Possible Essay Questions

Question 1

Describe proposed mechanisms of T. blagburni pathogenicity in cats.

Answer 1

• Infection via direct fecal oral route à no oocyst form & 1-stage asexual lifecycle
• Suspect colonic bacteria facilitate infection à nutrient source for T. blagburni or other potentiation
• Mucinase activity allows penetration thru mucus layer? May degrade mucus Ig and lactoferrin for nutrients
• Contact with epi à ameboid transformation, adherence & upregulation of virulence factors
  
  • Binds sialic acid portion of epi cell glycoconjugates OR may cleave it to use other adhesins after initial bindng
  • Trichomonad surface carbohydrates à lipophosphoglycan
  • Cysteine proteases
• Ameboid form à cytotoxicity via disruption of tight junctions, detachment & apoptosis
  
  • Cysteine proteases probably both adhesins and cytotoxic mediators
  • Phospholipases and porins
• Subepithelial invasion and host immunity evasion
  
  • Induce apoptosis in host innate immune cells & phagocytose leukocytes
  • Inhibits NF-kB activity à decreased TNFa and IL-12 activity
  • Enhances expression of anti-inflammatory cytokines IL-10, TGFb
  • Cysteine protease-mediated degradation of surface bound complement C3, IgGs, fibrinogen, albumin, others
  • Phenotypic variation & antigenic heterogeneity à not recognizable to immune system
  • BUT still characterized by influx of neuts, lymphs, plasma cells in to lamina propria
    
    • Likely contributes to diarrhea from T. blagburni

Question 2

Write out the arachidonic acid cascade.

Why are omega-3 fatty acids anti-inflammatory?

Where in the cascade do aspirin, NSAIDs, and glucocorticoids act?

Which NSAIDs are selective vs. nonselective COX inhibitors?

Question 3

1. What processes occur in fasting/insulin deficiency that lead to excessive ketone body production?

Answer 3

1. Fatty acids are processed via beta-oxidation into acetyl-CoA; normally would go to TCA cycle & electron transport chain to be fully processed into ATP
2. Insulin actions
   
   1. Upreg acetyl-CoA carboxylase; A-CoA to malonyl-CoA à reduces activity of carnitine palmitoyltransferase 1 which brings FAs into mitochondria for beta ox
   2. Inhibits hormone sensitive lipase, which cleaves a free fatty acid off a triglyceride stored in adipose tissue
   3. No insulin -> more free fatty acids & easier access to beta oxidation
3. Gluconeogenesis has used up available oxaloacetate, so the citric acid/TCA cycle isn’t working efficiently
4. Acetyl-CoA from beta oxidation accumulates & is shunted into ketogenic pathways

Question 4

Thyroid hormone synthesis, regulation, and degradation?

Sensitivity of basal TSH for hypothyroidism in dogs?

Effect of hypothyroidism on insulin sensitivity?

Effect of hyperadrenocorticism/GC administration on thyroid axis?

What drugs inhibit thyroid peroxidase activity?

Answer 4

basal TSH: 67-82% sensitive (normal in lots of hypothyroid dogs)

Question 5

Causes of hypoxia vs. hypoxemia? What’s the difference?

Answer 5

Hypoxemia = decreased PaO2 (dissolved O2 in the blood)

Hypoxemia causes

1. Decreased FiO2 (altitude) -> normal A-a
2. Hypoventilation -> normal A-a (hypoventilation decreases A)
3. V/Q mismatch
4. Diffusion defect
5. R-L shunt

Hypoxia = decreased oxygen delivery to tissues

1. Hypoxemia
2. Decreased cardiac output
3. Anemia
4. Carbon monoxide or cyanide poisoning