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SAM 2 > GI-vomiting Star! > Flashcards

GI-vomiting Star! Flashcards

1
Q

What muscles occur in the walls of the pharynx

A

Both circular and longitudinal

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2
Q

In what phase does the bolus move along the esophagus into the stomach

A

Esophageal (CN IX, X, SNS)

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3
Q

In what phase does pre-hend food form a bolus which moves to end of tongue

A

Oral (CN, V, VII, XII)

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4
Q

What happens in the pharyngeal phase

A

CN IX, XI
Propels bolus along pharynx
Closure of larynx by epiglottis and inhibition of breathing
Upper esophageal sphincter opens

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5
Q

What king of muscle is there in the dog esophagus?

A

Striated entire length

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6
Q

What kind of muscle is cat esophagus made of?

A

Distal aspect is smooth muscle

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7
Q

What is the pathophysiology of MG causing megaesophagus?

A

Ab produciton against ach receptors at neuromuscular junction

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8
Q

What are the possible endocrine associations with acquired megaesophagus?

A

Hypothyroid, addison’s disease

ALSO lead toxicity, and CNS brain stem lesion

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9
Q

What is the function of gastric juice?

A

Muscular walls churn food into chyme

Absorbs glucose + alcohol

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10
Q

What is the function of HCl acid

A

Kills bacteria brought in with food

Activates enzymes

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11
Q

What are the main physiologic actions of gastrin

A

Stimulates secretion of GASTRIC ACID and INTRINSIC FACTOR

stimulates secretion of PEPSINOGEN from chief cells

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12
Q

What are the main physiologic actions of somatostatin?

A

Inhibits secretion and action of many hormones

MASTER HORMONE

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13
Q

Where does most intrinsic factor come from in dogs?

A

The pancreas—B12 (cobalmin)

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14
Q

What are the clinical signs for gastric reflux?

A

Lip licking, pytalism, halitosis

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15
Q

What is zollinger-ellison syndrome?

A

Gastrinoma—gastrin secreting tumor

CS—reflux esophagitis

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16
Q

How do you tx bilious vomiting syndrome (BVS)

A

Frequent small feedings, gastroprotectants, novel protein diet

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17
Q

What is the main energy requirement of enterocytes?

A

Glutamine

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18
Q

What are the CS of small bowel diarrhea?

A

High volume, high frequency, melena, steatorrhea with malabsorption

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19
Q

What are the CS of AHDS

A

Looks like parvo
Hematemesis + hematochezia
PCV > 60% +/- TS not as high as expected (GI loss)

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20
Q

What are the CS of giardia duodenalis?

A

Small and large bowel diarrhea

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21
Q

How do you tx giardia duodenalis?

A

Fenbendazole, metronidazole, bathing on last day

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22
Q

What are the CS of tritrichomonas foetus?

A

Large bowel diarrhea

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23
Q

What are your PE findings for pythium insidiosum?

A

GI—palpable abd mass, dehydration, poor BC
Cutaneous:
Dog—lesions at base of tail, extremities, ventral neck, perineum
Cat—cervical, inguinal, and truncal

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24
Q

How do you tx small cell lymphoma?

A

CHLORAMBUCIL, pred

25
Q

What is the most common infiltrate in IBD?

A

Lymphoplasmacytic infiltrate

26
Q

How do you dx exocrine pancreatic insufficiency?

A

Trypsin like immunoreactivity (TLI)

Consider in older animals with hx of chronic GI signs, weight loss, diabetics

27
Q

How do you dx liver dz if not icteric?

A

ALT + AST —mostly for hepatocyte membrane integrity and maybe necrosis

ALP + GGT —cholestasis

Ammonium biurate crystals—u/a. Shunts, organ failure.

28
Q

T/F

The magnitude of elevation in serum bile acids allows differentiation of the category of dz

A

FALSE. IT DOESN’T.

While bile acids are quite useful for the dz of portosystemic shunts and cyrrhosis (high sensitivity), value is limited for the screening of most other hepatobiliary dz (low sensitivity)

Soooo if bilirubin is elevated then bile acids will be too

29
Q

What has been found to have the highest correlation with actual liver weight in dogs?

A

Measurements made from R lateral abd rads

30
Q

What diagnostic method can be useful for determining liver size, and for dx of hepatic mass lesions and portosystemic shunts?

A

CT

+ contrast—can help differentiate benign vs malignant

31
Q

What are the MC infectious causes of liver enzyme elevations?

A

Bacteria—GI or pancreas translocation
Lepto in dogs
Tick-borne infections
HWD

32
Q

What are the pre hepatic causes of icterus?

A

Primary IMHA—idiopathic, SLE, blood transfusion

PNS hemolytic anemia—LSA, HSA

Infectious HA—ehrlichia, lepto, endocarditis, piroplasmosis, dirofilariasis

Toxic origin HA—onion, zinc, copper, penicillins, cephalosporins

33
Q

What are hepatic causes of icterus?

A

Chronic hepatitis—hereditary, drug induced (phenobarb)

Acute hepatitis—toxic (NSAIDs), infectious

Neoplasia—LSA, hepatic mets, etc

Acute cholangitis

34
Q

What are post-hepatic causes of icterus?

A

Extra-hepatic bile duct obstruction (EHBDO)

Cholecystitis and cholangitis

Rupture of extra-hepatic biliary duct (mucocele, trauma, etc)

35
Q

What are the components of the vomiting reflex?

A

The emetic center
Higher brainstem and cortical structures
Vestibular apparatus

36
Q

T/F

Metoclopramide is better than cerenia as an antiemetic

A

FALSE

Cerenia acts directly on NK1 receptors in the antiemetic center

37
Q

How do you dx pancreatitis?

A

PLI

TLI is for EPI

38
Q

T/F bilirubinuria is always abnormal in the cat

A

TRUE

39
Q

What is the difference between dog and cat bile ducts?

A

Cat bile ducts converge with pancreatic ducts, while dogs are separate

40
Q

T/F

You restrict fat in cats with pancreatitis

A

FALSE

Lipidosis will occur if you do

41
Q

T/F

Dog’s with pancreatitis should be calorie restricted

A

FALSE
They should be fed whenever possible
Ultra-low-fat diet

42
Q

What is the most common disorder of the exocrine pancreas in cats?

A

Pancreatitis

And chronic pancreatitis is common as a primary dz

43
Q

Hypothyroid looking cat with diarrhea?

A

EPI!

44
Q

How does salmonella cause enterocolitits? Mechanism?

A

It attaches to epithelial cells and M cells in the SI and LI

45
Q

Neural control in pancreas

A

Stimulated by anticipation of meal—vagus nerve

46
Q

Mechanoreceptors in pancreas

A

Food distension

47
Q

Endocrine control in the pancreas

A

Stimulated by luminal contents of food
Cholecystokinin
Secretin
Gastrin

48
Q

What is the role of cholycystokinin and acetylcholine in the pancreas?

A

They are principal mediators of pancreatic enzyme secretion. They initiate fusion of zymogen granules with acinar membrane.

49
Q

What are the pancreatic enzymes?

A

Amylase and lipase

50
Q

PLE is associated with what?

A

Panhypoproteinemia—ALB + GLOB

If ALB + GLOB—GI protein loss MC, or liver failure —> not common

If only ALB—renal loss MC, not enough production

51
Q

What drugs would you use to treat a hypercoagulable state in PLE?

A

Low dose aspirin and/or clopidogrel

NSAID + steroid together? SCARY????

52
Q

What is lymph rich in?

A

Lipoproteins and lymphocytes

53
Q

What will show up in lab results as a result of lymph leakage?

A

Panhypoproteinemia, hypoCHOL, lymphopenia

54
Q

How do you dx whipworms?

A

HyperK + hyperNa —> psuedo-addison’s dz will be a ddx

ACTH stim results will normal

55
Q

T/F

HyperCa resolves with praziquantel tx in Heterobilharzia americana

A

FALSE

Px is good and neither hyperCa-induced renal failure nor ascites makes it worse o.o

56
Q

What is IBD?

A

Specturm of GI disorders

57
Q

What does clinical dx of IBD require?

A

1–chronic GI signs
2–histopath evidence of mucosal inflammation
3–inability to document other causes
4–inadequate response to therapeutic trials
5–clinical response to anti-inflammatory or immunosuppressive agents

*histopath changes in the abesence of these criteria does not allow a dx of IBD to be made

58
Q

What are PAMP receptors and what to they do?

A

Pathogen-associated molecular patterns. They are recognized by PRRs (pattern recognition receptors) in the innate immune system

TLRs are a kind of PRRs?

SAM 2 (2 decks)

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