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General Boards Flashcards

1
Q

What percentage of the body is fluid? What is the split of this amount between the intra and extracellular space?

A

60% of body weight is fluid

1/3 is in the extracellular space
2/3 is in the intracellular space

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2
Q

What ions are predominantly in the extracellular space, and what ions are predominantly in the intracellular space?

A

Extra - sodium, chloride, calcium, bicarbonate

Intra - potassium, phosphate, magnesium, proteins

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3
Q

Which organelle doesn’t have a membrane / phospholipid bilayer?

A

The nucleoulus - just an accumulation of RNA and proteins

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4
Q

What do the RER and SER manufacture, respectively

A

RER - proteins
SER - lipids

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5
Q

What organelle forms the nuclear membrane?

A

Endoplasmic reticulum

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6
Q

What organelle produces hyaluronic acid and chondroitin sulfate? What are these molecules?

A

The Golgi apparatus

Large saccharide polymers attached to a small protein backbone

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7
Q

What type of bond holds together the two strands of DNA? Is it strong or weak? What nucleotides bind together?

A

Weak, hydrogen bonds

Adenine bases bond with thymine
Cytosine bases bond with guanine

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8
Q

What is the term for the 3 adjacent nucleotides that determine the specific amino acid included in a future protein molecule?

A

Codon

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9
Q

What is the term for proteins that span the width of the cell membrane?

A

Integral proteins

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10
Q

What are four substances that have a high lipid solubility and can easily cross cell membranes?

A

Oxygen
Carbon dioxide
Nitrogen
Alcohol

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11
Q

What structures allow the free diffusion of water across lipophilic cell membranes?

A

Aquaporins

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12
Q

Via what type of transport mechanism does glucose use to get into cells from the bloodstream? What are the transport proteins called? Which transport protein is insulin-dependent?

A

Facilitated diffusion

GLUT transport proteins

GLUT-4

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13
Q

Definition for osmolality
Definition for osmolarity

A

Osmolality — osmoles in kilogram of water

Osmolarity — osmoles in liter of solution (ie the body)

These are essentially equivalent in the body given that the fluid in the body is almost all water.

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14
Q

Three functions of the Na-K-ATPase pump

A
  1. Maintain intra/extracellular concentration gradients of Na and K
  2. Establish negatively charged intracellular voltage gradient
  3. Maintain cell volume (via ions)
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15
Q

How much more calcium is located extracellularly compared to intracellularly?

How is this gradient maintained?

A

10,000 x

There is a calcium-ATPase pump in the cell membrane, and there is a similar pump located in certain organelles (sarcoplasmic reticulum - SERCA, mitochondria) that keeps the calcium levels in the intracellular fluid low.

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16
Q

What are two places in the body where active transport of hydrogen ions occurs?

What is the name of this pump?

A

Parietal cells in the stomach (for formation of HCl)

Alpha Intercalated cells in the distal tubules / collecting ducts of the nephron (excretion of excess H+ in the urine)

H+ - K+ - ATPase pump (proton pump)

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17
Q

What is the resting membrane potential of neurons, and how much is contributed by the Nernst potentials of Na and K, and how much is contributed by the Na-K-ATPase pump?

A

-90 mV

-86 mV is contributed to by the Nernst potentials

-4 mV is contributed to by the Na-K-ATPase pump

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18
Q

What ion alters the sensitivity of the voltage gated sodium channels, and what do high and low levels of this ion cause?

A

Calcium

High calcium - difficult to activate the VGSC

Low calcium - easy to activate the VGSC —> tetany / eclampsia

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19
Q

What is the functional unit of muscles?

Define the different parts of this structure.

A

Sarcomeres - one z line to another

I band - where there is just actin (immediately adjacent to z line)

A band - where there is myosin and actin overlapping, more centrally located

M line - center of A band

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20
Q

What protein helps hold myosin and actin in proximity to each other?

A

Titin

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21
Q

Explain how calcium allows for muscle contraction.

A

Calcium binds to troponin. This shifts the tropomyosin bands associated within the actin filaments to expose the active sites on the actin bands. Once the active sites are exposed, then the myosin heads can bind to them, and pull the actin filaments inwards, shortening the sarcomere (ie contraction)

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22
Q

What are the other names for fast and slow muscle fibers, and what are some distinguishing criteria between the two types?

A

Type 1 - slow
1. Good blood supply
2. Rely on oxidative metabolism
3. Have large amounts of myoglobin (red)
4. Lots of mitochondria
5. Smaller fibers / smaller nerve fibers

Type 2 - fast
1. Less blood supply
2. Rely more on anaerobic metabolism / glycolysis
3. Minimal myoglobin (white)
4. Less mitochondria
5. Large fibers with extensive sarcoplasmic reticulum

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23
Q

What are the receptors located in the skeletal muscle sarcoplasmic reticulum that release calcium when triggered by an AP called?

A

Ryanodine receptors

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24
Q

The presence of what channel results in the plateau phase of the action potential of cardiac muscle, compared to the short AP of skeletal muscle?

A

Slow calcium channels

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25
Q

What does the strength of cardiac contractability depend on primarily?

A

Concentration of extracellular calcium

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26
Q

The ____________ calcium concentration is more important for skeletal muscle conduction because most calcium is released from __________.

The ____________ calcium concentration is more important for cardiac muscle contraction, as most calcium enters the cardiac myocytes via the __________.

A

Intracellular, sarcoplasmic reticulum

Extracellular, T tubules

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27
Q

What is the AV node delay designed for?

A

To allow the atria to contract prior to ventricular contraction, resulting in more blood in the ventricle when it does contract (ventricular priming).

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28
Q

What is the difference between the VGSC in the pacemaker cells of the heart versus the true myofibers?

A

The VGSCs of the pacemaker cells are more leaky than those in the muscle. This allows for a slow, steady depolarization of the cell (with the help of slow calcium channels) following repolarization. The VGSCs of the cardiac myofibers are quick to shut and not leaky.

This difference also explains the difference in RMPs between these two cell types.

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29
Q

What is the RMP for the pacemaker cells in the heart, and for the cardiac myofibers?

A

Pacemaker cells: -55 to -60 mV
Cardiac myofibers: -90 mV

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30
Q

What cellular feature results in the AV nodal delay?

A

Less gap junctions in the AV node, forces the signal to travel slower between the cells

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31
Q

How does stimulation of the vagus nerve decrease heart rate?

A

It results in release of ACh at the SA node, which increases permeability of the node to potassium, making the RMP more negative. This means we have to wait longer for the leaky sodium (and calcium) channels to depolarize back to threshold from this more negative RMP (thus making each heart beat take longer to happen).

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32
Q

Why do we observe a ventricular repolarization T wave, but not an equivalent finding for the atrial repolarization?

A

The atrial repolarization wave occurs during ventricular depolarization, and is therefore hidden by the QRS complex.

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33
Q

What percentage of dogs with MMVD have tricuspid valve involvement?

A

30%

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34
Q

What are the four criteria that distinguish between a B1 and B2 MMVD patient?

A
  1. Murmur > 3/6
  2. Elevated LA:Ao ratio (>1.6)
  3. Elevated LVIDDn (>1.7)
  4. Elevated VHS (>10.5)
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35
Q

How do you measure VLAS?

A

Either right or left lateral projection.

Line from ventral most aspect of carina to the intersection of the left atrium and the dorsal border of the caudal vena cava.

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36
Q

What blood test can be used in dogs and cats to help determine if clinical signs of heart failure are truly related to heart failure or not?

A

NT-proBNP concentrations (normal / near normal results make CHF unlikely)

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37
Q

What dose of furosemide needs to be reached prior to considering a dog as stage D MMVD?

A

8 mg/kg/d

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38
Q

Which retinal cell layer provides the axons that form the optic nerve?

A

Ganglion cells

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39
Q

What are the receptors for light in the eye?

Which receptors are more sensitive to light, and which have better acuity / detail?

A

The cones and rods.

The cones have better acuity - they synapse on just one bipolar cell (which then synapses one just one ganglion cell).

The rods have better sensitivity to light - they synapse into multiple bipolar cells, which then activate many ganglion cells (which then travel as the optic nerve).

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40
Q

Information from which side of retina crosses at the optic chiasm?

A

Nasal portions, which perceive information from the lateral (temporal) planes.

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41
Q

What transport protein is located in both the thick ascending loop of Henle and the stria vascularis of the inner ear?

A

Na-2Cl-K cotransporter

Loop diuretics that inhibit this protein can result in deafness via changes in the electrolyte concentration of the endolymph.

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42
Q

What are the four most common skin tumors of cats?

A

Basal cell tumors
Mast cell tumors
Squamous cell carcinoma
Fibrosarcoma

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43
Q

Most common skin tumor in dogs

A

Mast cell tumor

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44
Q

What locations impart a worse prognosis for melanomas?

A

Digit and oral cavity, more likely to be malignant

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45
Q

What is a squamous cell carcinoma in situ, and what is it called when one develops secondary to excessive UV radiation?

A

It is a SCC that has not crossed beneath the basement membrane of the epithelium.

Actinic keratosis

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46
Q

What is the most common malignant neoplasm of the ear in dogs and cats?

A

Ceruminous gland adenocarcinoma

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47
Q

What is the most common malignant neoplasm of the digit, and in what type of dog is it most common in?

A

Squamous cell carcinoma

Black haired dogs

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48
Q

Digit tumors in cats have a high (~90%) chance of being what?

A

Metastatic from the lungs (lung-digit syndrome)

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49
Q

What is the most common oral tumor in dogs?

A

Melanoma

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50
Q

Mutations in this gene has been associated with worse prognosis in mast cell tumors?

What class of proteins is created by this gene?

A

C-kit

Tyrosine kinase receptor — this allows for cell proliferation and differentiation. The mutation allows this receptor to function independent of its ligand.

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51
Q

What is the most reliable prognostic factor for canine MCTs?

A

Histologic grade (low, intermediate, high)

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52
Q

What stains can be used to highlight mast cell granules in those MCTs that don’t stain with traditional H&E / diff quik stains?

A

Wright Giemsa
Toluidine blue

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53
Q

What breed of dog tends to have more benign acting MCTs?

A

Boxers

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54
Q

What are some side effects of toceranib phosphate?

A

Bone marrow suppression (leuko mostly)

GI (vomiting, diarrhea, hyporexia)

Hypertension

Proteinuria

Muscle pain

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55
Q

Which subtype of histamine receptors are present in the stomach?

A

H2

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56
Q

What are the 3 clinical syndromes of MCTs in cats?

A
  1. Cutaneous
  2. Visceral / splenic
  3. Intestinal
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57
Q

What is a unique subtype of feline MCTs?

A

Histiocytic - can occur in young cats, and also regress spontaneously

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58
Q

Most common cause of splenic disease in cats

A

Mast cell tumor

40-100% of cases are associated with a peripheral mastocytosis

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59
Q

What infectious agent can cause soft tissue sarcoma development?

What types of sarcoma?

What is the main location?

What other radiographic sign can be detected?

A

Spirocerca lupi

OSA, FSA, undifferentiated

Caudal thoracic esophagus

Ventral spondylitis from T6-T12

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60
Q

What is the main STS to occur in young dogs?

A

Rhabdomyosarcoma

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61
Q

Nerve sheath neoplasms can arise from what cell types?

A

Schwann cells
Perineural cells
Perineural or endoneural fibroblasts

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62
Q

Nerve sheath neoplasms can be differentiated from perivascular wall tumors via what stains?

A

S-100, vimentin, GFAP, nerve growth factor receptor, and neuron specific enolase.

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63
Q

What is the most common location of intermuscular lipomas? (what muscles do they arise in between?)

A

Caudal thigh in between the semitendinosus and semimembranosus muscles.

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64
Q

What type of biopsy procedure is not recommended for soft tissue sarcomas?

A

Excisional biopsy

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65
Q

Suggested margins for STS removal

A

2-3 cm lateral, 1 facial layer deep

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66
Q

What are the recurrence rates for incompletely excised grade I and II STSs, and what is the clinical implication of this?

A

Grade I — 7%
Grade II — 34%

Incomplete excisions of these tumors could be amenable to active surveillance as there is a relatively high chance that they may not recur.

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67
Q

What is the site of highest resistance in the circulatory system? What controls this resistance?

A

The arterioles

The autonomic nervous system
(Alpha 1 innervation to the arterioles of skin, splanchnics, and renal, beta 2 to arterioles of the skeletal muscle)

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68
Q

What two types of blood vessels are supplied by alpha 1 receptors?

A

Arterioles of skin, splanchnics, and kidneys

Veins (unspecified)

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69
Q

What are arterial murmurs called?

A

Bruits

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70
Q

What portion of the heart does not have parasympathetic innervation?

A

Ventricles

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71
Q

What is the formula for ejection fraction, and what is a normal EF?

A

Stroke volume / end diastolic volume

55-60%

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72
Q

What is the mechanism of action for cardiac glycoside medications?

A

Na-K-ATPase pump inhibition —> reduced Na gradient —> less activity of the Na-Ca exchanger —> accumulation of intracellular Ca —> stronger heart muscle contraction

Positive inotrope

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73
Q

What do S3 and S4 heart sounds refer to? What disease states in dogs / cats can cause these? What is it called when one is heard?

A

S3 — occurs immediately after ventricular systole (aka onset of ventricular diastole); large volume of blood in the atria rapidly entering the ventricle

S4 — occurs during atrial systole; ejection of atrial blood into the ventricle

S3 can be heard in dogs with DCM, and S4 can be heard in cats with HCM.

Gallop rhythm

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74
Q

What cranial nerve innervates the baroreceptors in the carotid sinus / carotid bifurcation?

A

Cranial nerve IX via the carotid sinus nerve

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75
Q

Action of aldosterone on Na and K?

A

Save sodium
Pee potassium

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76
Q

What are four actions of angiotensin II?

A
  1. Increase aldosterone secretion
  2. Increase Na-H antiporter activity in proximal tubule
  3. Increase thirst
  4. Arteriolar vasoconstricter
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77
Q

What three organs demonstrate auto regulation?

A

Heart
Brain
Kidneys

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78
Q

How do substances like histamine and bradykinin result in edema?

A

They cause arterial vasodilation and venous vasoconstriction

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79
Q

What is the most important determinant of cerebral bloodflow?

Why don’t other factors play a role?

A

Carbon dioxide —> elevated levels cause vasodilation

The blood brain barrier

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80
Q

Most common oral tumor
- Dog
- Cat

A

Dog: malignant melanoma
Cat: squamous cell carcinoma

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81
Q

For oral SCC, does the potential for metastasis increase or decrease as you move rostral to caudal?

A

Increase

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82
Q

What oral tumor commonly occurs between the canines and carnassial teeth, and what is a unique feature of this tumor?

A

Fibrosarcoma

They often appear histologically benign, but exhibit locally aggressive behavior

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83
Q

What is the main difference between peripheral odontogenic fibromas and acanthomatous ameloblastomas?

A

POF do not invade bone while AA do.

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84
Q

What form of SCC is highly metastatic?

A

Tonsillar SCC

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85
Q

What percent of all OSAs involve the axial skeleton?

A

25%

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86
Q

Which has a better prognosis: mandibular OSA or maxillary OSA?

A

Mandibular

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87
Q

What tumor of the tongue has a good prognosis even with marginal surgical resection?

A

Granular cell myoblastoma

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88
Q

What are some characteristic features of “undifferentiated malignancy of young dogs”?

A
  • occurs in dogs under 2 years of age
  • rapidly growing mass in the upper oral cavity / orbit
  • high metastatic rate
  • most dogs euthanized in 1 month after diagnosis
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89
Q

What location carries the best prognosis for MLO?

A

Mandible (~1500 days)

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90
Q

Most common type of salivary gland tumor

A

Adenocarcinoma

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91
Q

What is a unique paraneoplastic syndrome of pancreatic adenocarcinoma in the cat?

A

Alopecia

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92
Q

What is the pathophysiologic mechanism behind paraneoplastic hypoglycemia with leiomyo(sarco)mas?

A

secretion of insulin-like growth factor 2

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93
Q

What cell type do GISTs arise from, and what do the commonly express? What is the clinical significance of this?

A

Interstitial cells of Cajal

Commonly express c-kit and CD34

Helps distinguish from smooth muscle tumors

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94
Q

What is the main morphologic difference between gastric carcinomas and mesenchymal gastric tumors?

A

Carcinoma - broad based

Mesenchymal - focal / pedunculated

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95
Q

Most common hepatic tumor in dogs, cats?

A

Dogs - HCC
Cats - biliary cystadenoma (biliary duct adenoma)

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96
Q

What breed of dog is over-represented for HCC, and what breed of dog has a link with vacuolar hepatopathy?

A
  1. Miniature schnauzer
  2. Scottish terriers
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97
Q

Four main hepatic tumors in dogs and cats?

Three main distributions?

A
  1. Hepatocellular carcinoma
  2. Biliary duct tumors
  3. Neuroendocrine
  4. Mesenchymal / sarcomas
  5. Massive
  6. Nodular
  7. Diffuse
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98
Q

What are three reasons for a patient with a hepatic mass to present with neurologic signs?

A
  1. Hepatic encephalopathy
  2. Paraneoplastic hypoglycemia
  3. CNS metastasis
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99
Q

Which division for HCC carries a worse prognosis and why?

A

Right sided, surgical manipulation of the caudal vena cava

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100
Q

Most common and second most common intestinal tumor in dogs and cats

A

Lymphoma
Adenocarcinoma

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101
Q

What location along the GI tract is more likely to develop a GIST or leiomyo(sarco)ma than an adenocarcinoma?

A

The cecum

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102
Q

What is a carcinoid?

A

Neuroendocrine tumor of the GI tract, arising from the endocrine cells in the GIT. They are histologically similar to carcinomas, but contain secretory granules.

They are highly aggressive.

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103
Q

What perianal tumor in dogs is androgen related, and why can this tumor occur in female dogs occasionally?

A

Perianal (hepatoid) tumors

Hyperadrenocorticism

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104
Q

What is the major difference regarding treatment for perianal gland adenocarcinoma and adenoma?

A

Castration does not make a difference for adenocarcinomas because they are not testosterone induced.

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105
Q

How much of the anal sphincter can be removed without causing significant fecal incontinence?

A

~50%

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106
Q

True or false - size of a primary AGASACA is positively correlated with metastatic potential

A

False - very small tumors can met, while large ones often don’t. Regional lymph node metastases are the most common.

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107
Q

What percentage of dogs with AGASACA have bilateral tumors (either simultaneously or temporally)? Cats?

A

Dogs 15%
Cats 0%

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108
Q

What are two distinguishing characteristics of AGASACA cytology?

A
  1. Classic ‘neuroendocrine’ look
  2. Minimal criteria of malignancy
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109
Q

What tumor type has a significant survival benefit with lymph node extirpation?

A

AGASACA

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110
Q

What muscles are part of inspiration and what are part of expiration?

A

Inspiration - diaphragm and external intercostals

Expiration - abdominal muscles and internal intercostals

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111
Q

What is different about fetal and adult hemoglobin? Why is fetal hemoglobin like this?

A

Fetal hemoglobin is composed of gamma subunits instead of beta ones (a2y2 v a2b2). This makes fetal hemoglobin less susceptible to binding to 2,3-DPG, and thus it binds tighter to oxygen.

The point of this is so that oxygen can get passed from the mother to fetus.

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112
Q

What things shift the oxygen-hemoglobin association curve to right? To the left?

A

To the right (reduced hemoglobin binding): decreased pH, increased CO2, increased temperature, increased 2,3-DPG

To the left (increased hemoglobin binding): increased pH, decreased CO2, reduced temperature, less 2,3-DPG, fetal hemoglobin

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113
Q

What are five causes of hypoxemia?

Which ones have a normal A-a gradient, and which don’t?

What is A-a gradient?

A
  1. Decreased FiO2 - normal Aa gradient
  2. Hypoventilation - normal Aa gradient
  3. V/Q mismatch - increased Aa gradient
  4. Diffusion impairment - increased Aa gradient
  5. Right to left shunt - increased Aa gradient

A-a gradient = PAO2 (alveolar) - PaO2 (arterial); normal is 0-10 mmHg

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114
Q

Five causes of hypoxia

A
  1. Hypoxemia
  2. Decreased cardiac output
  3. Anemia
  4. CO poisoning
  5. Cyanide poisoning
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115
Q

What is the last anatomic portion of the conducting zone and the first anatomic portion of the respiratory zone?

What happens here in regards to gas transport? Why?

A

Terminal bronchioles
Respiratory bronchioles

The forward velocity of inspired gas slows dramatically. Movement of gas from here forward primarily relies on diffusion. It happens because the cross sectional area of the lungs dramatically increases at this level.

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116
Q

What is the normal pressure in the main pulmonary artery? Is the pulmonary system high or low resistance?

A

15 mmHg

Low

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117
Q

Why is it unsafe for patients with pulmonary hypertension to fly / move to a higher altitude?

A

On planes / at higher altitudes, the FiO2 is lower. As a result, the pulmonary vessels vasoconstrict (hypoxic pulmonary vasoconstriction), raising the resistance and workload on the right heart, potentiating signs of PH.

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118
Q

What is vital capacity? What is the volume following this?

A

It is the volume of air moved from a maximum inhale to a maximum exhale.

The remaining volume is called residual volume.

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119
Q

What lung volumes cannot be measured via spirometry?

A

Total lung capacity
Functional residual capacity
Residual volume

(It all boils down to residual volume - to know total lung capacity and FRC, you would have to know residual volume)

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120
Q

What radiation therapy technique is used to provide a highly conformative RT dose in an effort to spare normal tissues?

In what tumor type (anatomic) is this very helpful in?

A

Intensity modulated radiation therapy (IMRT)

Sinonasal tumors (allows avoidance of the eyes and brain)

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121
Q

What is the main determinant regarding the risk of late term RT side effects? What broad group of protocols has a higher risk?

A

The dose of radiation delivered per fraction (higher dose = more risk)

Stereotactic protocols

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122
Q

Most common sinonasal tumor in dogs, cats?

A

Dogs - carcinoma (ACA, SCC)
Cats - lymphoma

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123
Q

The real term for ‘lung digit syndrome’

A

Acrometastasis

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124
Q

Aside from the lungs themselves, what are two common sites that pulmonary tumors can metastasize to?

A

Brain and bone

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125
Q

A cause of lameness in dogs with either primary or metastatic pulmonary neoplasia:

A

Hypertrophic osteopathy (HO)

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126
Q

What is the width of an intra-pulmonary structure able to be detected on thoracic CT v thoracic radiography?

A

1 mm (CT) v 7-9 mm (rads)

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127
Q

What type of cells secrete surfactant?

A

Type 2 alveolar cells

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128
Q

What is p53 and what do increased amounts of staining for this mean?

A

p53 is a tumor suppressor gene. Mutations in this gene can allow for the formation of cancers. When this gene is mutated, the protein it produces is no longer broken down well and will remain in tissues, and can be stained for.

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129
Q

What does mTOR stand for? What is this molecule?

A

Mammalian target of rapamycin

This is a protein kinase that is often up-regulated in cancer pathways.

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130
Q

How does one distinguish OSAs from other tumors of bone on a histological basis?

A

The presence of osteoid produced by the neoplastic cells (will only be present with OSA, not other primary bone tumors)

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131
Q

What percent of dogs with OSA will have metastasis at the time of diagnosis? At euthanasia?

A

15%, 90%

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132
Q

What is the mechanism of action of bisphosphanates?

A

These cause apoptosis / inhibition of osteoclasts, and therefore reduce bony lysis.

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133
Q

Along what portion of the bone do metastases most frequently occur and why?

A

Diaphysis; proximity to the nutrient foramen.

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134
Q

Multiple cartilaginous exostoses occur secondary to derangement in this process.

A

Endochondral ossification

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135
Q

What percentage of dogs with PDH will develop neurologic signs secondary to their tumor?

A

15-25%

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136
Q

What is the MOA for trilostane?

A

Inhibition of the 3-beta-hydroxysteroid dehydrogenase enzyme

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137
Q

What is a common and unique sign of feline hyperadrenocorticism?

A

Thin, fragile skin

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138
Q

What clinical sign in a patient that has insulin resistant DM should increase suspicion for hypersomatotropism?

A

Weight gain

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139
Q

What percent of cats with DM likely have hypersomatotropism? What percent with insulin-resistant DM?

A

10-15%
30%

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140
Q

What is the most common adrenocortical disorder in cats?

What are two main consequences of this disease?

A

Primary hyperaldosteronism

Hypokalemia (and resultant muscle weakness) and hypertension.

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141
Q

Which commonly used diuretic is an aldosterone antagonist? Why is this different from furosemide?

A

Spironolactone

Potassium sparing

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142
Q

What is the most common location for a chromaffin cell tumor? What are two other names for these tumors outside their most common location?

A
  • Adrenal medulla (pheochromocytoma)
  • paraganglioma or extra-adrenal pheochromocytoma
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143
Q

What is the best way to distinguish between pheochromocytoma and other types of adrenal tumors?

A

Measurement of plasma or urinary normetanephrines

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144
Q

What are three indications that an incidentally identified adrenal mass should be surgically removed?

A
  1. Size - greater than 2.5 cm
  2. Functional
  3. Locally invasive

Small, inactive tumors can be monitored serially with AUS q3 months.

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145
Q

What is the best way to work up a suspected thyroid tumor? What test should absolutely be avoided?

A
  • cervical CT
  • biopsy
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146
Q

Most common endocrine disorder in cats

A

Hyperthyroidism

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147
Q

What percentage of hyperthyroid cats have a total T4 within normal limits?

A

10%

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148
Q

What is the treatment of choice for feline hyperthyroidism?

A

Radioactive iodine therapy

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149
Q

Proliferation of this cell type results in primary hyperparathyroidism?

A

Chief cells

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150
Q

What breed of dog is predisposed to primary hyperparathyroidism?

A

Keeshonds

151
Q

Most common presenting complaint in dogs with primary HPT?

A

Urinary - related to either stones or UTI

152
Q

What should the phosphorus be in a patient with primary HPT?

A

Low to low normal. High phosphorus would be indicative of vitamin D toxicosis or renal failure.

153
Q

Over what value for the Ca x P factor is the risk of mineralization?

A

> 70

154
Q

What is Zollinger-Ellison syndrome and what tumor type is it associated with?

A

Non-beta cell pancreatic tumor
Hypergastrinemia
GI ulceration

Gastrinoma

155
Q

What percentage of insulinomas have metastasized at time of diagnosis? Gastrinomas?

A

Insulinoma - 50%

Gastrinoma - 85%

156
Q

What is a unique paraneoplastic feature of glucagonamas?

What is a more common cause of this condition?

What cell type do these tumors arise from?

A

Necrolytic migratory erythema / superficial necrolytic dermatitis

Liver disease

Alpha cells of pancreas

157
Q

What percentage of feline pancreatitis cases are idiopathic?

A

> 95%

158
Q

Activation of this enzyme is the initiating event for acute pancreatitis?

A

Trypsinogen

159
Q

What are the normal MRI features of the pancreas?

A

T1W hyperintensity
T2W iso to hypointensity

160
Q

What lab work abnormality is not seen in feline pancreatitis that is commonly seen in canine (and human) counterparts?

A

Hyperlipidemia (either triglycerides or cholesterol)

161
Q

Do prions generate an inflammatory response? Why?

A

No. They are just mis-folded proteins and the immune system doesn’t recognize them as pathologic.

162
Q

How do viruses obtain a surrounding envelope / lipid bilayer?

A

When they exit a cell, they can do so by budding, and a piece of the cell membrane now covers the virus.

163
Q

Define incubation period

Define prepatent period

A

Time from when an animal is infected by a pathogen to the onset of clinical signs

Time from when an animal is infected to shedding of eggs / larvae in feces

164
Q

CD4 and CD8 are present on which cell type (broadly speaking), and what are their colloquial names?

A

T lymphocytes

CD4 T lymphs = helper T cells
CD8 T lymphs = cytotoxic T cells

165
Q

What CDs can be used to distinguish T cells and B cells?

A

T cells - CD 3
B cells - CD 20, 21, 45 and 79

166
Q

What is the main difference between the innate and adaptive immune response (ie how they recognize stuff)?

A

The innate immune response relies on pattern recognition receptors (PRRs) to recognize the non-specific PAMPs and DAMPs.

The adaptive immune response relies on lymphocytes recognizing pathogen-specific antigens.

167
Q

What type of antigens do B cells recognize; how?

A

Extracellular antigens; B cells express the antibody that they would secrete along their plasma membrane, and this can bind to any of the antigen as long as it is extracellular (exposed to the antibody)

168
Q

What do helper T cells bind? Cytotoxic T cells?

A

Helper T cells (CD4+) bind MHC II
Cytotoxic T cells (CD8+) bind MHC I

169
Q

What are MHC molecules?

A

These bind the antigens of various pathogens for presentation to T lymphocytes.

170
Q

What cell types express MHC type I and which express type II

A

Type I - all nucleated cells
Type II - antigen presenting cells (dendritic cells, macrophages, B lymphs)

171
Q

Difference between plasma and serum

A

Serum does not have clotting proteins in it, while plasma does

172
Q

What are toll-like receptors, what part of the immune response are they are part of, and where can they be found?

A

They are pattern recognition receptors (PRRs) that respond to PAMPs. They are part of the innate immune response. They can be located along the cell membrane or in the cytoplasm.

173
Q

What are some examples of sentinel cells? What part of the immune response do they belong to?

A

Macrophages, mast cells, and dendritic cells; surface epithelial cells of the GI and respiratory tracts as well.

They are part of the innate response given that they carry PRRs (specifically TLRs). They are also part of the adaptive response as they function as APCs to lymphocytes.

174
Q

Which toll-like receptor detects LPS, and where is it located?

A

TLR-4
Cell surface

175
Q

Against what major pathogen do interferon molecules act?

A

Viruses

176
Q

What is another name for DAMPs?

A

Alarmins

177
Q

What are the three major pro-inflammatory cytokines produced by sentinel cells?

What do these cytokines cause that we can detect on exam?

A

TNF-alpha, IL-1 and IL-6

Fever

178
Q

Most common uterine tumor

A

Leiomyoma

179
Q

A mutation in the Birt-Hogg- Dube gene results in the following signs in this breed of dog?

A

German Shepherds

  1. Bilateral renal cystadenomas
  2. Multiple uterine leiomyomas
  3. Nodular dermatofibrosis
180
Q

Most common tumor in female dogs

A

Mammary neoplasia (50:50 benign v malignant)

181
Q

Lifetime likelihood of developing mammary gland cancer if spayed before first, second or third estrus?

A

0.5%, 8%, 26%

182
Q

Which mammary glands are most likely to develop tumors? Why?

What is the percentage of dogs presenting with more than 1 mammary gland tumor at the time of diagnosis?

A

Caudal two - larger mammary tissue

70%

183
Q

What is the most common mesenchymal tumor to affect the mammary gland in the dog?

A

Osteosarcoma

184
Q

What are three prognostic factors for mammary gland carcinomas?

A

Size of tumor (>5cm - worse)
Lymph node metastases
WHO staging system (which also incorporates size)

185
Q

Use of this type of medication can result in mammary gland tumors in cats and dogs?

A

Progestins

186
Q

What surgical dose is recommended for treatment of feline mammary gland tumors?

A

Either unilateral or bilateral chain mastectomy (bilateral is probably superior)

187
Q

What type of testicular tumor is associated with feminization, and what is the pathophys? What percentage of dogs with this tumor demonstrate this? What is a fatal complication of this?

A

Sertoli cell tumors; 50%; estrogen production; irreversible bone marrow suppression

188
Q

Does castration provide a protective effect for canine prostatic cancer?

A

No - castrated dogs actually seem to have more aggressive tumors

189
Q

What is a unique site of metastasis for prostatic neoplasms?

A

Bone - lumbar vertebrae & pelvic most common

190
Q

What non-chemotherapy medication has shown a significant survival benefit for canine prostatic tumors?

A

NSAIDs - these tumors often over express COX2

191
Q

What is the formula for osmolarity?

A

2Na + (Glu/18) + (BUN/2.8)

192
Q

What percentage of cardiac output do the kidneys receive?

A

25%

193
Q

How do NSAIDs cause renal injury?

A

Normally, prostaglandins promote renal blood flow via vasodilation of the renal arterioles. Inhibitors like NSAIDs reduce this blood flow.

194
Q

Where is glucose reabsorbed along the nephron, what protein does this?

A
  • Proximal tubule
  • Sodium glucose cotransport 2 (SGLT-2)
195
Q

Where is sodium reabsorbed in the nephron, by what cells/proteins and what percentage?

A
  • proximal convoluted tubule - 67% - via cotransport with glucose, amino acids and bicarbonate
  • thick ascending limb - 25% - via the Na-2Cl-K cotransporter (inhibited by loop diuretics)
  • distal convoluted tubule - 5% - via the Na-Cl cotransporter (inhibited by thiazide diuretics)
  • Collecting duct - 3% - principal cells (inhibited by spironolactone)
196
Q

What two hormones act on the principal cells in the late distal collecting tubules / collecting ducts?

A

ADH - inserts aquaporins to reabsorb water

Aldosterone- inserts proteins (ENaC) that help reabsorb sodium and excrete potassium

197
Q

What are the various mechanisms of action that explain metoclopramide’s prokinetic activity?

A

D2 receptor ANTagonist (also antiemetic)
Muscarinic agonist
5HT4 receptor agonist

198
Q

How does cisapride work?

A

It enhances ACh release within the myenteric plexus via 5HT4 agonist properties, promoting GI motility

199
Q

What are the two sites of vitamin D activation? Via what enzyme? What hormone / values promotes this enzyme?

A

Liver and kidney

High Parathyroid hormone / low calcium / low phosphorus

Alpha-1 hydroxylase in the kidney

200
Q

How is actinomyces acquired? How does this relate to its pathogenesis? What type of bacteria is it?

A

It is a commendably bacteria of the oral cavity / GI, and is acquired when a lesion occurs in the mucous membranes (or when it is introduced via a bite wound). Since it is a normal commensal, the body has a harder time getting rid of it. It is acid-fast negative, gram-positive filamentous facultative anaerobe.

201
Q

What is the cellular location of steroid hormone action?

A

Nucleus

202
Q

Mechanism of action of buprenorphine? Butorphanol?

A

Buprenorphine - partial mu agonist
Butorphanol - mixed agonist (kappa) / antagonist (mu)

203
Q

Most common location for feline low-grade intestinal T cell lymphoma?

A

Small intestine (jejunum > ileum > duodenum) > stomach > colon

204
Q

What lab value is more commonly decreased in cats with GI lymphoma than chronic enteritis?

A

Cobalamin

205
Q

In what location of the intestinal wall (at a minimum) are all LPE and LGITL lesions present, and what is the clinical significance of this?

A

Both LPE and LGITL affect the lamina propria (just underneath the epithelial cells, still part of the mucosa), so endoscopic biopsies should be able to obtain a diagnostic sample. The only caveat to this is if the endoscope can’t get to where the lesion is (ie, mid-jejunal)

206
Q

What full thickness biopsy technique for assessment of the intestinal mucosa is unreliable / not recommended? Why?

A

Wedge shaped biopsies - this results in a large serosal surface area, but a very small / damaged / absent mucosal area.

207
Q

What form of a drug (ionized or non-ionized) can cross a cell membrane? What type of environment makes a drug ionized or not?

A

Non-ionized forms of drugs can diffuse across cell membranes, and do so primarily based off of concentration gradient.

When the pKa of a drug matches the pH of the surrounding environment, it becomes non-ionized. IE a weakly acidic drug will become non-ionized in a more acidic environment.

208
Q

What is p-glycoprotein?

A

This is a transport protein that pumps drugs / drug metabolites out of cells (or bacteria). It is a product of the ABCB-1 gene / MDR-1 gene.

209
Q

What explains the poor oral bioavailability of aminoglycosides?

A

The pKa of aminoglycosides is relatively high (8.4) - these drugs are generally weak bases. They don’t get absorbed in the GIT because of the acidity of the GIT. The weak base of aminoglycosides in combination with the acidic environment of the GIT means that these drugs stay in their ionized form, and don’t get absorbed as well.

210
Q

What is the absolute difference between pKa and pH required to cause a drug to be ionized to point where it won’t be absorbed?

A

2

(A weakly acidic drug that is in an environment that is 2 pH more basic than its pKa will not be absorbed - ie aminoglycosides in the GIT - pKa of 8.4 v pH of 6)

211
Q

What route of administration results in 100% bioavailability of a drug?

A

intravenous

212
Q

What value determines the bioavailability of a drug? If two drugs have the same AUC, are they equally bioavailable?

A

AUC

No, not necessarily- they need to be absorbed at the same rate and extent. Their AUC value could be identical but their peak concentrations, time to peak, etc could vary widely.

213
Q

What happens to PDC and elimination half life when volume of distribution is increased?

A

PDC decreases and elimination half life increases.

214
Q

What are the three main volumes of distribution, and what drug types are associated with each?

A
  1. Total body water (60% BW, large volume) — lipophilic drugs / drugs that go past cell membrane
  2. Extracellular space (20% BW, medium volume) - water soluble drugs
  3. Blood volume (5% BW, small volume) - highly protein bound drugs
215
Q

What is the goal of hepatic metabolism, how many phases are there, and which phase is cytochrome P450 a part of?

A
  • to make drugs/metabolites more water soluble so they can be excreted by the kidneys
  • two phases
  • phase one
216
Q

What are phase 1 hepatic reactions? Phase 2?

What is the most common type of a phase 2 reaction?

What species lacks some glucuronide synthetic enzymes?

A

Phase 1 - oxidation, hydroxylation, or reduction - these alter the efficacy of the parent drug

Phase 2 - conjugation, a large water soluble molecule is added

Glucuronadation

Cats

217
Q

What medication is a glutathione precursor? What is glutathione?

A

N-acetylcysteine

Glutathione is a phase II hepatic enzyme that focuses specifically on detoxification of free radicals. It can be rapidly depleted

218
Q

What is the term for stereoisomers that differ due to orientation of four different groups around a single carbon atom and are NON-superimposable on each other?

A

Enantiomers (S v R)

219
Q

Where is intrinsic factor produced in dogs and cats? What is its role? Where is it absorbed?

A

Exocrine pancreas

Facilitates absorption of cobalamin in the ileum

220
Q

Most common urinary bladder tumor and location

A

Urothelial carcinoma
Trigone

221
Q

Breed of dog most at risk for UC?

A

Scottish terrier

222
Q

What is the difference between COX-1 and COX-2?

Name 2 COX-1 selective inhibitors, and 4 COX-2 selective inhibitors.

Which one might be non-selective?

A

COX-1 is constitutively expressed (ie in health) and is found in platelets, GI mucosa, and renal tubule cells

COX-2 is expressed in disease, and is up-regulated in sites of inflammation

COX-1 — aspirin, naproxen
COX-2 — piroxicam, carprofen, meloxicam, deracoxib

Piroxicam (per Winthrow oncology text)

223
Q

What percentage of all brain tumors are secondary / metastatic?

What are the four most common types?

A

50%

HSA, LSA, pituitary, carcinoma met

224
Q

Three most common primary brain tumors in dogs?

A
  1. Meningioma
  2. Glioma
  3. Choroid plexus tumor
225
Q

Four breeds at risk for intracranial meningiomas

A
  • golden retriever
  • boxer
  • miniature schnauzer
  • rat terrier
226
Q

What percentage of brain tumors result in seizures?

A

50%

227
Q

MST for dogs with rostrotentorial brain tumors treated palliatively? Caudal fossa?

A

Up to 25 weeks (~5 months) v 1 month

228
Q

Percentage of ED, ID-EM, and IM spinal cord tumors and the most common ones

A

50% ED - osteosarcoma
35% ID-EM - meningioma
15% IM - glioma / ependymoma

229
Q

What type of lymphoma is most frequently associated with hypercalcemia?

A

Mediastinal

230
Q

What is the other term for epitheliotropic T cell lymphoma?

A

Mycosis fungoides

231
Q

What is the most common hematologic abnormality associated with lymphoma?

A

Anemia (typically of chronic disease)

232
Q

What is the most common type of lymphoma in the cat?

What is the most common location for extra-nodal (non-GI) in the cat?

A

GI-indolent (LGITL - low grade intestinal T cell lymphoma)

Nasal

233
Q

What myeloproliferative disorder can be associated with neurologic signs?

A

Polycythemia vera

234
Q

What two broad classes of molecules are produced from arachadonic acid? By what enzymes?

A
  • prostaglandins via cyclo-oxygenase
  • leukotrienes via lipo-oxygenase
235
Q

What interleukin of acute inflammation drives the hepatic production of acute phase proteins?

What are some common acute phase proteins?

A

IL-6

C-reactive protein, serum amyloid A, fibrinogen

236
Q

What do APC cells do, and what cell types are APCs?

A

They present antigens bound to MHC II molecules to helper T cells.

Dendritic cells, macrophages, and B lymphocytes.

237
Q

What are two major cytokines that T regulatory cells secrete?

A

IL-10, transforming growth factor beta (TFG-B)

238
Q

What are the five main ways that T helper lymphocytes can differentiate?

A

TH1 — potentiate macrophages killing their intracellular pathogens

TH2 — increase IgE production (IL-4) and activate eosinophils (IL-5)

TH17 — recruit / produce neutrophils indirectly by telling fibroblasts and epithelial cells to secrete appropriate cytokines

TFH cells — activate B cells into plasma cells

Treg— modulate the adaptive immune response

239
Q

Once differentiated, where do most plasma cells end up secreting their immunoglobulins?

A

Bone marrow

240
Q

What type of lymphocyte functions primarily in the innate immune response? What does it do?

A

Natural killer cells (also termed large granular lymphocytes)

It kills stressed cells. Also secretes IFN-gamma to activate macrophages (similar to the TH1 response).

241
Q

What type of hypersensitivity reactions are IMHA, ITP, lymphocytic thyroiditis and myasthenia gravis?

A

Type II hypersensitivity where auto-antibodies are directed against cell membrane proteins

242
Q

In which form of hypersensitivity does the formation of immune complexes occur? What are immune complexes? What are four examples of this hypersensitivity reaction?

A

Type III

Immune complexes are antigen:antibody complexes that form when soluble antigens come in contact with their respective antibodies.

Glomerulonephritis, vasculitis, uveitis, IMPA

243
Q

What type of hypersensitivity is not associated with antibodies? What are the two MOAs for this hypersensitivity? What are two examples of this?

A

Type IV

Activation of TH1 response (macrophage activation) and activation of cytotoxic T cells.

Flea allergy dermatitis and superficial necrolytic dermatitis (drug associated)

244
Q

What is the mechanistic difference between type 2 and type 3 hypersensitivity reactions?

A

Antigen location - in type 2, the antigen is associated with a cell membrane usually; in type 3, the antigen is solubilized (not with a cell membrane)

245
Q

True or false - dogs have natural antibodies to other blood group antigens

A

False - they do not. This explains why a dog’s first transfusion is ‘free’ / not at risk for a transfusion reaction

246
Q

In what domestic animal do naturally occurring antibodies to RBC antigens occur? What is the clinical significance of this?

A

Cat - almost all Type B cats have anti-A antibodies, and giving a type B cat type A blood can cause a severe and fatal transfusion reaction. The converse is similar, but less severe (only 35% of Type A cats have anti-B antibodies)

247
Q

What is the purpose of cross matching? Explain major versus minor cross matching.

A

Cross matching aids in the detection of potential transfusion reactions to other blood groups besides the main ones (DEA1 or AB).

Major - donor RBCs + recipient serum
Minor - recipient RBCs + donor serum

248
Q

How does a Coombs test work?

A

Involves adding an anti-globulin molecule to patient blood sample. If there are antibodies bound to the surface of the RBCs, then the added anti-globulin will bind to these RBC antibodies and cause agglutination.

249
Q

What is different about total body water in neonates?

A

More than 60% of BW

250
Q

What happens to the intracellular osmolarity when an excess amount of NaCl is taken in?

A

The osmolarity of the ECF increases. This creates a concentration gradient for water to move out of the ICF compartment. This increases the volume of the ECF at the expense of the ICF, whose osmolarity also increases.

251
Q

These substances (5) increase renal blood flow via arteriolar vasodilation.

This substance causes vasoconstriction of the renal efferent arteriole, increasing GFR.

This substance causes the same (renal efferent arteriolar vasoconstriction) AND renal afferent arteriolar vasodilation.

A
  • PGE2, PGI2, NO, dopamine, bradykinin
  • Angiotensin II
  • Atrial natriuretic peptide
252
Q

What are the renal thresholds for glucose in dogs and cats?

What transporter is responsible for reabsorption of glucose in the kidneys? Where is it?

A

Dogs - 180-200

Cats - 280-290

Sodium glucose cotransporter 2 (SGLT2)

Proximal tubule (early)

253
Q

What is the pathophysiology behind hypokalemia induced digoxin toxicity?

A

Digoxin binds to the potassium aspect of the Na-K-ATPase pump. When there is hypokalemia, more binding sites are exposed, functionally increasing the effective concentration of digoxin, potentiating toxicity.

254
Q

True or false - the same amount of sodium and potassium are reabsorbed by the proximal tubule

A

True - 67% of both are reabsorbed along the proximal tubule.

255
Q

In what situation do the kidneys conserve potassium? Where and how?

A

Dietary K deficiencies / (hypokalemia?)

In the late distal convoluted tubules / early collecting ducts via a H-K-ATPase associated with alpha-intercalated cells.

256
Q

What cells in the distal nephron secrete potassium? Reabsorb it?

A

Principal cells secrete, alpha-intercalated cells reabsorb

257
Q

Name 5 mechanisms by which urinary potassium excretion can be increased?

A
  1. High K+ diet
  2. Hyperaldosteronism
  3. Alkalosis (via H+ and K+ exchange)
  4. Diuretics (loop and thiazide, decrease K luminal concentration via flow)
  5. Excessive luminal anions (charge)
258
Q

Where is most of the phosphate reabsorbed in the kidney? What inhibits it?

A
  • 85% is reabsorbed in the proximal tubule (with sodium)
  • PTH, and fibroblast growth factor
259
Q

Where are osmoreceptors and what do they do when they sense a high plasma osmolarity?

A

In the hypothalamus; they tell the posterior pituitary / neurohypophysis to secrete ADH.

260
Q

What portions of the nephron dilute the urine / are impermeable to water?

A
  • thick ascending loop of Henle
  • early distal convoluted tubule

In both of these locations are ion transport proteins (Na-2Cl-K, Na-Cl) that reabsorb ions but not water.

261
Q

What is the formula for anion gap, and what is a normal anion gap?

A

(Na+K) - (Cl+HCO3)

15-25

262
Q

In metabolic acidosis, the _______ is decreased.

To compensate (for electroneutrality state), the anion gap can either be increased or static. What causes either?

A
  • Bicarbonate
  • in increased anion gap, an unmeasured anion is present (phosphate, lactate, ketone, formate, salicylate)
  • in normal anion gap metabolic acidosis, chloride must have increased
263
Q

Which acid-base disorder can cause hypocalcemia?

A

Respiratory alkalosis —> the plasma proteins trade H+ for Ca++, lowering the ionized calcium concentration

264
Q

Mortality rate associated with status epilepticus?

A

25-38.5%

265
Q

What are the two definitions of status epilepticus?

A
  • Seizure lasting longer than 5 minutes
  • 2 seizures without recovery of consciousness between
266
Q

What defines success for a benzodiazepine bolus for SE?

When should a second bolus be given?

A

seizures stop within 5 minutes and do not relapse within 10 minutes

In 2 minutes

267
Q

What is the order of medications to be used as third line agents in treatment of SE?

A
  1. Ketamine or dexmedetomidine
  2. Propofol
  3. Barbiturate anesthetics (pentobarbital or sodium thiopental)
  4. Gas anesthetics
268
Q

What two things can cause increased aldosterone secretion?

A
  1. Decreased circulating volume via activation of RAAS. (Renin — angiotensin I — angiotensin II — aldosterone)
  2. Hyperkalemia
269
Q

Which intestinal nervous plexus controls motility, and controls secretion / blood flow?

A

Submucosal - secretion and blood flow

Myenteric - motility

270
Q

What hormone is involved in the formation of saliva? What are the biochemical characteristics of saliva?

A
  1. Aldosterone
  2. Low sodium, high potassium, high bicarbonate, hypotonic
271
Q

What is unique about the autonomic innervation of the salivary glands?

A

Saliva production is stimulated by both parasympathetic and sympathetic innervation. Production is decreased with parasympatholytics (atropine).

272
Q

What cell types in the stomach secrete what?

A
  • Parietal cells: HCl
  • Chief cells: pepsinogen
  • G cells: gastrin
273
Q

Why doesn’t atropine completely inhibit gastric acid secretion?

A

It inhibits the direct pathway involving vagally mediated Ach release / muscarinic receptor at the parietal cell. However, the indirect pathway with the vagally mediated gastrin release from G cells relies on release of GRP (gastrin releasing peptide) not Ach.

Also it doesn’t block histamine receptors.

274
Q

What things (3) promote parietal cell H+ release? What things (5) inhibit it?

A
  • Acetylcholine, gastrin, histamine
  • High H+ levels, somatostatin, prostaglandins, secretin, GIP
275
Q

What is the “alkaline tide”?

Where does the “tide” go?

A

It refers to transient elevation (more basic) in blood pH due to bicarbonate secretion from the parietal cells. The bicarbonate comes out of the parietal cells into the blood while the H+ goes into the stomach as a part of HCl.

The bicarbonate then is secreted in pancreatic juices to balance out the acidity of the chyme.

276
Q

What three things stimulate pancreatic secretion / increase the bicarbonate concentration in the pancreatic juices?

What else does CCK do?

A

Acetylcholine, secretin, CCK

CCK also cause gall bladder contraction, sphincter of Oddi relaxation, and inhibits gastric emptying.

277
Q

What forms of carbohydrates are absorbed by enterocytes? How?

How do they then leave the enterocyte?

A
  • glucose and galactose; absorbed by sodium glucose cotransporters (SGLT1); this is secondary active transport
  • fructose: via facilitated diffusion

They leave the enterocyte via GLUT-2.

278
Q

What activates pepsinogen to pepsin?

What activates trypsinogen to trypsin?

A

Low gastric pH (1-3)

Enterokinase in the intestinal brush border

279
Q

What happens to lipid products once they make it into the enterocytes?

A

They are reformed into triglycerides and packaged into chylomicrons with the aid of apoproteins. These are then secreted into the lymphatic system.

280
Q

What are three places in the body where aldosterone results in Na and K adjustments?

In the third location, what is the clinical consequence of high flow (ie diarrhea)?

A
  • kidneys, salivary glands and colon
  • when there is diarrhea and high flow rates through the colon, this keeps the relative K+ concentration low, increasing the gradient for K+ to flow into the colon, which can cause excessive K+ losses.
281
Q

What is the main electrolyte secreted by the intestines?

A

Chloride

282
Q

What are the fat soluble vitamins?

A

A D E K

283
Q

What are the storage states / various transport proteins for iron?

A

In the blood stream, iron attached to its transport protein is termed transferrin. The same protein when not bound to iron is called apotransferrin.

In the tissues, iron is stored as ferritin. Ferritin not bound to iron is termed apoferritin.

Apo = unbound

284
Q

What causes insulin release in response to oral glucose?

A

Oral glucose stimulates glucose-dependent insulinotropic peptide, that then triggers insulin secretion.

285
Q

What is octreotide, and what can it be used to treat?

A

Octreotide is a somatostatin analogue, and can be used to treat acromegaly because somatostatin inhibits growth hormone release.

286
Q

What are the two main actions of ADH?

A
  • increase water permeability in the kidney via insertion of aquaporins
  • vasoconstriction
287
Q

Which is more biologically active: T3 or T4?

Which one is higher in serum? Where does the conversion happen?

A

T3 is more biologically active, but more T4 is present. The conversion from T4 to T3 occurs in peripheral tissues.

288
Q

What impact does thyroid hormone have on the autonomic nervous system?

A

Unregulates beta-1 receptors in the heart

289
Q

What cells in the anterior pituitary produce POMC, and what tells them to do so?

A
  • corticotrophs, CRH from the hypothalamus
290
Q

What are the enzymes / molecules involved in the RAAS?

A

Renin is secreted by juxtaglomerular cells of the kidney in response to low flow in the renal arterioles; convert angiotensin to angiotensin 1.

Angiotensin 1 is concerted to angiotensin 2 by ACE in the lungs.

Angiotensin 2 increases production of aldosterone in the zona glomerulosa of the adrenal.

291
Q

What are three ways that steroids inhibit the immune response?

A
  1. Phospholipase A2 inhibition (no production of arachadonic acid)
  2. Reduce T lymphocytes differentiation and IL-2 secretion (this is what cyclosporine does)
  3. Inhibit mast cell release of histamine and serotonin
292
Q

What part of the autonomic nervous system is cortisol dependent?

A

Alpha-1 receptors on arterioles

293
Q

What do the delta cells of the pancreas secrete?

A

Somatostatin and gastrin (source of pancreatic gastrinomas?)

294
Q

Explain the mechanism behind renal secondary hyperparathyroidism.

A
  • renal disease causes phosphate retention
  • higher phosphate complexes with circulating calcium
  • renal disease also reduces activation of vitamin D
  • both result in reduced Ca++ and subsequent PTH increases
295
Q

What increases a-1 hydroxylase activity?

A

PTH, hypocalcemia and hypophosphatemia

296
Q

What is the most important reservoir host for leptospirosis?

A

Brown rat

297
Q

How is leptospirosis most commonly transmitted?

A

Urine or liquid (pond water, etc) carrying infectious leptospira bacteria cross a mucous membrane or cut/macerated skin. Once past the epithelium, they enter into the bloodstream and spread from there.

298
Q

Two main organ systems impacted by leptospirosis?

What percent of people have evidence of aseptic meningitis associated with leptospirosis?

A

Kidney and liver

25%

299
Q

What is a unique organ system that can affected by leptospirosis, and what happens in this organ system?

What diagnostic test should be done to screen for this, even in the absence of obvious clinical signs of this organ involvement?

A

Lungs

Leptospiral pulmonary hemorrhage syndrome (bleeding into alveoli)

Chest xrays

300
Q

What is a common clinical finding in dogs when initially symptomatic for leptospirosis?

Are bloodwork changes present at this time?

A

Fever

No (always worry about leptospirosis in the acutely sick / febrile animal even if bloodwork isn’t very exciting).

301
Q

Why should a single negative MAT not rule out leptospirosis? A single positive MAT?

When should one be repeated?

A

A single negative MAT could occur due to slow formation of antibodies to the organism (have not seroconverted yet).

A single positive MAT could be secondary to previous exposure / vaccination.

A repeat (convalescent) titer should be repeated in 7-14 days after the first one.

302
Q

What does the WITNESS leptospirosis snap test look for? What is the specificity of this test?

A

IgM antibodies; > 97%

303
Q

When should samples be collected for leptospira PCR? What samples?

Antibiotic treatment regimen for lepto?

A

Prior to antibiotic administration.

Blood and urine.

IV ampicillin followed by 2 weeks worth of oral doxycycline

304
Q

What dogs are at-risk for leptospirosis? Clinical implications of this? What type of vaccine is the lepto vaccine? What serovars are covered by it in the US?

A

All dogs!! All dogs should therefore be vaccinated. It is a bacterin vaccine, that covers Grippotyphosa, Icterohemorrhagiae, Canicola and Pomona.

305
Q

How is babesiosis normally transmitted? What is the one species of babesia that is often transmitted differently, and how?

A

Infected ticks release sporozoites into the blood stream when feeding on dogs.

Babesia gibsoni has been shown to be transmitted through bite wounds (blood), especially in fighting Pitbull dogs.

Infected dogs can also transmit the infection transplacentally.

306
Q

What are four classic clinical signs / lab findings associated with babesiosis?

A

Fever (considered classic, but often waxing/waning)
Thrombocytopenia (most common)
Hemolytic anemia
Splenomegaly

307
Q

What is the most likely mechanism by which babesiosis could cause neurologic signs?

A

Parasitized RBCs cause sludging of blood in capillaries. This can result in ischemic or hemorrhagic infarcts in the brain.

308
Q

Which babesia organism is large on cytology? Small?

A

Large - B. canis
Small - B. gibsoni (ironic because Pitbulls are big dogs)

309
Q

What does insulin do to promote fatty acid synthesis and storage?

A

Insulin promotes formation of fatty acids in the liver (excess glucose gets transformed into fatty acids). These are secreted as triglycerides, which circulate attached to lipoproteins. Insulin then promotes activity of lipoprotein lipase in adipose tissue capillaries so the triglycerides can be absorbed / stored into the adipocytes.

310
Q

What is the storage form of lipid?

A

Triglycerides — they are put into the adipose tissue via activity of lipoprotein lipase (activated by insulin), and taken out by hormone sensitive lipase (inhibited by insulin).

311
Q

What is the juxtaglomerular apparatus/complex composed of? What is its goal and how does it achieve it?

A

The JGC is composed of the macula densa cells located in the distal tubule, and the juxtaglomerular cells in the afferent renal arteriole. These are all in close physical proximity along with the actual glomerulus.

Its goal is to restore GFR to normal.

The macula densa detects the amount of NaCl passing through the distal tubule. There is less when GFR is low because flow through the nephron is slow and allows the NaCl more time to be reabsorbed. The macula densa then causes the afferent arteriole to dilate, and triggers release of renin, which ultimately produces AT2, which causes renal efferent arteriolar constriction. The combo of the afferent dilation and efferent constriction results in increased GFR.

312
Q

What are the definitive hosts for neospora? Intermediate hosts?

A

Definitive - dogs and wild canids

Intermediate - livestock (cattle primarily)

Dogs pass sporozoites in their feces, which are ingested by cattle. These sporozoites turn into bradyzoites in cattle and cause tissue cysts. Dogs then eat tissues infected with these cysts, and then can become infected.

313
Q

What is the MOA of cyanide toxicity?

A

Disruption of oxidative phosphorylation / electron transport chain in mitochondria by inhibiting a protein called cytochrome C.

314
Q

What are the medications used to treat GI pythium if non-resectable?

A

Itraconazole, terbinafine, and prednisone

315
Q

Where are the enzymes that break carbohydrates down into monosaccharides located?

A

Brush border of enterocytes.

316
Q

What are the five classes of anti-arrhythmic medications? Examples of each?

A

Class 1 - sodium channel blockers (lidocaine)
Class 2 - beta blockers (atenolol)
Class 3 - potassium channel blockers (sotalol, amiodarone)
Class 4 - calcium channel blockers (diltiazem)

And then just digoxin

317
Q

What is the difference between the carotid sinus and carotid body?

A

The carotid sinus is a baroreceptor and feeds back on HR (U in sinus for pressUre). Low pressures = increased heart rate (and vice versa).

The carotid body is a chemoreceptor that assesses PaO2. Low oxygen levels stimulate respiratory drive (and not vice versa).

318
Q

How do natural killer cells know what cells to kill?

A

Cells that lack normal MHC I molecules (as seen in some viral infections or cancers).

Cells that are expressing stress molecules.

319
Q

What increases as the prevalence of a disease decreases?

What decreases?

A

The number of false positives increases and the positive predictive value decreases. If you are testing a low risk population (ie low prevalence of disease) and get a positive result, make sure to perform a confirmatory test.

320
Q

What is a more potent stimulator of the classical complement pathway? Why?

A

IgM > IgG

IgM has five Fc binding sites and one molecule is able to activate the pathway, while at least 2 IgG’s that are close together are needed to activate the pathway.

321
Q

What percent of cats with dry FIP present with sole neurologic signs?

A

22%

322
Q

Most common cause of hyperbilirubinemia in young cats?

A

FIP - not liver associated, but due to RBC destruction and a relative lack of hepatic conjugation (common in cats) to clear these byproducts.

323
Q

What cell tropism does feline enteric coronavirus demonstrate? FIP?

A

Epithelium (mostly GI)

Macrophages

324
Q

What are the creatinine cutoffs for the IRIS CKD staging levels?

Protein?

A
  1. <1.5
  2. 1.5-2.8 (actually 1.4 in dogs and 1.6 in cats)
  3. 2.9-5.0
  4. > 5

Non-proteinuric is <0.2
Borderline = 0.2-0.5 (dog) and 0.2-0.4 (cat)
Proteinuric >0.5 (dog) and 0.4 (cat)

325
Q

What is the explanation for toxoplasma oocysts present in canine feces?

A

The dog must’ve eaten cat poop with oocysts in it, and mechanically passed them through their GIT.

326
Q

What is unique about toxoplasmosis in rodents?

A

It makes them less scared of cats, so they are more likely to be eaten and cats more likely to become infected after ingesting the tissue cysts.

327
Q

How long does it take fecally excreted toxoplasma oocysts to sporulate / become infective? Clinical implications?

A

1-5 days; as long as the cat box is cleaned within 24 hours, then humans won’t be at risk for coming into contact with an infective toxoplasma sporozoite.

328
Q

How do cats most commonly become infected with toxoplasmosis? Dogs / people?

A

cats - ingestion of bradyzoites in intermediate hosts

Others - ingestion of infective sporozoites from poop or from bradyzoites in uncooked meats.

329
Q

What scenario in cats and other species allows for subclinical toxoplasmosis to become clinical?

A

Immunosuppression; it is not uncommon for a cat to develop clinical toxoplasmosis following another infection, especially FIV.

330
Q

What vector borne disease can cause impaired neutrophil function, and allow for opportunistic infection?

A

Anaplasma phagocytophilum

331
Q

What cell line is decreased in patients with granulocytic anaplasmosis?

A

Platelets - these patients present with moderate thrombocytopenias, not neutropenias

332
Q

What organism is the cause of infectious canine cyclic thrombocytopenia?

How often does the cycle occur?

A

Anaplasma platys
Every 1-2 weeks

333
Q

What cell type does E. canis preferentially affect?

A

Monocytes / mononuclear cells

334
Q

What infectious organism can cause a profound monoclonal gammopathy and lymphocytosis?

A

Ehrlichia canis

335
Q

What two vector borne diseases can result in morulae in neutrophils? In monocytes/mononuclear cells?

A

Anaplasma phagocytophilum and Ehrlichia ewingii

Ehrlichia canis and chaffeensis

336
Q

What is the reservoir host for cytauxzoonosis?

How is this parasite transmitted from bobcats to cats?

A

Bobcats

Ticks ingest infected erythrocytes from bobcats. The organism undergoes a complete lifecycle in the tick, and then transmit infected sporozoites to a cat when it is fed upon.

337
Q

What is the main pathogenesis of cytauxzoonosis in cats?

A

The infectious sporozoites infect the mononuclear phagocytes in blood. These infected cells then have the organism undergo asexual reproduction inside of them, causing them to become severely enlarged, full of schizonts. These enlarged monocytes then cause vascular obstruction.

338
Q

What happens following infection of mononuclear cells in cytauxzoonosis? How does this relate to diagnosis? What is the most important diagnostic test in these cats?

A

The organisms rupture out of the giant monocytes, and then infect the RBCs. Visualization of the organism in the RBCs (piroplasms) or in mononuclear cells (schizonts) on blood smear is often how these cats are diagnosed.

CBC with smear evaluation

339
Q

What are cytologic features that can help distinguish Mycoplasma hemofelis from Cytauxzoonosis felis?

CBC change?

A

Mycoplasma is typically epicellular and often occurs in pairs or chains

Mycoplasma is typically associated with a regenerative anemia, while cytauxzoonosis is not.

340
Q

What percent of dogs with lymphocytic (immune mediated) thyroiditis (ie hypothyroidism) have elevated TSH levels?

A

75%

341
Q

What are the four main areas of the CNS that are affected by thiamine deficiency in cats?

A
  • oculomotor nuclei
  • vestibular nuclei
  • lateral geniculate nuclei
  • caudal colliculi
342
Q

Are cats or dogs more susceptible to thiamine deficiency? What is the difference?

A

Cats; they require 2-4x more than dogs

343
Q

What does secondary hypoadrenocorticism refer to?

A

This refers to when the pituitary doesn’t release ACTH. This results in the signs of ‘atypical addisons’ where only glucocorticoid deficiency is present.

344
Q

What are the clotting factors for the extrinsic pathway? Intrinsic? Common?

What is another name for the extrinsic pathway?

A

Extrinsic - 7

Intrinsic - 8, 9, 11, 12

Common - 1, 2, 5, 10

Tissue factor

345
Q

What are the alternative names for factor 1, 2, 3, 4?

What does thrombin do?

A
  1. Fibrinogen
  2. Thrombin
  3. Tissue factor
  4. Calcium

Thrombin activates fibrinogen to fibrin.

346
Q

What is the main way that lungworms get to the lungs?

What is slightly different about angiostrongylus?

A

Infective forms are ingested and pass into the GIT. They then penetrate through the intestinal wall and gain access to either the lymphatics or hepatic portal circulation. From there, they entire into the right heart, and go into the pulmonary vasculature, from which they emerge into lungs.

Angiostrongylus adults live in the right heart / pulmonary vasculature, and then their eggs release L1s which then escape into the airways.

347
Q

What causes the neurologic signs associated with Angiostrongylus vasorum?

A

These dogs develop a systemic coagulopathy that can result in CNS hemorrhage.

Occasionally, larval migrans can occur as well.

348
Q

What is the goal of a Baermann test?

Which lungworms are and are not often detected on it?

A

Detect motile lungworm larvae that have been coughed up from the lungs and then swallowed.

Detectable - Aelurostrongylus, angiostrongylus, and crenosoma vulpine

Not detectable - filaroides, oslerus osleri, and capillaria

349
Q

Describe the lifecycle of trichuris vulpis.

How long is the PPP?

A

Eggs are ingested from environment.

Larvae develop in the small intestine for a couple of weeks.

Larvae then migrate to cecum and colon, where they penetrate into the mucosa, and develop into adults.

The adults literally have their faces in the mucosa and their butts in the lumen, where eggs are shed into the feces.

Long relative to others: 70-100 days (3 months)

350
Q

What is the PPP of hookworms and roundworms?

A

Hooks — 2 weeks
Rounds — 1 month

351
Q

What is the main form of brucella that affects dogs? What are the other three possibilities?

A

Canis

Abortus
Suis
Melitensis

352
Q

Traditionally, what is a patient side test that is commonly used as a screening test for brucellosis? What are two confirmatory tests?

A

Screening (high sensitivity) - RSAT (rapid slide agglutination test); high sensitivity (70%), but low specificity so has high false positive rate that necessitates use of a confirmatory test.

Confirmatory tests include ME-RSAT or AGID; highly specific, but poorly sensitive (30%)

353
Q

Aside from the reproductive tract, what three organ systems are commonly affected by brucellosis?

A

Spine / intervertebral disc
Eyes
Kidneys

354
Q

What hormone increases and what hormone decreases appetite?

A

Ghrelin increases, leptin decreases

355
Q

What is a potential side effect of misoprostol?

A

Abortion

356
Q

What are four classic labwork changes in dogs with H. americanum?

A
  1. Severe neutrophilic leukocytosis
  2. Mild to moderate ALP elevation (bone related)
  3. Hypoglycemia (spurious due to extremely high WBC counts)
  4. NORMAL CK
357
Q

What is unique about the transmission of Hepatozoon?

A

It is acquired via ingestion of an infected tick, not being bit by the tick.

358
Q

What are some major differences regarding H canis and H americanum infections?

A

H canis is much less pathogenic and subclincial infection is more common.

H canis affects lymphoid organs and bone marrow, while americanum affects muscle. This means that americanum is more likely to result in lameness and muscle pain.

H canis is associated with mild lab changes with anemia as the most common clinical sign, while americanum is associated with dramatic leukocytosis.

They are transmitted by different ticks. H canis is associated with the brown dog tick (Rhipicephalus sanguineus) and Americanum is associated with the gulf coast tick (Ambylomma maculatum).

359
Q

What is a unique PE finding in dogs with H. americanum? Radiographic finding?

A

Ocular discharge

Periosteal bone proliferation, usually smooth / not aggressive

360
Q

What is the colloquial term for the histopathological lesion associated with H americanum? How does this relate to the clinical signs?

A

Onion-skin cyst - formed by the host cell (likely a mononuclear cell) that produces large amounts of mucopolysaccharide to protect itself

When these rupture following significant parasite reproduction, it causes a severe inflammatory myositis.

361
Q

How can hepatozoonosis be diagnosed on blood smear?

A

Gamonts will be present in neutrophils for both forms, but is significantly more common for H canis.

362
Q

What is the most reliable way to diagnose Hepatozoon americanum?

A

Muscle biopsy

363
Q

How do the pancreatic cells know when to release insulin?

A

They take up glucose via GLUT2 into the beta cell. It gets converted to ATP. The ATP then blocks a ATP-K pump, which prevents potassium from leaving, allowing the cell to depolarize. This triggers VGCC and then vesicles of insulin are released.

364
Q

Via what vector is bartonella transmitted?

What is the main reservoir host for bartonella?

A

Fleas

Cats

365
Q

What is the main clinical manifestation of bartonellosis in dogs?

A

Infective endocarditis

366
Q

What cell types does bartonella commonly infect?

A

Vascular endothelial cells and RBCs

367
Q

How many stages does EG toxicity have, and what are they?

A

Three

  1. Initial clinical signs — GI and neuro (vomiting, nausea, ataxia, seizures and PU/PD); first 12 hours
  2. Apparent resolution in clinical signs; 12-24 hours
  3. Onset of acute kidney injury secondary to calcium oxalate crystalluria; 24-36 hours onward
368
Q

What is another name for the ornithine cycle and what molecule is needed for this cycle?

A

Urea cycle; arginine

369
Q

What is the etiologic agent of salmon poisoning? Where is this disease located to and why? What is the lifecycle of this organism?

A

Neorickettsia helminthoeca

Pacific northwest — this is the location of intermediate host (snail) of the trematode (fluke) vector (Nanophyetus salmincola).

Snails become infected via contact with infectious feces from dogs. The snails then release more infectious organisms in water that get into salmon/fish, and then the dog eats the fish.

370
Q

What are two common findings on exam for salmon poisoning disease, and what are two common historical complaints?

A

Peripheral lymphadenopathy and fever

Vomiting and diarrhea, often bloody

371
Q

What cell type does Neorickettsia helminthoeca infect?

A

Macrophages

372
Q

How is salmon poisoning typically diagnosed?

A

Identification of trematode eggs on fecal analysis

373
Q

What is the pathophysiology behind pemphigus foliaceus lesions?

A

Auto immune attack against desmoglein 1, a desmosome holding keratinocytes together. This results in free floating keratinocytes, which are called acanthocytes.

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