Environmental/GI/Endocrine

Question 1

According to Burkitt Creedon (2015), what defines Critical Illness-Related Corticosteroid Insufficiency (CIRCI) in veterinary patients?

Answer 1

CIRCI is a state of inadequate corticosteroid activity for the severity of illness, often characterized by vasopressor-resistant hypotension and reduced responsiveness to ACTH despite normal cortisol levels.

Question 2

What are the two main diagnostic challenges of CIRCI in dogs and cats, as discussed by Burkitt Creedon (2015)?

Answer 2

1) Lack of validated diagnostic tests (e.g., baseline cortisol or ACTH stim). 2) Overlap of clinical signs with critical illness.

Question 3

According to Burkitt Creedon (2015), what is the rationale for low-dose corticosteroid therapy in suspected CIRCI?

Answer 3

Low-dose corticosteroids (e.g., hydrocortisone 0.5–1 mg/kg IV q6–8h) are intended to restore vascular tone and improve catecholamine responsiveness without significant immunosuppression.

Question 4

According to Mignan et al. (2020), what are the four subtypes of acquired myasthenia gravis in dogs and cats?

Answer 4

1) Focal, 2) Generalized, 3) Fulminant, 4) Paraneoplastic (especially thymoma-associated).

Question 5

What distinguishes congenital myasthenic syndromes (CMS) from acquired MG in dogs and cats, per Mignan et al. (2020)?

Answer 5

CMS are inherited defects in neuromuscular transmission (often presynaptic or synaptic), while MG is immune-mediated and involves anti-AChR antibodies.

Question 6

Which breeds are predisposed to CMS as described by Mignan et al. (2020)?

Answer 6

Jack Russell Terriers, Springer Spaniels, and Smooth Fox Terriers.

Question 7

According to Bruchim et al. (2017), what are the major mechanisms of heatstroke-induced organ dysfunction?

Answer 7

Heat cytotoxicity, endotoxemia from GI barrier failure, systemic inflammation, coagulopathy, and direct cellular injury from hyperthermia.

Question 8

What key organ systems are most affected in canine heatstroke per Bruchim et al. (2017)?

Answer 8

CNS, gastrointestinal tract, liver, kidneys, and coagulation system (often manifesting as DIC).

Question 9

How does heatstroke lead to coagulopathy according to Bruchim et al. (2017)?

Answer 9

Endothelial injury and cytokine release trigger procoagulant pathways and consumption of clotting factors, leading to DIC.

Question 10

What are the core goals of therapy in canine heatstroke per Bruchim et al. (2017)?

Answer 10

Rapid cooling, fluid resuscitation, correction of coagulopathy, and organ support.

Question 11

According to Brodeur et al. (2017), what are the three phases of therapeutic hypothermia in dogs and cats?

Answer 11

1) Induction, 2) Maintenance, 3) Rewarming.

Question 12

What is the physiologic rationale for targeted temperature management (TTM) in veterinary patients per Brodeur et al. (2017)?

Answer 12

TTM reduces cerebral metabolic demand, stabilizes cell membranes, attenuates inflammation, and reduces excitotoxic neurotransmitter release.

Question 13

What are the complications of hypothermia in dogs and cats discussed by Brodeur et al. (2017)?

Answer 13

Bradycardia, coagulopathy, arrhythmias, decreased drug metabolism, shivering, and infection risk.

Question 14

According to the VITAMINS RCT (Fujii et al., 2020), what was the effect of adding vitamin C and thiamine to hydrocortisone in septic shock patients?

Answer 14

There was no significant difference in vasopressor-free days compared to hydrocortisone alone; the combination therapy did not improve outcomes.

Question 15

What is the mechanistic rationale behind using vitamin C and thiamine in septic shock (Fujii et al., 2020)?

Answer 15

Vitamin C supports endothelial function and catecholamine synthesis, thiamine is essential for aerobic metabolism, and both may reduce oxidative stress.

Question 16

What are the most common enteropathogenic bacteria in dogs and cats as reviewed by Marks et al. (2011)?

Answer 16

Salmonella, Campylobacter, Clostridium perfringens, Clostridium difficile, and E. coli.

Question 17

According to Marks et al. (2011), which tests are recommended for diagnosing enteropathogenic bacteria in small animals?

Answer 17

Fecal culture, PCR, ELISA for toxins (e.g., C. difficile), and electron microscopy in some cases.

Question 18

What are the main treatment principles for enteropathogenic bacteria in dogs and cats (Marks et al., 2011)?

Answer 18

Supportive care, judicious use of antimicrobials (based on pathogen), and infection control measures to prevent zoonosis.

Question 19

According to Lidbury et al. (2016), what are the key pathophysiologic mechanisms of hepatic encephalopathy (HE)?

Answer 19

Ammonia accumulation, inflammation, impaired neurotransmission (GABA, glutamate), cerebral edema, and altered blood-brain barrier permeability.

Question 20

What clinical signs are associated with hepatic encephalopathy in dogs and cats per Lidbury et al. (2016)?

Answer 20

Altered mentation, ataxia, seizures, head pressing, ptyalism (cats), and episodic dullness.

Question 21

What diagnostic tests support the diagnosis of hepatic encephalopathy (Lidbury et al., 2016)?

Answer 21

Elevated fasting/fed ammonia, abnormal bile acids, low BUN, low albumin, and imaging (microhepatica, portosystemic shunt).

Question 22

What treatments are recommended for hepatic encephalopathy according to Lidbury et al. (2016)?

Answer 22

Lactulose, antibiotics (e.g., ampicillin, metronidazole), protein restriction (for acute episodes), and addressing underlying hepatic disease.

Question 23

What is the role of lactulose in HE management (Lidbury et al., 2016)?

Answer 23

Acidifies colonic contents, traps ammonia as ammonium, and reduces systemic absorption of nitrogenous compounds.

Question 24

According to Burkitt Creedon (2015), what defines Critical Illness-Related Corticosteroid Insufficiency (CIRCI) in veterinary patients?

Answer 24

CIRCI is a condition where cortisol activity is inadequate relative to the severity of illness, often seen with hypotension unresponsive to vasopressors, despite normal or low-normal cortisol concentrations.

Question 25

What physiologic systems are impaired in CIRCI, per Burkitt Creedon (2015)?

Answer 25

Impaired hypothalamic-pituitary-adrenal (HPA) axis responsiveness, reduced cortisol receptor sensitivity, and altered tissue metabolism of glucocorticoids.

Question 26

What is the function of cortisol in the stress response?

Answer 26

Cortisol maintains vascular tone, enhances catecholamine responsiveness, modulates immune function, and regulates glucose metabolism during critical illness.

Question 27

What defines an "adequate" adrenal response in ACTH stimulation testing?

Answer 27

A post-ACTH serum cortisol > 2–5 µg/dL above baseline or an absolute value > 10–15 µg/dL, though criteria vary.

Question 28

What is the mechanism of action of hydrocortisone in treating CIRCI?

Answer 28

Hydrocortisone mimics endogenous cortisol, restoring receptor activation, increasing adrenergic receptor expression, and improving vasomotor tone and perfusion.

Question 29

According to Mignan et al. (2020), how does myasthenia gravis impair neuromuscular transmission?

Answer 29

Autoantibodies target nicotinic acetylcholine receptors (AChR) at the neuromuscular junction, reducing signal transmission and leading to muscle weakness.

Question 30

What pathophysiologic defect underlies congenital myasthenic syndromes (CMS)?

Answer 30

Genetic mutations affecting presynaptic vesicle release, synaptic cleft enzymatic function (e.g., acetylcholinesterase), or postsynaptic receptor function.

Question 31

What clinical signs suggest fulminant MG in dogs or cats (Mignan et al., 2020)?

Answer 31

Rapidly progressive generalized weakness, megaesophagus, respiratory failure, and often a poor prognosis.

Question 32

According to Bruchim et al. (2017), what are the initiating mechanisms of heatstroke-induced systemic inflammation?

Answer 32

Hyperthermia damages epithelial and endothelial cells, disrupts GI integrity, promotes endotoxemia, and activates DAMPs, TLRs, and proinflammatory cytokines (e.g., TNF-α, IL-6).

Question 33

What is the role of the gut in heatstroke pathogenesis (Bruchim et al., 2017)?

Answer 33

Heat-induced intestinal ischemia and epithelial barrier disruption allow bacterial endotoxin translocation, promoting systemic inflammation and DIC.

Question 34

How does hyperthermia impair cellular function (Bruchim et al., 2017)?

Answer 34

It denatures proteins, disrupts membrane fluidity, impairs mitochondrial function, and induces oxidative stress and apoptosis.

Question 35

What is the definition of targeted temperature management (TTM), per Brodeur et al. (2017)?

Answer 35

TTM refers to deliberate reduction and maintenance of core body temperature to reduce ischemia-reperfusion injury, especially after cardiac arrest or neurologic insult.

Question 36

What are the neuroprotective mechanisms of hypothermia during TTM?

Answer 36

Decreased cerebral metabolic rate (CMRO₂), inhibition of excitotoxic neurotransmitters (e.g., glutamate), reduced free radical generation, and stabilization of the blood-brain barrier.

Question 37

Why is controlled rewarming important in TTM (Brodeur et al., 2017)?

Answer 37

Rapid rewarming can cause vasodilation, hypotension, electrolyte shifts (e.g., rebound hyperkalemia), and cerebral edema.

Question 38

According to Fujii et al. (2020), what hypothesis did the VITAMINS trial test in septic shock?

Answer 38

That combination therapy with vitamin C, thiamine, and hydrocortisone would improve time alive and free of vasopressors compared to hydrocortisone alone.

Question 39

Why might vitamin C be beneficial in septic shock (Fujii et al., 2020)?

Answer 39

It supports vasopressor synthesis, scavenges reactive oxygen species, improves endothelial function, and may modulate inflammation.

Question 40

Why is thiamine given in sepsis (Fujii et al., 2020)?

Answer 40

Thiamine is a cofactor for pyruvate dehydrogenase and α-ketoglutarate dehydrogenase, supporting aerobic metabolism and reducing lactic acidosis.

Question 41

According to Marks et al. (2011), which enteropathogens are most relevant in veterinary patients?

Answer 41

Salmonella, Campylobacter spp., Clostridium perfringens, Clostridium difficile, enterotoxigenic E. coli, and Yersinia.

Question 42

What is the role of bacterial culture vs PCR in diagnosis (Marks et al., 2011)?

Answer 42

Culture is traditional but lacks sensitivity for some pathogens; PCR is more sensitive but detects DNA regardless of viability or clinical relevance.

Question 43

What infection control practices are critical for zoonotic bacterial enteropathogens (Marks et al., 2011)?

Answer 43

Isolation, hand hygiene, glove use, proper sanitation, and communication with owners about zoonotic risks.

Question 44

What is hepatic encephalopathy (HE) as described by Lidbury et al. (2016)?

Answer 44

A neuropsychiatric syndrome due to hepatic insufficiency or portosystemic shunting, characterized by ammonia and neurotoxin accumulation leading to CNS dysfunction.

Question 45

How does ammonia contribute to HE pathophysiology?

Answer 45

Ammonia crosses the BBB, is metabolized by astrocytes to glutamine, causing astrocyte swelling, cerebral edema, and impaired neurotransmission.

Question 46

What are the key neurotransmitters disrupted in HE (Lidbury et al., 2016)?

Answer 46

Increased GABAergic tone (neuroinhibition), altered glutamate signaling, and serotonin/dopamine imbalance.

Question 47

What treatment mechanisms reduce ammonia levels in HE?

Answer 47

Lactulose acidifies the colon and traps ammonia, antibiotics reduce ammonia-producing bacteria, and dietary protein restriction reduces substrate load.

Question 48

What is the function of astrocytes in HE-associated brain injury?

Answer 48

Astrocytes uptake ammonia and convert it to glutamine, but excessive glutamine causes osmotic swelling and oxidative damage.

Question 49

What are the systemic consequences of HE that may worsen critical illness?

Answer 49

Seizures, cerebral edema, hypokalemia (from lactulose), hypoglycemia, coagulopathy, and systemic inflammation.

Question 50

What defines the 'controller algorithm' in TTM physiology?

Answer 50

The hypothalamus functions as the central controller, adjusting thermoregulatory responses based on feedback from peripheral temperature sensors.

Question 51

What are the physiologic feedback loops involved in TTM and hypothermia?

Answer 51

Negative feedback loops involving peripheral thermoreceptors → hypothalamic thermoregulatory centers → autonomic and behavioral responses (shivering, vasoconstriction).

Question 52

What mechanism contributes to CIRCI despite normal cortisol levels (Burkitt Creedon, 2015)?

Answer 52

Tissue-level glucocorticoid resistance, due to downregulation or dysfunction of glucocorticoid receptors and post-receptor signaling, can render cortisol ineffective.

Question 53

What is the role of 11β-hydroxysteroid dehydrogenase in CIRCI?

Answer 53

11β-HSD type 1 activates cortisol from cortisone; decreased activity in critical illness may impair local cortisol bioavailability at tissues.

Question 54

In myasthenia gravis (Mignan et al., 2020), why is thoracic imaging recommended?

Answer 54

To identify thymoma or mediastinal masses associated with paraneoplastic MG, which may influence prognosis and treatment.

Question 55

What is a clinical test to differentiate MG from CMS in practice (Mignan et al., 2020)?

Answer 55

A positive response to an acetylcholinesterase inhibitor (e.g., edrophonium or pyridostigmine) supports acquired MG; CMS may have poor or paradoxical responses.

Question 56

Why can dogs with CMS deteriorate when given pyridostigmine (Mignan et al., 2020)?

Answer 56

In some CMS variants, excess acetylcholine or prolonged receptor activation worsens the synaptic defect.

Question 57

What post-rewarming complication is associated with TTM (Brodeur et al., 2017)?

Answer 57

Rebound hyperkalemia and vasodilation due to sudden shifts in vascular tone and potassium efflux from cells during rewarming.

Question 58

How does shivering during TTM physiologically impact oxygen balance (Brodeur et al., 2017)?

Answer 58

Shivering increases VO₂ up to 500%, counteracting the neuroprotective goals of TTM by elevating metabolic demand.

Question 59

Why does hypothermia mask clinical signs of shock or pain (Brodeur et al., 2017)?

Answer 59

Hypothermia suppresses metabolic activity, cardiac output, and neurohormonal responses, leading to falsely reassuring exam findings.

Question 60

What distinguishes heatstroke from simple hyperthermia (Bruchim et al., 2017)?

Answer 60

Heatstroke involves CNS dysfunction, SIRS, DIC, and MODS, whereas hyperthermia alone does not cause systemic failure or cytotoxicity.

Question 61

What causes delayed DIC after heatstroke (Bruchim et al., 2017)?

Answer 61

Ongoing endothelial damage, cytokine release, and exposure of tissue factor activate coagulation pathways even after normothermia is restored.

Question 62

Why is it inappropriate to treat all C. perfringens PCR-positive dogs with antibiotics (Marks et al., 2011)?

Answer 62

Asymptomatic carriage is common, and PCR detects DNA regardless of toxin production or clinical relevance—overuse promotes dysbiosis.

Question 63

Which test confirms clinically relevant C. perfringens infection (Marks et al., 2011)?

Answer 63

Detection of Clostridium perfringens enterotoxin (CPE) via ELISA or PCR with supportive clinical signs.

Question 64

What are Alzheimer type II astrocytes and how do they relate to HE (Lidbury et al., 2016)?

Answer 64

These are swollen astrocytes with pale nuclei seen in HE, reflecting ammonia-induced metabolic stress and cytotoxic edema.

Question 65

What is the role of systemic inflammation in hepatic encephalopathy (Lidbury et al., 2016)?

Answer 65

Proinflammatory cytokines (TNF-α, IL-6) worsen neurotoxicity by amplifying astrocyte dysfunction and disrupting neurotransmitter balance, even without hyperammonemia.

Question 66

Why might lactulose worsen dehydration or electrolyte status in HE?

Answer 66

Overuse can lead to diarrhea, volume depletion, and hypokalemia, which in turn exacerbate HE symptoms.

Question 67

What is the hypothalamus’s role as a controller in TTM physiology?

Answer 67

It integrates signals from peripheral thermoreceptors and regulates autonomic and endocrine responses to maintain a target setpoint.

Question 68

What defines an 'input sensor' in thermoregulation?

Answer 68

Thermoreceptors in the skin, spinal cord, and hypothalamus detect environmental and core body temperature changes.

Question 69

What is the ‘actuator’ in TTM or thermoregulatory response?

Answer 69

Effectors like sweat glands, vasomotor tone, skeletal muscles (shivering), and behavior (seeking warmth/cold) that execute the thermal response.

Question 70

How does ammonia cross the blood-brain barrier in HE?

Answer 70

Ammonia diffuses passively into the brain and is taken up by astrocytes, where it is converted to glutamine by glutamine synthetase.

Question 71

Why does glutamine accumulation cause cerebral edema in HE?

Answer 71

Glutamine is osmotically active, and its accumulation in astrocytes causes cytotoxic swelling and increased intracranial pressure.

Question 72

How does GABAergic tone change in hepatic encephalopathy?

Answer 72

There is increased GABAergic neuroinhibition due to elevated endogenous benzodiazepine-like substances and altered receptor activity.

Question 73

What neurotransmitter pathways are altered in HE beyond GABA?

Answer 73

Glutamate, serotonin, dopamine, and histamine pathways are also affected, contributing to altered mentation and behavior.

Question 74

What is the rationale behind titrating lactulose to soft stools in HE treatment?

Answer 74

To ensure sufficient reduction in ammonia absorption without causing dehydration or hypokalemia.

Question 75

Why might a septic patient with CIRCI not respond to vasopressors alone?

Answer 75

Glucocorticoid deficiency or resistance impairs adrenergic receptor function and vascular tone, requiring corticosteroid supplementation for hemodynamic stability.