q

Why is GGT more specific for liver than ALP in dogs

A

ALP is steroid inducible

376
Q

If patient is icteric, dont need to do what test?

A

Serum bile acids- bc bili follows same metabolic pathway, so if that is elevated, you already know there is something wrong with that system

377
Q

What type of test is serum bile acids

A

Liver true function test- yes or no to normal function, not what type

378
Q

What does very high (over 100) pre or post bile acids indicate

A

PSS - dont go this high in regular dysfunction

379
Q

Describe fasting bile acids

A

fast, give a meal, GB dumps in BA to SI, reabsorbed in ileum, taken up by liver and small amount escapes (bump from pre to post prandial)

380
Q

Effect of PSS/parenchymal dz on BA

A

When liver not functioning or being bypassed, more bile acids get past the liver

381
Q

How could fecal evidence of GI bleed indicate liver dz

A

Clotting function, portal hypertension backup leading to exudate

382
Q

Liver disease- rads or U/S better?

A

Rads- can see size, effusion, ascites

383
Q

Pros and cons of aspiration cytology in liver dz

A

not invasive, good for neoplasia, lipidosis, not good for inflammatory, cant tell where lesions are

384
Q

Best way to get bx in liver dz

A
  • laparoscopy
385
Q

Causes of hepatocellular damage

A

Toxins (sago), drugs, infection (lepto), idiopathic/unseen

386
Q

ALP

A

Hepatocellular damage much more likely than cholestasis

387
Q

Magnitude of increase of ALT indicates

A

Severity of hepatocellular damage

388
Q

T/F- biopsy useful in dx hepatocellular damage

A

False

389
Q

Tx for hepatocellular damage besides supportive/antiemetics

A

Antioxidant therapy- N-acetlycysteine IV, silymarin, SAMe

390
Q

Define extrahepatic bile duct obsruction

A

Any impairment of bile flow in biliary system between liver and duod (intra to extra hepatic bile ducts, common, cystic)

391
Q

Causes of extrahepatic bile duct obstruction in dog: top two most common

A

Pancreatitis #1, GB mucocele (+ tumors, stones rare)

392
Q

Causes of extrahepatic bile duct obstruction in cat: top two most common

A

Biliary neoplasia, liver flukes

393
Q

CS- EHBDO

A

inapp, icterus, V (esp in dogs with panc involved)

394
Q

Dx EHBDO

A

U/S, cofirm via laparotomy catheterize duodenal papilla

395
Q

Chronic hepatitis ddx

A

lepto, chronic infection

396
Q

Causes of Chronic hepatitis

A

drug induced (phenobarb, rimadyl), copper, diet toxin, breed, idiopathic

397
Q

Copper-associated hepatopathies- breeds

A

dobie, westie, dalmatian, lab

398
Q

Copper storage dz breed and cause

A

Bedlington- COMMD1, MURR1

399
Q

ALP&raquo_space; ALT, icterus, inappetence

A

EHBDO

400
Q

Copper-associated hepatopathies- CS

A

Non-specific, wax/wane, acute illness with weight loss (or can be icterus w/o illness)

401
Q

Best Dx for Copper-associated hepatopathy and findings

A

Bx- mononuclear inflammation (no neuts- infection), single cell/piecemeal necrosis

402
Q

Bile duct hyperplasia indicates-

A

Chronic inflammation

403
Q

Bridging indicates

A

Fibrosis replacing irreversibly danaged cells then connecting betwee portal tracts- Far progression, poor prognosis

404
Q

Dx copper

A

Bx- rhodanine stain red, quantitative tissue analysis >400 ug/g

405
Q

Differentiate between chronic hepatopathies and reactive hepatopathies-

A

Necrosis makes it chronic hep, (but no necrosis found does not mean its NOT, just should consider RH)

406
Q

Primary copper vs secondary copper

A

Primary- found in centrilobular around vein; secondary from infection in periportal area (think PC-SP)

407
Q

Tx chronic hepatopathy

A

Pred with ALT monitoring until it plateaus

408
Q

Good bile acids

A

Hydrophilic

409
Q

Patient feels good but has mild elevation in enzymes- what should you think of

A

Reactive hepatopathies- like abdominal disease, oral disease)- consider before starting steroids for chronic inflammation

410
Q

UDCA- function, main SE

A

increases bile flow by thinning bc hydrophillic, contracts GB, anti-ox and antiinflamm; V

411
Q

When should UDCA be used

A

Evidence of cholestasis add-on therapy

412
Q

Tx copper hepatitis

A

D-penicillamine, trientine- chelation tx; Zinc to prevent GI absorption- DONT use WITH chelator

413
Q

Mechanisms of liver fibrosis

A

Stellate cells activated to fibroblastic cells when liver injured, replace parenchyma= less compliant

414
Q

Regenerative nodules in liver indicate

A

Normal age change and chronic hepatitis

415
Q

Persistent increase in ALT and ALP (but less) progressing to ALP >ALT, low albumin, BUN, chol; hyperbili +/- abnormal BA

A

Copper associated hepatopathies

416
Q

Cirrhosis- describe

A

Consequence of long term damage causing diffuse fibrosis, losing liver function bc less tissue- end stage of chronic liver dz

417
Q

Cirrhosis- CS

A

Inapp, encephalopathy, weight loss, icerus first, ascites or peripheral edema

418
Q

Describe portal hypertension’s role in ascites

A

In cirrhosis, Starling forces increase hydrostatic pressure and pushes fluid out to abdomen- less circulating volume- activate RAS system to retain water and Na, which worsense ascites

419
Q

Cause of hepatic encephalopathy-

A

loss of detox function and acumulation of toxic metabolites (esp ammonia, others hard to measure)- toxic to neurons, act as false neurotransmitters

420
Q

Dx hepatic encephalopathy-

A

bile acids test (fasting ammonia might be WNL due to no liver challenge) to confirm liver dysfunction

421
Q

Tx ascites from cirrhosis

A

antagonize RAS system aldosterone- spironolactone diuretic

422
Q

Tx hepatic encephalopathy-

A

Lactulose po or enema to change colon pH so ammonia converted, Abx (neomycin, amox) to stop bacteria converting protein to ammonia (acute, not helpful in long term)

423
Q

Why cant’ ALP be monitored in tx chronic hepatitis

A

Steroid administration will raise the enzyme level

424
Q

CPSS, PSS- describe

A

Some connection between portal and systemic system bypassing liver

425
Q

ALP elevated without bilirubin elevation

A

Vacuolar hepatopathy

426
Q

What is the most common cause of increased liver enzymes

A

Reactive hepatopathy (extrahepatic dz- GI, panc, dental, systemic)

427
Q

What condition is inflammation centered around biliary ducts-in periportal areas

A

Cholangitis in cats!

428
Q

Types of cholangitis

A

Neutrophilic- acute from ascending, has fever; lymphocytic- immune mediated, persians, NO fever

429
Q

Cholangitis CS

A

anorexia, V, jaundice, ascites, weight loss

430
Q

Bloodwork in cholangitis cats

A

ALP less than ALT bc of shorter half life, inflammatory leuk with left shift, non/normo/normo anemia

431
Q

Dx cholangitis best

A

Bx- type of inflammation (neut vs lymphocytic); bile culture (> tissue), FISH techniqe to find bacteria

432
Q

Tx cholangitis- neutrophilic

A

Neut- Abx via culture or fluroquin+metro; can also give potentiated penicillin (clavamox)- not as broad but once a day, and no metro po

433
Q

Tx cholangitis- lymphocytic

A

Pred, abx, +/- add on UDCA

434
Q

Mechanism of hepatic lipidosis

A

Below 50% RER for 1-3 weeks= derangement in metabolism, FFA shittled to liver as triglycerides

435
Q

Risk factors of hepatic lipidosis

A

Obseity, weight loss, decreased intake leading to negative nitrogen balance

436
Q

Only exception where predominant liver enzyme isnt the primary type of dz

A

Cholangitis in cats- ALP lower than ALT only bc of half life

437
Q

Tx hepatic lipidosis

A

60-90 kcal/kg/d, start wtih NE 24-48 h (no anesthesia), then E tube, high protein, carb restricted, vitamins E, K, B12

438
Q

Rx hepatic lipidosis

A

Mirtazipine, cisapride

439
Q

Fxn of lysosomes

A

Clean things in the cell

440
Q

Jaundice, hepatomegaly, vaculoar congestion, dramatic inc ALP

A

Hepatic lipidosis

441
Q

Function of stellate cells

A

Liver repair

442
Q

Cholesterol- high or low in liver dz-

A

Low, not being taken up/made by liver

443
Q

Liver dz breeds

A

dobies, spaniels, labs, bedlingtons, yorkie

444
Q

High ALP with normal GGT

A

Hepatic lipidosis (GGT enzyme from bile canaliculi that increases in all cholestatic except hep lipidosis

Small animal GI (1 decks)

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