Final Flashcards
(444 cards)
1
Q
Avg max gastric capacity, comfortable capacity
A
80 ml/kg, 40-60 ml/kg
2
Q
2 components of gastric filling
A
Receptive relaxation, accommodation
3
Q
Where does accommodation occur
A
fundic region
4
Q
Causes of dysfunction of filling
A
Inflammatory proces or neoplasia
5
Q
Consequence of failure to receptively relax, accommodate
A
increase in post-prandial intragastric pressure causing vagal afferents to stimulate emetic center
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
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
8
Q
Erosions/ulcers more common in
A
Dogs
9
Q
Secretions from: chief cells, endocrine cels, G cells, parietal cells
A
Chief: pepsinogen digestive hormone; endocrine: histamine; G- gastrin; parietal: H+
10
Q
Activate proton pump in stomach
A
Vagus Ach to receptors for gastrin and H+ which activate H-K-ATPase
11
Q
Stomach Rx- function of: Atropine
A
Blocks Ach from vagus - no gastrin
12
Q
Stomach Rx- function of: Cimetidine
A
Blocks endocrine cells- no histamine
13
Q
Stomach Rx- function of: omeprazole
A
H-K-ATPase to stop H+
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)
15
Q
Meal composition effects on emptying- carb vs fat/protein
A
Carbs faster than protein/fat
16
Q
Emetic center- what affects
A
cerebral cortex (anxiety), CRTZ (drugs, toxins, cardiac glycosides), oculo-vestibular system- motion (stimulates CRTZ first in dogs)
17
Q
Three phases of the vomiting reflex
A
Nausea, retching, V
18
Q
Define diarrhea
A
Increase in water content of feces changing freq, fluidity, volume
19
Q
Fecal water sources
A
25% intake, remainder secretions
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
21
Q
Where do cells from intestines start
A
Villous crypt cells, migrate upwards towards tips of villi
22
Q
Crypt cell functions
A
When in crypt- secrete electrolytes/fluids; towards tip- absorptive
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
24
Q
Mechanisms of D; which most common
A
Osmotic, secretory, exudative, disordered motility, mixed; Mixed most common!
25
Mechanism of osmotic diarrhea
Osmotically active particles retained in GI tract from lack of digestion/absorption
26
Mechanism of secretory diarrhea
Stimulation of excess secretion overwhelms ability to absorb- loss of fluid, protein, +/- blood
27
Mechanism of exudative D
increased mucosal permeability from injury to barrier
28
What are the two most important diagnostics for any condition
Hx and PE
29
Name the 14 signs of GI dz
V, regurg, D, abd pain, tenesmus, dyschezia, hematochezia, constipation, flatus, salivation, shock, weight loss, anemia, appetite change
30
THreshold of normal cat V frequency
No more than 1/month
31
Clinical sources of V
GI vs non-GI (endocrine, neuro, metabolic, systemic, abdominal)
32
Does fasting improve osmotic diarrhea
Yes
33
Time needed for V to be chronic
2-3 weeks
34
Define delayed emptying parameter
more than 12 hours after eating
35
Main causes of acute V
single insult to stomach, proximal GI tract, pancreas
36
Which type of V is rarely self-limiting
Chronic
37
Does fasting improve secretory diarrhea
No, stimulation to secrete outpacing absorption is the cause
38
Regurgitation more common in
Dogs, rare in cats
39
EPI, intestinal dysbiosis, acute viral diseases will all cause what type of diarrhea
Osmotic
40
What differentiates V from retching
Retching/abdominal contractions
41
Premonitory signs of regurg
very few- some ptyalism in obstructive/esophageal inflammatory
42
Premonitory signs of V
ptyalism, pacing, swallowing, tachycardia (from nausea)
43
SI diarrhea- volume
normal to increased
44
SI diarrhea- mucus content
Rare, but can happen as disease progresses to include LI
45
SI diarrhea- blood
Melena (digested), rare
46
Flatulence and halitosis absent in
LI D
47
What kind of D caused by fat malabsorption
Osmotic and partially secretory (osmotically active particles, hydroxyl fatty acids converted by bacteria stimulate secretion)
48
SI diarrhea- frequency
Normal-mild inc (2-3x/day)
49
Dyschezia- type of D
LI
50
Enterotoxic e. coli causes what type of D
Secretory- stimulation of cAMP
51
Weight loss common in which D
SI
52
Increased urgency in what type of D
LI
53
Lymphangiectasia causes what kind of D
Exudative
54
LI diarrhea- volume
Normal to decreased
55
LI diarrhea- frequency
increased (>5x)
56
Tenesmus- type of D
LI
57
LI diarrhea- weight loss
Rare
58
What kind of D commonly has mucus
LI
59
Hematochezia from what kind of D
LI
60
Causes of constipation
diet, environment, anorectal dz, obstruction, neuro dz of spine, endocrine, metabolic, iatrogenic (opioids)
61
Low oncotic pressure (hypoalbuminemia) and high hydrostatic pressure (RHF, portal hypertension) causes what kind of D
Exudative
62
Cause of tenesmus
Distal alimentary (colon, rectum, anus) or urogenital system
63
Cause of flatus
Swallowed air or bacterial degradation of unabsorbed carbohydrates
64
What condition frequently has flatus
IBD
65
What condition in cats can cause ptyalism
Portosystemic shunt
66
Define malassimilation
Liver dysfunction- unable to convert food to useful molecules
67
Mechanism of bacterial translocation
Breakdown of GI mucosal barrier allowing bacteria into bloodstream
68
What causes sepsis
Bacterial translocation exceeds liver's ability to filter them out
69
Most common causes of anemia in GI dz
tumor, ulcer, bleeding disorder, parasites; defective RBC production from malabsorption (B12) or bone marrow suppression
70
When patient has polyphagia or pica, thought think of
Increased utilization or malabsorption
71
Cat with increased appetite and weight loss- 4 ddx
Hyperthyroidism, IBD, GI lymphoma, DM
72
Dog with increased appetite and weight loss
DM, IBD, lymphoma, EPI
73
Top 7 signs of GI dz- high to low
D, V, appetite change, weight loss, tenesmus, abdominal pain, salivation
74
Common nutrient deficiency in chronic GI dz
Cobalamin
75
Fecal test for PLE
alpha proteinase inhibitor test- supposed to be in blood stream, in feces during PLE
76
Radiographs better for chronic or acute V and D; signs
Acute; ileus, effusion, foreign body, mass effect, pneumoperitoneum,
77
US utility in GI dz
non-specific changes, might show other issues or need for only FNA
78
Mutual interaction of microbiota with host cells is called
Intestinal microbiome
79
What are the normal intestinal microbiota
Bacteria, protozoa, archaea, viruses, fungi
80
Pros of characterizing microbiome with bacterial culture
Pro: can tell viability, susceptibility, analyze genotype, metabolism and virulence
81
Ways of characterizing microbiome via molecular technique
PCR, analysis of amplicons, qPCR/FISH quantification
82
What molecular technique answers "who is there?"
Analysis of amplicons- fingerprint, phylogenetic info
83
What molecular technique answers "What is there?"
PCR- specific genes
84
FISH and qPCR answer what question
How much is there
85
What study tells species, what they are doing, what they are making
Metagenomics
86
What % of gut bacteria is cultureable
5%
87
Where is there a spike in anaerobic, bacteroides, and spore forming anaerobes
Ileum to cecum
88
What starts almost non-existant and increases in number from D-J-I
Aerobes and facultative anaerobes
89
What are gut flora control mechanisms
gastric acid, bile salts' Abx quality, intestinal motility to sweep, intestinal mucus helps motility, immune response, bacterial products stifling pathogenic bacteria
90
Function of archaea
Take H+ from fermentation and convert to methan (instead of HS which damages enterocytes and colonocytes)
91
Main fungi, main viruses
Yeast, bacteriophages
92
Where are TLRs found
Toll-like receptors are found on and in enterocytes luminal and apical borders
93
Function of TLRs
Communication with microbiota
94
What are the good bacteria and how do they inhibit pathogenic growth
Bacteriocins- compete for O2, nutrients and adhesion sites, create a physiologic restrictive barrier
95
What is the source of 7% of ME in dogs
VFAs from fermentation in colon
96
Most common pathogen colonization when bacteriocins fail
Salmonella, c. diff, campylobacter
97
Term for the overgrowth of commensals, what results from it
Intestinal dysbiosis- change of bacteria and communication with immune system leading to inflammation, cytokine and dz
98
How can EPI cause intestinal dysbiosis
True overgrowth from poor digestion of dietary nutrients
99
Microbiome causes of disease
Pathogen colonization, overgrowth of commensals, altered communication
100
Inflammatory bowel disease is a microbiome disease of what cause
Altered communication
101
Describe the altered communication route of disease, name two outcomes
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
102
What shift in dysbiosis stimulates an inflammatory response
Towards gram negative organisms
103
How should you tx histiocytic ulcerative colitis?
Abx (no longer immunosuppressives
104
What causes histiocytic ulcerative colitis
AIEC- adherent and invasive e. coli
105
Former and current approaches to change gut microbiome
Previously Abx (metronidazole and tylan) now using pre/pro/sym- biotics
106
What makes up prebiotics
non-digestible dietary carbs- fructooligosaccharides, bran, psyllium
107
Mechanism of prebiotics
Increase short chain FA
108
Benefits of probiotics
Improved epithelial barrier, modulation of immune system, inhibit pathogenic colonization
109
Minimum requirements for probiotic packaging
Reputable mfgr, list genus and species (+/- strain), 1x10^8 cfu/g
110
What org is in prostora
b. animalis
111
What org is in Proviable
mix of 7
112
Study outcomes of probiotics (4)
Evidence of shorter days to D resolution with some breed difference, improved fecal score, faster days to remission, increased T-regulator markers
113
What is the ultimate probiotic, what conditions has itbeen shown to help
Fecal transplant: IBD, ulcerative colitis, c. diff
114
Causes of dysphagia
Oral, pharyngeal and cricopharyngeal dz
115
Dysphagia can be secondary to
Pharyngitis or tonsilitis- oral cavity inflammation
116
Dysphagia ddx
oral or pharyngeal dz (or tongue), cricopharyngeal achalasia/asyncrhony, neuromuscular dz (myositis, myasthenia, trauma)
117
First dx of dysphagia, other useful followups
Survey rads of head, neck, chest for mass effect, neoplasia; fluoroscopy, EMG
118
What muscles make up UES
thryopharyngeus and cricopharyngeus
119
Site of achalasia
Cricopharyngeus
120
Dog vs Cat esophagus
dog- all skeletal; cat- lower 1/3 smooth muscle
121
Esophagus- rather than serosal layer beyond muscularis, have what layer
Adventitial thin coating
122
What causes stricture
Damage penetrates mucosa and submucosa and exposes muscularis where fibroblasts can make scar tissue
123
Describe primary peristaltic wave
Pharynx contracts as UES relaxes, activates nerve fibers to propagate swallowing reflex down esophagus, moves bolus to stomach via receptive relaxation of LES
124
Describe secondary peristaltic wave
Clearance mechanism- food that didnt make it to stomach with primary- distension of esophagus activates
125
Ages for congenital and acquired esophageal dz
Congenital young, older acquired
126
Causes of esophageal dz
Caustic/abrasive material ingestion, gastric reflux in anesthesia, doxy/clindamycin in cats
127
Name the four causes of regurgitation
Inflammatory disease (usually esophagitis), extraluminal compression, intraluminal obstruction, neuromuscular dz
128
Best dx for esophagitis
Endoscopy is the only definitive; might see stricture with contrast rads
129
Most common cause of extraluminal compression in regurgitation; name three others
PRAA- vascular ring anomaly; thymoma, intrathoracic tumor, hilar lymphadenopathy
130
Signs of PRAA present when?
6-8 weeks, weaning
131
Causes of intraluminal obstruction causing regurgitation
Stricture, foreign body, tumor, diverticulum
132
Dx stricture
Esophagram or endoscopy
133
Causes of stricture-
foreign body, drugs, anesthesia, tumor, esophagitis
134
Tx stricture
Balloon dilation, bougienage blunt dissection, steroids in lesion, mitomycin C chemo agent, +/- gastrotomy tube. PREVENT!! by tx esophagitis
135
Rx stricture
Omeprazole, cisapride, sucralfate liquid
136
Most common site of foreign body
thoracic inlet, heart base, distal esophagus
137
Causes of congenital megaesophagus
unknown, familial, efect in vagal afferents from esophagus
138
Tx foreign body
remove, push, sucralfate, omeprazole, rest with tube
139
Congenital megaesophagus ddx, differentiate between them
R/o vascular ring anomaly- usually focal/segmental dilation; true congenital is generalized
140
regurgitation, ptyalism, inappetance, nasal d/c, +/- cough and fever- name the condition
Esophageal dz
141
Causes of acquired megaesophagus, name biggest category
tox (lead, organophosphates), endocrine (hypoadreno, hypothy), neuromuscular (myasthenia, polyneuritis/myositis); Idiopathic most common
142
Megaesophagus congenital breeds
GSD, irish setter, mini schnauzer, great dane
143
Dx megaesophagus
Survey rads- d not use barium!; CBC for aspiration, serum chem for neuro/addisons, CK for myositis
144
What tests for myasthenia gravis
Ach receptor Ab test
145
What tests for organophosphate toxicity
Cholinesterase activity
146
Tx megaesophagus
fluids, nutrition, elevation, tx aspiration if present
147
Tx myasthenia gravis and myositis
pyridostigmine and prednisone
148
What is the most common cause of acute vomiting in the dog and cat
acute gastritis
149
Mechanism of acute gastritis
Mucosal damage from food/foreign/etc results in increased permeability for acid and inflammatory irritation of vagal afferents for emetic center
150
What causes hematemesis in acute gastritis
Necrosis and erosion of epithelial cells
151
What is the most common sign of acute gastritis
V
152
Acute gastritis Ddx
gastric foreign body, obstruction; acute pancreatitis, infectious dz (parvo, corona), systemic (liver, kidney, toxin)
153
Most effective tx for acute gastritis
Brief fast (12-24 h)
154
Define chronic gastritis
Persistent insult present in GI
155
Causes of chronic gastritis
Inflammatory (lymphoplasma, eosino), FRD, helicobacter gastritis, reflux gastritis (bilious V syndrome)
156
CS of lymphoplasmacytic chronic gastritis
V, hematemesis, appetite change in cats
157
T/F degree of cellular infiltrate corresponds with degree of CS in chronic gastritis
False
158
Rx- lymphoplasmacytic chronic gastritis
Acid reducer (omeprazole or famotidine); prokinetic (cisapride, metoclopramide); prednisone +/- rx to increase
159
Rx to add to pred for dogs with lymphoplasmacytic chronic gastritis
Azathioprine or cyclosporine
160
Rx to add to pred for cats with lymphoplasmacytic chronic gastritis
Chlorambucil
161
Gross lesions- eosinophilic inflammatory chronic gastritis
Nodules filled with eos
162
eosinophilic inflammatory chronic gastritis breeds
Rotties
163
Tx eosinophilic inflammatory chronic gastritis
dietary manipulation +/- corticosteroids
164
Cause of helicobacter chronic gastritis
h. felis
165
Vomiting, lethargy, polydipsia, hematemesis, mild-moderate cranial abdominal pain- name the condition
Acute gastritis
166
Patient has chronic vomiting and all other causes have been r/o, what should you test for?
Helicobacter via warthin-starry stain
167
Tx helicobacter
amoxicillin with clarithromycin +/- metronidazole
168
Mechanism of bilious vomiting syndrome (reflux gastritis)
defect in pyloric sphincter tone allowing reflux or gastric motility allows prolonged contact of bile with mucosa
169
T/F helicobacter can cause ulceration in dogs and cats
False
170
What kind of substance is bile
Detergent
171
Tx bilious vomiting syndrome
BID feeding, prokinetic (cisapride, metoclopramide), acid reducer (omep or ranitidine)
172
Why is ranitidine indicated for bilious V synd
Has some possible prokinetic effect on stomach
173
Ulcer vs erosion
ulcer penetrates to muscularis, erosion only to submucosa
174
Causes of ulcer/erosion
Drugs (steroids and NSAIDs), liver dz (shunts, portal hypertension), tumors, malnutrition, uremia/stress?
175
Tumors that cause ulcer/erosion
mast-histamine release, gastrinoma- gastrin release, LSA
176
Cause of lymphoid follicular hyperplasia lesions and bx result lymphocytic gastritis
Helicobacter gastritis
177
Dx ulcer
Endoscopy! (also contrast rads, biopsy)
178
Best Tx ulcers
Omeprazole PPI- longest/greatest acid reducer, tx underlying dz
179
Causes of gastric outlet obstruction
GDV, gastric tumor, foreign body, stenosis
180
Types of stenosis, which more common, breeds predisposed
Congenital- boxers, bulldogs, boston, cats- pyloric; Acquired-- male small breeds (lhasa, shih, pekingese)- antral
181
Blood findings in advanced gastric outlet obstruction
Hypochloremia, hypokalemia, metabolic acidosis
182
Most common gastric tumor in dogs
adenocarcinoma in distal stomach at antrum angularis incisra- circumferential
183
Most common gastric tumor in cats
LSA
184
What is the cat puke worm
Ollulanus
185
Dog vomits first thin in the morning before eating, green yellow with a little bit of blood- waht is this?
Bilious vomiting syndrome
186
Tx gastric parasites
Pyrantel or fenbendazole
187
Most common gastric parasite, CS
Physaloptera from dung beetle; chronic V
188
Life threatening SI diarrhea causes
Parvovirus, intussusception
189
Life threatening LI diarrhea causes
Pythium, histoplasmosis
190
Causes of infectious acute diarrhea
Parasitic (helminths and protozoa), bacterial (clostridium>e.co, salm, campylo), viral (parvo, corona)
191
Name 3 helminths
ascarids (round), whips, hooks
192
See beak sign on rads- what is this?
Contrast funneling through plyorus= gastric outlet obstruction
193
Coccidia, giardia, cryptospor, tritrich are all what parasite type
Protozoa
194
Which parasite causes worst CS
hookworms
195
What fecal test is best for motile parasites
Direct smear
196
What fecal test is most sensitive for giardia
ELISA or PCR
197
Clostridium primarily causes what type of D, how?
Large intestine; Undergoing sporulation and releasing enterotoxins
198
Y-U pylorostomy and pyloromyotomy tx for?
Gastric outlet obstruction (muscular cutting)
199
Intermittent V becoming projectile, contains food hours after eating, starting to show signs of hypo-Cl, K, metabolic acidosis
Aquired stenosis causing gastric outlet obstruction
200
Tx clostridium
Metronidazole, amoxicillin
201
Dx coronavirus
EM of fresh feces, PCR
202
Which viral D agent will show signs of fever, leukopenia
Parvo (not coronavirus)
203
Tx coronavirus
Self limiting, resolution in 1.5 weeks
204
Depression, strawberry jam diarrhea, V +/- blood, prolonged CRT, normal MM
Hemorrhagic gastroenteritis
205
Hemorrhagic gastroenteritis- labs
Increased PCV, normal TP, thrombocytopenia, metabolic acidosis
206
Tx Hemorrhagic gastroenteritis
12-24 hr NPO until V stops, antiemetics, fluids, electrolytes (titrate fluids to normal PCV)
207
Name two extra-intestinal causes of D
Addison's and hyperthyroidism
208
Sudden onset of D, vomiting rare, orange smelly feces; resolves in 8-10 days
Coronavirus
209
What causes feline panleukopenia
Parvovirus
210
Mechanism of parvovirus
Fecal-oral transmission, Epitheliotropic enterovirus invading rapidly dividing cells lining intestinal tract
211
Parvovirus breed susceptibility
Black and tans
212
Incubation time of parvovirus
3-7 days before shedding in feces; can shed 5-6 days before CS; remember subclinical infections in adults-
213
Where does parvo replicate, travel?
oro-pharyngeal lymph tissue (LN, tonsils) then circulates to other lymphoid tissue, bone marrow, intestines
214
Parvo- cbc findings
lymphopenia with first neutropenia due to bone marrow invasion/necrosis and their short half life
215
What kind of diarrhea is parvo and why
Exudative bc epithelial cell loss leads to exposed lamina propria
216
What day will some regrowth of epithlium be seen? What day will they start to look normal
7, 8 (when diarrhea resolved)
217
Parvo CS
D and V from subclinical to peracute, fever
218
Dx parvo
EM fresh feces, intestinal histopath, ELISA
219
If parvo patient is hypoproteinemic- tx
Plasma/albumin
220
Parvo abx
cephalosporin, amikacin, enrofloxacin
221
Antiemetics- parvo
Metaclopramide CRI, cerenia (some dont respond), ondansetron
222
Two alternative parvo tx
Feline omega interferon, hyperimmune plasma
223
Best tx for parvo
Good nursing
224
Nutrition approach in parvo
EEN- early enteral nutrition- prevents further breakdown of gut barrier leading to shock that can be caused by fasting
225
Parvo- monitoring parameters
Glucose, PCV/TP, weight, electrolytes, azotemia
226
Major causes of chronic D in dog
IBD, ARD, FRD, intestinal parasites, lymphangiectasia, EPI, intestinal neoplasia, fungal
227
Major causes of chronic D in cat
IBD, intestinal tumors (diffuse), FRD, ARD, viral, intestinal parasite
228
Age and chronic D
Younger- parasites, older- neoplasia, IBD
229
Vomiting indicates what kind of diarrhea location
Upper GI, but can be any part
230
What type of D is dehydration most seen in
Acute- chronic compensates
231
How does chronic D hypoproteinemia present
subcu edema on ventral neck, pitting edema in legs of large breed, ascites in small breed
232
Severe V and D, fever, depression, leukopenia, dehydration
Parvovirus
233
Why is Ca decreased in chronic D
hypoalbuminemia affects bound portion
234
What part of chronic D causes panhypoprot'a
PLE, hemorrhage
235
Dx FRD
Diet trial for 2-4 weeks, takes 6-8 weeks to resolve
236
Cause of ARD
Altered or increased bacteria from antibiotics, abnormal host response
237
Most important dx in ARD/intestinal dysbiosis
Cobalamin- tx not successful if low
238
Mechanism of cobalamin loss
cobalamin+R protein in stomach --> IF (intrinsic factor) from parietal cells/stomach/pancreas --> IF needed to bind receptors in ileum for cobalamin uptake
239
Species difference- cat cobalamin
IF only comes from pancreas, not stomach, so this is why pancreatitis often linked to enteropathies- lack of production
240
Dx LI chronic D; name best
Diet trial, clostridium test, response to deworm or Abx, contrast radiography for intussusception; colonoscopy/bx
241
Rx for chronic D
metro, tylan
242
Define IBD
Disorder of SI characterized by persistent or recurrent GI signs and histo evidence of inflammation
243
Describe IBD infiltration
Lymphocytes and plasmacytes invade lamina propria
244
Pathogenesis of IBD
Alteration in TLRs, Epithelial lining, immune system receptors under epithelial layer- genetic loss of tolerance to bacterial or food antigens; environmental; microbiome;
245
Most important TLRs in dogs
4 and 5, esp in GSD- altered expression leads to risk
246
What causes the cinical signs of IBD
mucosal cell infiltrates and inflammatory mediators (complement, leukotrienes, inflammatory cytokines, etc)
247
IBD breeds
Nasenji, lundehund, wheatons, irish setters
248
Most common sign of IBD in cats
V clear foam/bile
249
Cats or dogs, more PLE in IBD
Dogs, so cats no edema (but more mesenteric LN enlargement)
250
Dx IBD
BIOPSY via endoscopy or laparotomy- confirm inflammation, r/o infection/neoplasia
251
IBD-SI endoscopic findings
50% normal grossly, erythema, erosions, lymphangiectasia, granular, friable
252
IBD-SI histo
Mucosal atrophy, villous atrophy, erosion, eos debris in crypts, lymphangiectasia
253
Tx SI IBD
diet --> abx --> steroids
254
Effect of steroids on IBD-SI
dec neut migration, dec mac fxn, dec cytokine production, inhibit arachidonic acid pathway of inflammation
255
IBD-SI Rx
Pred, dex (more potent, less dosing), budesonide (better for liver, suppresses HPA axis)
256
Taper IBD-SI steroids
25% reduction q 2-4 weeks to lowest effective dose
257
Alternative IBD-SI Rx
Azathioprine, cyclosporine, chlorambucil
258
Use and benefit of azathioprine in IBD-SI
Cheaper, combine with pred, use in PLE/large breed cases
259
Rx IBD-SI with PLE
cyclosporine (or pred/aza)
260
Adjunctive tx for IBD- SI
plasma/alb, cat cobalamin, nutrition, pancreatic enzymes
261
Tx IBD-LI, mild
Diet- hypoallergenic or high fiber; Rx- metronidazole
262
Tx IBD-LI, moderate-severe
Sulfasalazine or pred- sulfasalazine wont compromise bx results
263
D, hematochezia, tenesmus- used to be called IBD
Histiocytic ulcerative colitis from AIEC (adherent/invasive)- large intestine disease
264
HUC tx
NO STEROIDS- enro +/- amoxicillin/metronidazole - some need long term
265
What specific cell type is in HUC
PAS+ macrophages
266
FRD diet recommendation
Hypoallergenic (no cross linking to Ig); novel protein, bland
267
What type of dz is fiber response colitis
Mostly LI
268
Most frequent breed with intestinal dysbiosis
GSD
269
Tx intestinal dysbiosis
tylan, amox, tetracyc metro/enro, probiotics, fecal transplant
270
Mechanisms of PLE
Lymphatic obstruction/rupture, increased mucosal permeability (exudative), mechanical (ulcers)
271
Dz assoc with PLE
inflammatory, infectious infiltrative, neoplasia (LSA, mast), lymphangiectasia, addisions
272
Primary vs secondary lymphangiectasia
1- congenital, 2- inflammation obstruction
273
Lymphangiectasia- breed most common
Yorkie
274
Lymphangiectasia- CS
muscle wasting, edema, ascites, pleural effusion- clear transudate- panhypoproteinemic (30-40% are hypoalb only due to increased immune Ig)
275
Define hypoproteinemia in lymphangiectasia
Loss of protein-rich lymph
276
2 main causes for panhypoproteinemia
GI loss or hemorrhage
277
Other causes of hypoalbuminemia
liver dz, kidney loss
278
Loss of protein in Lymphangiectasia leads to a decrease in what minerals
Ca--> vitamin D
279
Dx Lymphangiectasia
Intestinal biopsy- dilated lymphatics
280
Cause of lymphopenia in Lymphangiectasia
Loss of lymphocytes to GI tract
281
Mainstay Tx Lymphangiectasia
low fat diet (to reduce chylomicrons in blood to increase flow)- Purina HA (low fat and hydrolyzed)
282
Causes of infectious colitis
Clostridium, pythium, prototheca, histoplasma
283
Geography of clostridium
Gulf atlantic states
284
Clostridial infection- location, CS
LI chronic D
285
Drug response dx for clostridium
Metronidazole, amoxicillin
286
Location of pythium
ileo-colic junction but can be anywhere dermal or GI- not usually both
287
Dx pythium
Abdominal LN enlargement, org in intestinal wall
288
Infectious colitis source from Ohio river valley- rectal scrape, LN aspirate, wall aspirate all dx
histoplasma
289
Exocrine panc fxn
Digestive enzymes and cofactors into duodenum via acini and ducts with buffer for enzymes
290
Speckled/perpendicular striation pattern of mucosal layer of intestine on U/S- dz
Lymphangiectasia
291
Endocrine panc fxn
into portal blood- islets with hormones to portal vein
292
Test for histoplasma
histo/blasto Ag with GI signs only
293
Panc enzyme synthesis location
RER
294
How are digestive enzumes from panc secreted
Zymogens
295
Yorkie with ascites, muscle wasting, panhypoprot, hypoCa, hypoMg, low cholesterol, low vitamin D- name the dz
Lymphangiectasia
296
Pancreatic enzymes
Amylase, lipase, proteolytic, trypsinogen
297
How are proteolytic enzymes secreted
In inactive zymogens to have terminal am ac removed to activate
298
What mineral is critical to activation of pancreatic zymogens
Calcium
299
Path/actions of trypsinogen
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
Inhibitory mechanism of trypsin, source
PSTI (panc secretory trypsin inhibitor) filling active site on trypsin- secreted at same time from acinar cells, works in duct areas
301
Mechanisms stopping autodigestion of the pancreas
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
Alpha1-proteinase inhibitor function
Binds trypsin in blood stream so proteases not activated outside GI
303
Alpha1-macroglobulins
Form buffer around trypsin to block active site so proteases not activated outside GI
304
Age groups for cat/dog pancreatitis
Dog >4yr, Cat >1yr, usually chronic but can be acute
305
Pathogenesis of pancreatitis
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
Risk factors of pancreatitis
Dietary indescretion, panc ischemia (trauma, anesthetic hypertension), duodenal reflux of bile, drugs (not steroids), duct obstruction, genetics, idiopathic 50%
307
Dog CS pancreatitis (most to least)
V, weakness, abdominal pain, dehydration, D (LI, colon in chronic)
308
Cats CS pancreatitis (most to least) +acute signs
Lethargy, anorexia, dehydration; acute: hypothermia, subtle abdominal pain
309
Co-diseases for pancreatitis
IBD, cholangiohepatitis (triaditis)
310
Cat labs pancreatitis
anemia in >1/3, dehydration, +/- leukocytosis
311
Dog labs pancreatitis
Neutrophilia with left shift (inflammation), thrombocytopenia
312
Both dog and cat labs- pancreatitis
Pre-renal azotemia, hypoalbuminemia (esp in dogs with peritonitis), hyperglycemia, hypoCa, hyperlipidemia, hyperbilirubinemia, increased liver enzymes
313
Dog vs cat pancreatic anatomy
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
Dx pancreatitis
cPL and fPL 200/400
315
Snap test- cPL, fPL- limitations
Good sensitivity (no false neg), poor specificity (foreign body, panc tumor, GI inflamm)
316
Test to confirm pancreatitis Snap
Pancreatic lipase test >400
317
U/S changes in pancreatitis
hypoechoic pancreas enlarged, hyperecholic fat surrounding- fibrosis might make it look normal if previously dz'd
318
Tx pancreatitis
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
EEN study results
Early enteric nutrition tx in pancreatitis showed less V than parenteral but more post-prandial pain
320
Indications for pancreatitis sx
Pancreatic abscesses, prolonged bile duct obstruction
321
When can steroids be used in cats with pancreatitis
When biopsy has confirmed diagnosis
322
What is EPI
lack of pancreatic enzymes due to defenerative atrophy in dogs- esp GSD and mixes
323
What causes EPI in cats, CS
Chronic pancreatitis: polyphagia, weight loss, steatorrhea, voluminous D
324
Dx EPI
Trypsin-like immunoreactivity TLI
325
Tx EPI
Powdered enzymes, oral Abx, cobalamin
326
Exception of blood from from tributaries of GI organs to liver
Rectal vessels straight to venous system
327
Liver function
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
Blood flow into and out of liver
Portal vein + hepatic artery into liver, branch to venules/arterioles to capillary beds- feed sinusoids, come out hepatic veines to vena cava
329
Cause of ALP, bili and GGT rise in cats with pancreatitis
Early merge of bile duct and pancreatic duct makes GI-inflammatory obstruction back up all three systems
330
How does biliary system flow in liver
Countercurrent to portal vein and hepatic arteries
331
Biliary vessel tract
Biliary vessels join into bile duct, merge into common bile duct, out to pancreas then to GI tract via duodenal papilla
332
Liver lobule arrangement
lobule radially arranged around central hepatic venule with portal triads at periphery
333
Lobular terminology- define
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
Increased appetite, decreased weight, large stool volume and frequency, steatorrhea-
EPI
335
Alternative terminology for hepatocytes
Acinar- portal triad in middle, each point of hexagon a central vein; periportal, intermediary and central vein zones (1-3)
336
Portal triad
hepatic a, portal v, biliary duct
337
Sinusoids in liver lined by
Hepatocytes
338
Liver immune cells
Kupfer cells
339
Location of stellate and dendritic cells in liver
Between vascular wall and hepatocytes (space of dis)
340
Detox and excretion functions of the liver
hepatic biotransformation of lipophilic compounds to promote excretion, metabolism of steroids, bilirubin, ammonia activate or clear drugs,
341
Ammonia
Byproduct of protein metabolism in liver
342
Why are liver dz hard to diagnose early
Vague signs due to functional reserve and regeneration
343
% of the liver that can be lost without evidence of dysfunction
70
344
Most specific CS of liver dz
Jaundice of oral mucosa, skin, sclera- cats soft palate way early!
345
Forms of portal hypertenison
Primary- obstruction (cirrhosis fibrosis) or secondary to obstruction further upstream than the liver causing backflow
346
Causes of low protein ascites
Portal hypertension, hypoalbuminemia (liver not making enough)
347
Causes of high protein ascites
RHF causing CaVC backup into hepatic veins, HWDz caval syndrome, mass lesions, thrombi in vena cava or hep vein
348
Cats- liver disease differences
Ascites uncommon, no cirrhosis, RHF congestion to chest
349
ALT increase in cats NOT from primary hepatic dz
Hyperthyroid
350
Copper eyed cat
Liver shunt
351
Define reactive hepatopathy
Dz elsewhere impacts liver- ex IBD, LSA in GI, periodontal dz- cytokines and bacteria from GI
352
Greatest increases in liver enzymes indicates
Necrosis
353
Leakage/cellular damage enzymes
ALT, AST (think almost always liver leakage and sometimes)
354
T/F liver enzymes are not markers of function
True
355
Liver-specific enzyme found in cytoplasm
ALT
356
Widespread, acute necrotic damage to liver will cause very high elevation of what
AST
357
Liver pseudofunction tests, name and define
(pulled from blood by liver, but liver not only source of abnormal level) Bili, albumin, BUN, Gluc, cholesterol
358
Causes of increased bilirubin
Pre-hepatic (hemolysis), hepatic (hepatitis, lipidosis, neoplasia, cirrhosis, etc), post-hepatic (panc-, cholang-, cholecyst-itis, liths, biliary neoplasia, GB mucocele, dudoenal dz)
359
First liver enzyme to leak in cell damage
ALT
360
AST > ALT
Probably muscle, not liver, check CK- if it is from the liver, more irreversible damage done
361
ALP comes from
Bone, liver, drugs (+others with short half-lives) (different isoenzymes)
362
Location of cholestatic liver enzymes
Membrane bound (ALP, GGT)
363
Liver cholestasis enzymes
ALP, GGT
364
Bilirubinuria- form excrete
conjugated (water soluble)
365
Dog vs cat bilirubinuria differences
dog has low renal threshold for conj bili, common in urine- cat has high so bili in urine is significant
366
Path of bilirubin
Mostly unconjugated bili in blood, liver conjugates, dumped into bile, gets unconjugated back to blood
367
Dog vs cat ALP
Cat only 6 hr half life (72 in dog)- ALP always significant in cat
368
Ddx of low albumin from liver dz
PLE and PLN (anorexia will not cause)
369
Steroids increase what liver enzyme in dogs but not cats
ALP (alk phos)
370
BUN in liver dz- high or low? why?
Low BUN bc liver converts ammonia to urea
371
Liver true function tests
Blood ammonia, serum bile acids, post-prandial bile acids
372
Causes of high blood ammonia
Bypass liver in PSS, hepatitis not allowing uptake, cirrhosis acquired shunts
373
Biliary neoplasia is a _____ cause of bilirubinemia
post-hepatic
374
Effect of high serum bile acids on liver
No contribution to hepatic enceph or anything negative- stable in serum
375
Why is GGT more specific for liver than ALP in dogs
ALP is steroid inducible
376
If patient is icteric, dont need to do what test?
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
What type of test is serum bile acids
Liver true function test- yes or no to normal function, not what type
378
What does very high (over 100) pre or post bile acids indicate
PSS - dont go this high in regular dysfunction
379
Describe fasting bile acids
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
Effect of PSS/parenchymal dz on BA
When liver not functioning or being bypassed, more bile acids get past the liver
381
How could fecal evidence of GI bleed indicate liver dz
Clotting function, portal hypertension backup leading to exudate
382
Liver disease- rads or U/S better?
Rads- can see size, effusion, ascites
383
Pros and cons of aspiration cytology in liver dz
not invasive, good for neoplasia, lipidosis, not good for inflammatory, cant tell where lesions are
384
Best way to get bx in liver dz
- laparoscopy
385
Causes of hepatocellular damage
Toxins (sago), drugs, infection (lepto), idiopathic/unseen
386
ALP
Hepatocellular damage much more likely than cholestasis
387
Magnitude of increase of ALT indicates
Severity of hepatocellular damage
388
T/F- biopsy useful in dx hepatocellular damage
False
389
Tx for hepatocellular damage besides supportive/antiemetics
Antioxidant therapy- N-acetlycysteine IV, silymarin, SAMe
390
Define extrahepatic bile duct obsruction
Any impairment of bile flow in biliary system between liver and duod (intra to extra hepatic bile ducts, common, cystic)
391
Causes of extrahepatic bile duct obstruction in dog: top two most common
Pancreatitis #1, GB mucocele (+ tumors, stones rare)
392
Causes of extrahepatic bile duct obstruction in cat: top two most common
Biliary neoplasia, liver flukes
393
CS- EHBDO
inapp, icterus, V (esp in dogs with panc involved)
394
Dx EHBDO
U/S, cofirm via laparotomy catheterize duodenal papilla
395
Chronic hepatitis ddx
lepto, chronic infection
396
Causes of Chronic hepatitis
drug induced (phenobarb, rimadyl), copper, diet toxin, breed, idiopathic
397
Copper-associated hepatopathies- breeds
dobie, westie, dalmatian, lab
398
Copper storage dz breed and cause
Bedlington- COMMD1, MURR1
399
ALP >> ALT, icterus, inappetence
EHBDO
400
Copper-associated hepatopathies- CS
Non-specific, wax/wane, acute illness with weight loss (or can be icterus w/o illness)
401
Best Dx for Copper-associated hepatopathy and findings
Bx- mononuclear inflammation (no neuts- infection), single cell/piecemeal necrosis
402
Bile duct hyperplasia indicates-
Chronic inflammation
403
Bridging indicates
Fibrosis replacing irreversibly danaged cells then connecting betwee portal tracts- Far progression, poor prognosis
404
Dx copper
Bx- rhodanine stain red, quantitative tissue analysis >400 ug/g
405
Differentiate between chronic hepatopathies and reactive hepatopathies-
Necrosis makes it chronic hep, (but no necrosis found does not mean its NOT, just should consider RH)
406
Primary copper vs secondary copper
Primary- found in centrilobular around vein; secondary from infection in periportal area (think PC-SP)
407
Tx chronic hepatopathy
Pred with ALT monitoring until it plateaus
408
Good bile acids
Hydrophilic
409
Patient feels good but has mild elevation in enzymes- what should you think of
Reactive hepatopathies- like abdominal disease, oral disease)- consider before starting steroids for chronic inflammation
410
UDCA- function, main SE
increases bile flow by thinning bc hydrophillic, contracts GB, anti-ox and antiinflamm; V
411
When should UDCA be used
Evidence of cholestasis add-on therapy
412
Tx copper hepatitis
D-penicillamine, trientine- chelation tx; Zinc to prevent GI absorption- DONT use WITH chelator
413
Mechanisms of liver fibrosis
Stellate cells activated to fibroblastic cells when liver injured, replace parenchyma= less compliant
414
Regenerative nodules in liver indicate
Normal age change and chronic hepatitis
415
Persistent increase in ALT and ALP (but less) progressing to ALP >ALT, low albumin, BUN, chol; hyperbili +/- abnormal BA
Copper associated hepatopathies
416
Cirrhosis- describe
Consequence of long term damage causing diffuse fibrosis, losing liver function bc less tissue- end stage of chronic liver dz
417
Cirrhosis- CS
Inapp, encephalopathy, weight loss, icerus first, ascites or peripheral edema
418
Describe portal hypertension's role in ascites
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
Cause of hepatic encephalopathy-
loss of detox function and acumulation of toxic metabolites (esp ammonia, others hard to measure)- toxic to neurons, act as false neurotransmitters
420
Dx hepatic encephalopathy-
bile acids test (fasting ammonia might be WNL due to no liver challenge) to confirm liver dysfunction
421
Tx ascites from cirrhosis
antagonize RAS system aldosterone- spironolactone diuretic
422
Tx hepatic encephalopathy-
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
Why cant' ALP be monitored in tx chronic hepatitis
Steroid administration will raise the enzyme level
424
CPSS, PSS- describe
Some connection between portal and systemic system bypassing liver
425
ALP elevated without bilirubin elevation
Vacuolar hepatopathy
426
What is the most common cause of increased liver enzymes
Reactive hepatopathy (extrahepatic dz- GI, panc, dental, systemic)
427
What condition is inflammation centered around biliary ducts-in periportal areas
Cholangitis in cats!
428
Types of cholangitis
Neutrophilic- acute from ascending, has fever; lymphocytic- immune mediated, persians, NO fever
429
Cholangitis CS
anorexia, V, jaundice, ascites, weight loss
430
Bloodwork in cholangitis cats
ALP less than ALT bc of shorter half life, inflammatory leuk with left shift, non/normo/normo anemia
431
Dx cholangitis best
Bx- type of inflammation (neut vs lymphocytic); bile culture (> tissue), FISH techniqe to find bacteria
432
Tx cholangitis- neutrophilic
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
Tx cholangitis- lymphocytic
Pred, abx, +/- add on UDCA
434
Mechanism of hepatic lipidosis
Below 50% RER for 1-3 weeks= derangement in metabolism, FFA shittled to liver as triglycerides
435
Risk factors of hepatic lipidosis
Obseity, weight loss, decreased intake leading to negative nitrogen balance
436
Only exception where predominant liver enzyme isnt the primary type of dz
Cholangitis in cats- ALP lower than ALT only bc of half life
437
Tx hepatic lipidosis
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
Rx hepatic lipidosis
Mirtazipine, cisapride
439
Fxn of lysosomes
Clean things in the cell
440
Jaundice, hepatomegaly, vaculoar congestion, dramatic inc ALP
Hepatic lipidosis
441
Function of stellate cells
Liver repair
442
Cholesterol- high or low in liver dz-
Low, not being taken up/made by liver
443
Liver dz breeds
dobies, spaniels, labs, bedlingtons, yorkie
444
High ALP with normal GGT
Hepatic lipidosis (GGT enzyme from bile canaliculi that increases in all cholestatic except hep lipidosis
