NMhbu
These two prostaglandins are responsible for blood pressure regulation and anti-coagulation at the site of the afferent arterioles, which are of major concern during NSAID toxicity with ischemic injury being a primary concern as a result.
PGE2 and PGI2 (prostacyclin)
TOSS UP ROUND:
Both teams will both write their best guesses for the reference intervals for the PT and aPTT.
The team with the lowest difference in intervals will take the points and pick the next question. (Use normal dog RI, source eClinPath.
PT: 0-10 seconds
aPTT: 15-20 seconds
Tiebreaker if needed: ACT with MAX-ACT tube (answer ss on ur phone)
Growth Hormone (GH) significantly decreases the sensitivity of target organs to PTH. Do the following alterations in hormone level increase/decrease phosphorus secretion in urine.
1. Decreased GFR 2. Increased PTH 3. Increased GH
1. Decreases sP
2. Increases sP
3. Decreases sP (as long as there is some action happening from PTH)
The "Bezold-Jarish" response is common in about 25% of human patients, in situations where they encounter their own blood or see needles. It is the most common cause of vasovagal syncope.
This results from decreased cerebral blood flow due to parasympathetic, and sympathetic alterations. Give one reason, for each, stating why changes in ANS stimulation might cause decreased cerebral flow.
ParaNS: Increased asf, -> decreased HR (will accept CO)
SympNS: decreased, -> decreased TPR
Amylase of any origin is responsible for the breakdown of what specific bond, between glucoses.
Glycosidic (a1-4) linkages
A post-ganglionic sympathetic neuron going to the heart will release ___ to a ___ receptor.
A post-ganglionic parasympathetic neuron going to bronchial smooth muscle will release ___ to a ___ receptor.
A post-ganglionic sympathetic nerve fiber going to sweat glands will release ___ to a ___ receptor.
1. NE:a1/a2/b1/b2
2. ACh:Muscarinic
3. ACh:Muscarinic
Name at least four types of cells that make up erythropoiesis (you can include the obvious one(s)).
Other team can steal if you CANT name four, only if they have more listed than you. (3>2)
Rubriblast, Prorubricyte, Rubricyte, Polychromatophillic rubricyte, Metarubricyte, Reticulocyte, Erythrocyte.
___ is excreted in urine while ___ is reabsorbed.
Describe an acid/base disturbance that could be caused by hypovolemia in a patient, and give me an example pH (where the primary disturbance is metabolic).
Protons/Bicarbonate
Metabolic acidosis as a result of decreased proton excretion in urine. The pH should be anywhere south of 7.35
Many people experience nausea during a heavy lift, or a long run. Describe a blood gas that is appropriately compensating for the acid/base disturbance, and prioritize the disturbance. (Include pH, pCO2, HCO3-, and SBE)
pH: 7.28, pCO2: 28mmHg, HCO3-: 13mEq SBE: -10
TOSS UP ROUND: Write out the entire pathway of Gastrin signaling to the H-K pump.
Team with the most correct steps wins points and next turn.
Gastrin is released by G endocrine cells, binds to CCK receptors, stimulates Gq receptor, activates PLC, activated PLC causes conversion of PIP2 to IP3, IP3 releases Ca2+ from SR, Ca2+ facilitates exchange for intracellular proton for luminal K+.
(Bonus points for PIP2, to DAG, to PKC, to proton exchanger)
Gocovri effects what type of receptor?
What is its action on this receptor?
What ultimately happens as a result of this action?
Gocovri is Amantadine
Amantadine effects NMDA receptors (Post-synaptic CNS Ca2+ channels)
It has an inhibitory effect on these receptors, making further neuron potentials less frequent while active. Decreasing action potentials in CNS pain pathways will also be correct.
Brodifacoum has a half life of how much time? (Be close)
The abbreviation "SNOT" is guideline for the half life of which molecules following the presence of Warfarin-like rodenticides (name them, in order of increasing half life).
220-300 days
Clotting Factors 7, 9, 10, and 2
Describe the mechanism, effect, and side effect(s) of Diaqua-2.
Na/K/Cl cotransporter inhibitor in the thick AL of the LoH, preventing reabsorption of Na/Cl/H2O. Causes diuresis and increases loss of K+.
ECF fluid loss. Kalemiuria.
Dehydration, hypokalemia, hyponaturemia, dur.
Decadron has a slow onset, but has many effects. Name the mechanism of action and name 3 effects it may have on the body.
Decadron is dexamethasone, and it halts the production of AA byproduct by phospholipase A2 at the site of inflammation.
(List of effects on my phone)
Popular in gay culture, a certain drug is commonly used to prevent messes in the bedroom.
Please list the drug name, trade name, and briefly describe how it minimizes messes in the bedroom (2 sentences max)
(Hint: It works on mu opioid receptors.)
loperamide, Imodium
Imodium works to decrease contractions in the small/large gut. Decreased motility allows for longer fluid and electrolyte absorption, causing less water content in stool and decreased trips to the bathroom.
Hypokalemia typically causes excitable cells to be less excitable, with the exception of this type of cell. Explain why this is the case.
Hypokalemia causes the membrane potential of cells to be more hyperpolarized (less excitable).
Pacemaker cells are more excitable in the presence of hyperpolarization due to "funny" channels, and therefore generate AP's quicker due to increased activation of funny channels causing quicker depolarization.
Describe the leukogram changes in a "physiologic leukocytosis" of a feline patieant?
Leukocytosis, neutrophilia, lymphocytosis. No other changes or left shift.
Name three scenarios where a normal dosage of NSAIDs (below toxic level of the patients species) can result in acute ischemic kidney injury.
Hemocomplicated patients are the most likely to suffer from ischemic AKI even when doses remain under the toxic serum levels. They rely on PGs to regulate a constant GFR when vasoconstrictive effects are highly systemic.
Scenarios: Dehydration, hemorrhage, anesthesia, heart failure, liver or current kidney disease.
Heartworm is a parasite in canines that commonly occupies the pulmonary arteries. Why do you think they occupy this area in particular (in early stages of disease)?
Heartworms typically cause inflammation and tissue damage to pulmonary artery endothelium, as well as occupying a large amount of space in these vessels. Use what you learned in block 3a to assume the progression of this pathophysiology resulting in death of patients. (Hint: Patients with HW typically have normal diffusion at rest.)
Since HWs cannot climb through pulmonary capillaries, all HWs will flow down the pressure gradient to the pulmonary arteries and stay there unless they grow longer. (Something about the lowest pressure being there is what I'm looking for.
As worms take up more space and cause more tissue damage, pulmonary vascular resistance increases, making the right side of the heart work harder and dilation (eccentric) hypertrophy, and resulting blood backing up will cause right-sided CHF signs and hemolysis/shock eventually killing your patient.
Clostridium perfringens enterotoxin (C-CPE) causes collapse of tight junctions formed by ____
Claudin-19
Mg2+ is the second most common intercellular cation in the body, and it is a natural Ca2+ antagonist.
A patient with hypomagnesemia will have ___ excitable cells, and will have a(n) ___ time contracting their skeletal muscles.
More/easier
Ceruloplasmin is a protein complexed with copper, that functions in macrophages exactly how Hephaestin does in enterocytes, both promoting the transport of Fe2+ out of their respective cells.
You think your patient may be copper deficient. Describe the anemia you expect to find in this very characteristic scenario.
1. Microcytic
2. Normo- to hypochromic
3. Non-regenerative anemia more likely, but can be regenerative. (Unlikely, because consumption of Fe2+ would need to be up to par with natural hemolysis, and copper deficiency decreases intestinal absorption).
Vomiting results in the loss of gastric hydrochloride, resulting in the loss of fixed protons
Sometimes the loss of protons in chronic cases of vomiting contributes(!!!) to a metabolic alkalosis. Why might a patient who's been vomiting frequently be hypokalemic.
As well as the loss of HCl, V+ also results in ECF volume contraction (similar/like hypovolemia)
We know that hypovolemic patients will release AGII, in order to restore fluid volumes via Aldosterone. Chronic Aldosterone release will increase K+ secretion and result in hypokalemia.
Bordetella pertussis releases an exotoxin called PTx. PTx acts on the alpha subunit of Gi coupled protein receptors, locking the subunit in an inactive state.
Name 3 clinical signs that may result from PTx toxicity.
List is too long to put here, but did you get it?
Staphylococcal enterotoxin A (SEA) is a common toxin produced by Staphylococcus aureus, which causes a retching reflex in mice.
Propose a mechanism for how SEA may cause retching. (Hint: there should be some sort of plot but be specific)
Enteroendocrine cells release 5-Ht (serotonin) in response to SEA.
Serotonin acts on sensory vagal neuron receptors to stimulate the emetic center causing retching. (or something like that)