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Boards: GI > GI Case Management > Flashcards

GI Case Management Flashcards

1
Q

Oropharyngeal Diseases

A

Patients with pharyngeal dysphagia more prone to regurgitation, aspiration esp in cases where large space-occupying lesion compressing CN IX, X – responsible for series of involuntary movements that transport food bolus into stomach, protect airway during swallowing

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2
Q

Why Mandiblectomies Prone to Hemorrhage

A

inferior alveolar artery (br mandibular artery) runs through ramus of mandible, almost always transected during surgery

Coags before sx

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3
Q

Why Maxillectomies Prone to Hemorrhage

A

transection of either or both major palatine artery, infraorbital artery
o Transection depends on location of tumor
o Both = branches of maxillary artery

Rostral maxillectomy: diffuse bleeding from highly vascularized nasal turbinates

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4
Q

Oral Pharyngeal Dz and Intubation

A

Potential challenges for intubation- retrograde

eg TMJ ankylosis, MMM

o Puncture cricothyroid membrane with needle or IVC
o Insert guide wire through needle and advanced retrograde through mouth opening then feed ET over guide wire into larynx
o Remove guidewire so further advanced ET into trachea

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5
Q

Reflex Assoc with Maxillofascial Sx

A

trigeminovagal reflex (rarely reported in vet med)

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6
Q

Bezold-Jarish Reflex

A

stimulation of [ventricular] cardiac chemoR or stretch R (mechanoR) – induction of sinus bradycardia, hypotension, peripheral VD

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7
Q

Bainbridge Reflex

A

increase HR caused by rise in BP in great veins as enter RA

Fluid Bolus

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8
Q

Vasovagal Reflex

A

decrease in venous return to heart (hypovolemia, compression of caudal VC, regional analgesia) – sinus bradycardia, vasodilation

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9
Q

Esophageal Composition

A

o Dogs: striated m
o Cats, pigs, horses, primates: proximal 2/3 striated m, distal 1/3 SmM

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10
Q

Muscles that Compose UES

A

cricopharyngeus, thyropharyngeus m

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11
Q

What is the most common cause of benign esophageal stricture in dogs, cats?

A

GA-related GER –> esophagitis

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12
Q

Esophagitis Related to GER

A

esophageal mucosa exposed to caustic substances for prolonged periods +/- esophageal defense mechanisms (EDMs) impaired/overwhelmed

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13
Q

What are esophageal defense mechanisms?

A

superficial mucus/bicarb layer, tight junctions btw epithelial cells, intracellular/interstitial buffering capacity dependent on BF

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14
Q

Incidence, Consequence of GER/esophagitis?

A

Signs: days to three weeks to appear

Mortality: 21-30%, low incidence (~0.1%)
 Greater risk with intraabdominal sx, esp OVH

CS perforation: pneumothorax, pleuritis, pyothorax, resp distress

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15
Q

MOA GER Esophagitis

A

Reduced LES pressure allows contents to enter esophagus more easily

Swallow reflex absent; acidic gastric acid contents (pH <4) cannot be neutralized by patient swallowing basic saliva

Reduced esophageal peristalsis

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16
Q

Factors that Increase GER/Decrease LES Pressure

A

 Older or younger animals
 Dogs >40kg
 Large, deep chested dogs esp in sternal recumbency
 Dorsal recumbency
 Change in Position During GA
 Prolonged fasting times (>10hr), shorter fasting times (3h)
 Intraabdominal sx, including laparoscopy
 Ax duration >105’
 GA during second half of pregnancy

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17
Q

What percentage of animals that experience GER will actually regurgitate?

A

Only 0-15% in patients experiencing GER will actually regurg

Incidence of GER in dogs, cats without hx of GI or esophageal dz: 12-67% based on esophageal pH meters

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18
Q

Treatment of Esophagitis/GER

A

H2RA tachyphylaxis may occur in 3-13d – PPIs more effective at treating reflux esophagitis, maintaining effects on pH

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19
Q

Should you include an anticholinergic indiscriminately in your canine, feline premeds?

A

NO!

 Decreases LES tone
 Minimal effect on gastric pH at clinical doses – higher doses, will inhibit H plus secretion by gastric parietal cells via M1

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20
Q

Congenital or Idiopathic ME

A

defect of vagal sensory innervation where esophageal peristalsis does not occur, no detection of dilation caused by food bolus

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21
Q

Acquired Megaesophagus

A

mechanical obstruction –> Vascular ring anomaly, esophageal stricture, hiatal hernia, tumor, granuloma, FBs
* Over time, dilation of esophagus proximal to lesion becomes irreversible

Idiopathic acquired: most common form in adults – loss of normal esophageal motility eventually results in dilation

Secondary to/assoc with other diseases:
* Peripheral neuropathy, laryngeal paralysis, MG, severe esophagitis, lead poisoning, lupus myositis, chronic/recurrent GD or GDV

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22
Q

Main Anesthetic Concerns Assoc with ME

A

GER, regurg, aspiration

Prolonged fasting not necessary: dysmotility, dilation prevent complete emptying of esophageal contents

Potential for repeated episodes of asp pneumonia, greater risk for postop hypoxemia

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23
Q

Stricture Ballooning/Upper GI Endoscopy

A

o Pyloric sphincter tone may increase with pure MOR agonists, ketamine

o Gastric distention: hypoventilation, decreased venous return; vagal nerve stimulation from distended viscous

o Overdistention of GIT = activation of stretch R within walls, sudden/profound vagally-mediated bradycardia, tx: immediate deflation, atropine

o Inflation of hollow viscus with air = dull cramping pain of poorly localized discomfort ; Intraop analgesia +/- TAP block: more stable plane of ax

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24
Q

Laparoscopy - Effects of CO2 Insufflation

A

Decrease venous return, impair ventilation
 Increase in SVR, decreased preload, potential for hypotension

Decreases FRC, reduced compliance – predisposed to VQ mismatch

Cranial displacement of diaphragm – more difficult for SpV to maintain adequate minute ventilation, IPPV may be required
 PPV: decreases HBF

CO2 freely diffuses into splanchnic circulation

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25
Q

Levels of Abdominal Pressure Assoc with Laparoscopy

A

Intraabdominal pressure 10-16 mmHg, HBF increased >12mm Hg (humans)
o Ideally want intraabdominal pressure as low as possible
o Decrease in blood flow to GIT
o Decreased GFR = AKI

Transient increases in hepatic transaminases up to 48hr after desufflation
o Increases in ALT, AST directly proportional to intra-abdominal pressure, duration of insufflation

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26
Q

Other Effects of Laparoscopy

A

VQ mismatch: potential for large differences btw ETCO2, PaO2, worse with Trendelenburg

Increased ICP

Hypercapnia

Air Embolism

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27
Q

Air Embolism with Laparoscopy

A

Absorption of CO2 via ruptured blood vessel, etc: rapid absorption of CO2 into tissues (as opposed to nitrogen) means that it seldom causes clinical problems

Microemboli don’t cause as severe issues as pass through right side of heart&raquo_space; Wedge in pulmonary vessels where they create V/Q mismatching/ pulmonary hypertension/ atelectasis, can be eliminated through lungs

Large gas emboli can become lodged in RA or RV or PA where they stop passage of blood through the heart&raquo_space; Rapidly fatal

If reach systemic circulation, obstruct BF - cause hypoxia in critical organs (eg cerebral, coronary arteries most vulnerable)

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28
Q

Tolerable Levels of Air in Circulation

A

0.35mL/kg/min in dogs, pigs 2mL/kg

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29
Q

How Reduce Risk of Embolism with Laparoscopy

A

by slowing rate of abdominal insufflation to <1 L/min  more time for pulmonary clearance of air bubbles

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30
Q

Diagnosis of Air Embolism

A

Behavior changes (agitation, change in demeanor)

changes in ETCO2 readings (V/Q mismatch with rapid drop in CO2 when ventilation held constant)

development of mill-wheel heart murmur (harsh, churning, splashing, metallic)

Hypotension, tachypnea

TEE = definitive diagnosis

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31
Q

Treatment of Air Embolism

A

Remove insufflated gas from abdomen

Address any non-ligated vasculature

increase CVP (to encourage bleeding rather than air entrainment)

discontinue N2O admin, administer 100% O2

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32
Q

Nitrous and Air Emboli

A

Admin of N2O: exacerbates gas emboli as diffuses into air pockets, expands them

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33
Q

Induction and Maintenance of Patients with GDV, Splenic Masses

A

TP, propofol sensitize myocardium to catecholamine-assoc arrhythmias
o Also why des, iso, sevo preferred for maintenance vs halothane
* DO NOT INDUCE VIA INHALANT TECHNIQUE

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34
Q

Pathogenesis of SI Intraluminal Obstruction

A

Intestine rostral to FB extends with gas, fluid (fluid DT increased secretion from intestinal glands, retention of fluid)

Fluid shifts from serosa into peritoneal cavity

Circulation in mucosa becomes ischemic, wall necrosis possible

Bacterial overgrowth, may translocate if normal mucosal barrier impaired by distention, ischemia

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35
Q

Consequences of Manipulation, Derotation of Ischemic Bowel

A

release of numerous inflammatory mediators that cause VD, cardiac dysfunction
 Ischemic reperfusion injury, endotoxemic shower/shock
 Lidocaine CRI, dexmedetomidine CRI

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36
Q

Analgesia in Abdominal Sx

A

Innervation: sympathetic chain T1-L3/4, abdominal wall innervation T11-13/L1-3

Innervated primarily by C fibers: poorly localized, may be assoc with autonomic responses DT adjacent travel with ANS fibers

Stimulus from distention, contraction, inflammatory mediators, ischemia

Referred pain: distant from source, DT convergence of afferent nerve pathwas onto same DH neurons

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37
Q

Pathophysiology of GDV

A

Gastric distention, torsion – compromised BF to stomach, surrounding organs

CV compromise DT obstruction of (low pressure) caudal VC, portal vein, splenic veins

Obstruction of vessels = decreases venous return, increased venous pressure –> severe hypovolemic shock, decreased oxygen delivery

DO CO, hypotension + splanchnic pooling/portal hypertension = interstitial edema, loss of IV volume
o Distention of stomach, increased abdominal pressure restricted ventilation via interference with diaphragmatic excursion

Respiratory compromise, possible partial lung collapse

Decreased VT, VQ mismatch – hypercapnia, hypoxemia despite increased RR, effort

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38
Q

Consequences of GDVs

A
  1. Arrhythmias
  2. Hemoabdomen - rupture of short, large bore gastric arteries
  3. Mixed Acid, base Disturbances
  4. Splenic Compromise/Vascular avulsion
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39
Q

Arrhythmias Assoc with GDV

A

Common – mainly ventricular, ~40% of GDV dogs

Coronary BF decreased by 50% in GDVs: myocardial ischemia establishes ectopic foci of electrical activity
* Supported by elevated cardiac troponins in GDV

Also circulating catecholamines, pro inflammatory cytokines

Tx: >160, multifocal, R on T, impact on hemodynamic status – lidocaine bolus, CRI

40
Q

Acid Base Disturbances with GDV

A
  • Initial hypochloremic metabolic alkalosis – sequestration of gastric HCl DT outflow tract obstruction, vomiting, salivation
  • High anion gap (lactate) acidosis secondary to low DO2
    –Ischemia, contributions from release of inflammatory mediators
  • Respiratory acidosis from hypoventilation, hypercapnia

Also hypokalemia

41
Q

MOA hypokalemia with GDV

A

administration of large volumes of low K containing fluids, loss of K via vomiting, hypochloremic metabolic alkalosis with transcellular shifting, RAAS activation, catecholamine-induced intracellular shifting of K+

42
Q

Gastric Necrosis with GDV

A

when >1 hemostatic test abnormal, lactate greatly elevated at presentation +/- fails to decrease significantly with fluid resuscitation predicting a poor outcome

MOA: gastric wall tension exceeds driving pressure in gastric wall arterioles, capillaries
 Reduced CO –> gastric necrosis –> increased mortality

43
Q

Risk Factors Assoc with Badness in GDVs

A

hypotension during hospitalization, combined splenectomy + partial gastrectomy, peritonitis, sepsis, DIC

Consider avoidance of hyperoxia – greater damage following reperfusion in patients maintained at higher than normal O2 levels

44
Q

GI Neoplasia Considerations

A

Main considerations with GI Neoplasia:
*Hypercalcemia of malignancy
–Muscle tremors, weakness, arrhythmias
*Hypoproteinemia
*Anemia
*Monitor BG with GI stromal tumors - secrete insulin, also lymphoma, leiomyomas
*MCTs: histamine release

45
Q

Hemoabdomen: volume replacement with crystalloids

A

3x volume for acute hemorrhage
8x gradual loss affecting intracellular volume

Losses 20-30% total blood volume replaced with FWB, plasma, colloids + pRBCs

46
Q

Mesenteric Traction Syndrome

A

tachycardia, hypotension, cutaneous hyperemia in humans undergoing abdominal surgery

Release of prostacyclin, histamine, other vasoactive substances cause fluctuations in hemodynamic status when tension placed on mesenteric vasculature

47
Q

Mortality with Septic Abdomen

A

31-64%

Higher survival rates with secondary peritonitis treated surgically vs medical management, primary peritonitis

Other risk factors: pre‐existing peritonitis, low albumin/protein levels, intraoperative hypotension, hyperlactatemia

48
Q

Diagnosis of Septic Abdomen

A

AXR/AUS – specific lesion with or without effusion in secondary peritonitis

Confirmation: septic infiltrate cytology of peritoneal effusion or lavage fluid

Lactate often increased in serum +/- abdominal fluid.

Peritoneal lactate, comparison of serum with peritoneal lactate diagnostic in ≥90% of dogs, not accurate in cats

49
Q

Sepsis

A

presence of SIRS in response to most often bacterial but fungal or protozoal infections
o May progress to severe sepsis with multiple organ dysfunction (MODS), poor perfusion, hypotension

50
Q

Septic Shock

A

Acute circulatory failure, persistent arterial hypotension despite volume resuscitation assoc with sepsis

SAP <90, MAP <60

51
Q

Bacteremia

A

Presence of live bacterial organisms in bloodstream

52
Q

Sepsis Definition

A

Clinical syndrome caused by infection, host’s systemic inflammarioty response to it

May be bacterial, viral, protozoal, fungal in origin

53
Q

SIRS - definition

A

Clinical signs of SIRS to infectious or noninfectious insults

54
Q

MODS - def

A

Physiologic deranges of endothelial, cardiopulmonary, renal, nervous, endocrine, GI systems assoc with progression of uncontrolled systemic inflammation or DIC

55
Q

Hypovolemic Shock

A

Decrease in circulating blood volume

hemorrhage, severe dehydration, trauma

56
Q

Cardiogenic Shock

A

Decrease in forward flow from heart

CHF, arrhythmias, tamponade, drug overdose

57
Q

Distributive Shock

A

Marked decrease or increase in SVR or maldistribution of blood

Sepsis, anaphylaxis, obstruction (HW dz, saddle thrombosis), catecholamine excess, GDV

58
Q

Metabolic Shock

A

Deranged Cellular Metabolic Machinery

Hypoglycemia, cyanide toxicity, mitochondrial dysfunction, cytopathic hypoxia of sepsis (maybe MH)

59
Q

Hypoxemia Shock

A

Decrease in PaO2

Anemia, severe pulmonary dz, CO toxicity, methemoglobinemia

60
Q

Type I Hyprsensitivity Run

A

Immediate, IgE dependent - histamine release

Anaphylaxis

61
Q

Type II Hypersensitivity Run

A

Cytotoxic, IgG, IgM dependent

62
Q

Type III Hypersensitivity Run

A

Immune complex mediated, IgG/ IgM complex dependent

63
Q

Type IV Hypersensitivity Run

A

Delayed, T lymphocyte dependent

64
Q

Type IV Hypersensitivity Run

A

Delayed, T lymphocyte dependent

65
Q

Histamine Receptors

A

H1, H2, H3

66
Q

Role of H1

A

● Mediate coronary artery VC, cardiac depression
● Rhinitis
● Pruritus
● Bronchoconstriction
● Stimulation causes endothelial cells to convert L-arginine into NO (potent vasodilator)

67
Q

Role of H2

A

gastric acid production

produce systemic coronary and systemic vasodilation, increases in HR/ventricular contractility

68
Q

Role of H3

A

On presynaptic terminals of sympathetic effector nerves that innervate heart, systemic vasculature

These receptors inhibit endogenous norepi release from sympathetic nerves, so activation accentuates degree of shock observed during antigen challenge because compensatory neural adrenergic stimulation is blocked

69
Q

Role of Epi in Anaphylaxis

A

Stimulation of beta-adrenergic receptors enhances production of adenyl cyclase, subsequent conversion of adenosine triphosphate to cAMP

Inhibits antigen-induced release of histamine and other anaphylactic mediators

Improvement in MAP attributed to increase in CO from epi’s beta adrenergic effects on the heart, not its alpha 1 vasoconstrictive effects on systemic vasculature

70
Q

Pathophysiology of Sepsis

A

organisms +/- toxins gain access to circulation
 Classic explanation: release of endotoxin from Gram-negative organisms (LPS) and exotoxins/peptidoglycans from Gram-positive organisms

Activation of WBCs > release of potent inflammatory mediators

Damage to microvascular endothelium = loss of control of permeability, develop coagulopathy

Body generates anti-inflammatory response to maintain homeostatic balance: initially SIRS phase, then CARS phase

71
Q

SIRS Phase

A

Initially: ‘hyperdynamic’ stage (in dogs) with increased CO, tachycardia, vasodilation (bright red MM), shortened CRT

72
Q

CARS Phase

A

counter anti-inflammatory response syndrome, immunosuppressive phase

73
Q

What happens following hyper dynamic phase of shock?

A

 Proinflammatory effects overwhelm anti‐inflammatory response = CV collapse ensues with continued VD, myocardial dysfunction, poor perfusion, decreased CRT, bluish or pale MM, obtundation, hypothermia.

74
Q

MODS

A

Progressive, potentially reversible dysfunction of two or more organ systems after acute life threatening disruption of homeostasis

Dysfunction of either respiratory, CV, renal, coag system independently associated with significantly increased odds of death

75
Q

MOA MODS

A

 Systemic activation, dysregulation of inflammatory cascade causes organ dysfunction and failure
 Combined effect of inappropriate host defense response, dysregulation of immune/inflammatory responses leads to cell injury, tissue and organ failure

76
Q

One Hit Model

A

 Massive initial insult - major trauma, septic peritonitis

77
Q

Two Hit Model

A

 Multiple insults over short period of hours to days, eg major trauma followed by aspiration pneumonia
 Second hit induces exaggerated inflammatory response, immune dysfunction

78
Q

Three Hit Model

A

Sustained eg drug resistant bacterial infection

79
Q

Cryptic Shock

A

Loss of hemodynamic coherence leading to hyperlactatemia, acidemia despite normal perfusion parameters

Normalization of CV parameters may not equate to improvements in microcirculatory perfusion – macrocirculation vs microcirculation

80
Q

GIT and Role in SIRS

A

important role in generation of SIRS, sepsis even when intestinal serosa intact, primary source located elsewhere

Inflammation damages barrier function of GI mucosal lining – allows absorption of non-microbial factors into lymphatic system
 Eventually drain into venous system via thoracic duct
 Pathway contributes to magnification of ongoing SIRS, resp distress/dysfunction, MODS

Translocation of bacteria, bacterial product thought to occur via lymphatics vs portal system - not necessary for development of SIRS/MODS

81
Q

SIRS Parameters in Dogs

A

Need at least 2

HR >120bpm
RR >40, PaCO2 <30
T <100.4, >104
Leukogram >18,000 or <5000

82
Q

SIRS Parameters in Cats

A

Need at least 2

HR <140, >225
RR >40
T <100, >104
WBC >19,000 or <5000

83
Q

Goals of Resuscitation Therapy

A

MAP >65mm Hg, central venous O2 saturation >70%, CVP 8-12mm Hg, urine output >0.5mL/kg/hr

First line therapy choice = Balanced crystalloid electrolyte solution
 +/- albumin if protein/albumin low

84
Q

4 Main MOA of Refractory Hypotension with Sepsis

A
  1. Unregulated synthesis of NO (increased with acidosis)
  2. Local acidosis from anaerobic metabolism - electrolyte changes prevent SmM contraction
  3. Activation of AC - prevents increased intracellular Ca
  4. Depletion of VP from neurohypophysis
85
Q

MOA for refractory hypotension: acidosis

A

Local acidosis with hydrogen, lactic acid production from anaerobic metabolism

Opens ATP sensitive K channels in vascular SmM

Allows influx of K, prevents Ca from entering cells – SmM does not contract, vasoplegia

Hyperpolarization of vascular SmM cells

86
Q

MOA for refractory hypotension: activation of AC, prevention of increased intracellular Ca

A

Prostaglandin, prostacyclin concentrations increase which activates adenylyl cyclase

AC –> stimulates formation of cAMP, activates PKA and prevents increase in cytoplasmic Ca leading to vasodilation

87
Q

MOA for refractory hypotension: depletion of VP

A

Concentration increases 20 to 200 fold in hypotensive states, acute septic shock to help maintain vasoconstriction

Levels rapidly depleted, deficiency may contribute to pathogenesis of irreversible shock

88
Q

Synthetic VP

A

V1A R in SmM – intense nonadrenergic VC at endothelial level, preferentially constricts arterioles in extracerebral tissues

Decrease in inducible NO synthase activity, inhibits VD in septic shock

Also modulates Na/KATP channels, potentiates adrenergic or other vasoactive agents, allows for decreased dose of other catecholamines, effective in presence of acidemia

89
Q

CIRCI

A

Critical Illness-Related Corticosteroid Deficiency

Inadequate endogenous corticosteroid activity in relation to severity of patient’s illness

Corticosteroids = necessary for responsiveness to vasopressor therapy

Underlying pathophysiology unknown

90
Q

Potential MOAs CIRCI

A

 HPA dysfunction
 Alterations in cortisol-plasma protein binding
 Changes in glucocorticoid receptor function
 Target cell enzymatic changes
 Decreased production of ACTH, corticotropin releasing hormone, cortisol
 Adrenal damage from infarction, hemorrhage
 Adrenal suppression from chronic exogenous glucocorticoid administration
 Inflammatory cytokines causing systemic inflammation associated with glucocorticoid release

91
Q

Vasopressor Therapy in Sepsis

A

VPs: NE > epi > VP

Dopamine, phenylephrine not recommended in humans
 No difference found with use of various VPs in animals
 Lowest effective dose to avoid ischemia, mask persistent hypovolemia

Inotropes: myocardial depression

Alterations in BG: hyper or hypoglycemia – maintain normal levels

Relative adrenal insufficiency occurs in sepsis: consider physiologic doses of steroids

92
Q

POI

A

horses, rabbits, ruminants, humans

Drugs: anticholinergics, opioids, a2, inhalants, N2O, induction agents

93
Q

Which drug does not induce POI?

A

KETAMINE

94
Q

Opioids and POI

A

delay gastric emptying, increase sphincter tone, variably affect SmM ctx

Inhibit propulsive motility, enhance segmental contractions esp in colon
 Absorption increased, secretions decreased
 Constipation: frequent SE
 Epidural morphine: much faster return of GI motility in dogs, humans

95
Q

Return of GI Motility

A

Dogs: distal intestine/colon first > proximal intestine stomach

96
Q

MOA of POI

A

Paralysis of muscularis externa layer
 Local inflammatory response within muscularis layer after intestinal handing
 Resident macrophage activation proportional to intensity of damage
 Increases NO –> Decreases motility

Exacerbated by effects of anesthetic agents on motility, presence or development of peritonitis/sepsis

Boards: GI (4 decks)

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