Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Specialty Boards Prep > Deck 8 > Flashcards

Deck 8 Flashcards

1
Q

What is this picture demonstrating?

A

A myotonic dimple in a dog with congenital myotonia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is cricopharyngeal achalasia? What is the main treatment option?

A

It is failure of the cricopharygneus muscle to relax during swallowing, causing significant dysphagia.

Treatment consists of myotomy / myectomy of this muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Scotty cramps may be caused by a functional deficiency of this neurotransmitter?

A

Serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Via what mechanism does hypokalemia result in myopathy / weakness is cats? Below what value do clinical signs start to occur?

A

Being hypokalemic increases the concentration gradient of potassium across the cell membrane. Thus, the resting membrane potential of the muscle cells moves closer to the Nernst potential of potassium (-90mV). This causes the RMP to become more negative, moving it further away from threshold.

Below 3.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the abnormal channel in horses with HYPP? What is the mechanism? What is the main bloodwork finding? What is the genetic defect?

A

Voltage gated sodium channel

When extracellular potassium raises, the concentration gradient of potassium across the cell membrane decreases. This means that the RMP is less dependent on the Nernst potential of potassium, and thus the RMP becomes more positive, moving closer to threshold potential.

When RMP moves closer to threshold, it is easier for the VGSCs to fire. Unfortunately, some of them are abnormal. The abnormal ones stay open for too long, and tons of sodium rushes into the cell.

Two things then happen. 1) a bunch of potassium effluxes from the cells, in an attempt to repolarize the cell. 2) the normal VGSCs that are present become inactivated, and not enough are available to allow for muscle contraction, resulting in the clinical signs of paralysis.

The main bloodwork finding is elevated potassium levels from the massive efflux of potassium.

So elevated potassium is both the inciting factor and the bloodwork finding — note that the initial potassium increase is just mild / physiologic as can be seen after exercise or just eating a potassium rich food (like alfalfa hay).

Genetic defect is SCN4A.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What type of muscle atrophy (histologically) is seen with Cushing’s myopathy?

A

Type 2 fiber atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Ragged red fibers on muscle histopathology are associated with __________.

A

Mitochondrial diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Malignant hyperthermia is due to an abnormality in what channel?

What is a commonly implicated trigger of clinical signs?

Drug for treating this?

A

The calcium channel associated with the ryanodine receptor, which is what lets calcium out of the sarcoplasmic reticulum.

Volatile anesthetic agents

Dantrolene — blocks this channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the function of carnitine?

If abnormal, what type of abnormalities will we see on histopath?

A

Binds to fatty acids, and enables their transport across the mitochondrial membrane. It can help get fatty acids to the mitochondria so that they can be processed for energy, or can remove them out of the mitochondria if they are starting to accumulate.

Abnormalities with carnitine will typically result in lipid accumulation within type 1 myofibers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Type 1 myofibers primarily rely on _______ for energy metabolism. What molecule is important in this process?

Type 2 myofibers primarily rely on _______ for energy metabolism.

A

Type 1 — free fatty acids via beta oxidation; carnitine.

Type 2 — glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How can a mitochondrial disorder lead to a lipid storage myopathy / secondary carnitine deficiency?

A

If the mitochondria can’t process fatty acids due to some defect in the respiratory / electron transport chain, then lipid will start to accumulate within the mitochondria. Carnitine will do the best it can to help remove this lipid and get it excreted in the urine, but eventually it will be used up, and lipid will build up within the mitochondria AND within the muscle (because no carnitine will be available to move the fatty acids into the mitochondria either).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What two breeds of dog develop polymyositis most frequently? In which breed can this be a “pre-neoplastic” syndrome?

A

Boxers and Newfoundlands

Boxers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Feline hyperesthesia syndrome is presumed to be what type of disease process?

A

Myopathy — specially an inclusion body myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which species is more resistant to tetanus - dogs or cats?

A

Both are relatively resistant, but cats are 10 times more resistant than dogs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does tetanus gain access to the nervous system?

A

It can either travel retrograde up the motor nerve axons after gaining access at the end plate, or it can get access hematogenously (presumably how it gets to the brain in some cases).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Mechanism of action of tetanospasmin

A

Inhibition of glycine (and GABA) at inhibitory interneurons in spinal cord (Renshaw cells) and brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Main risk of tetanus anti-toxin administration?

A

Anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is this dog’s diagnosis? Treatment options in the acute phase? Chronic phase?

A

Infraspinatus muscle contracture

Acute phase — fasciotomy to relieve compartment syndrome

Chronic phase — infraspintus tenotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What neuropathy can be seen in severe cases of iliopsoas muscle injury?

A

Femoral neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the molecular features of the nicotinic acetylcholine receptor. Where does acetylcholine bind?

A

It is composed of 5 subunit proteins. 2 alpha, 2 beta and one epsilon. It forms an ion channel in the middle of it. Two acetylcholine have to bind, one to each alpha subunit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the toxic component of black widow venom? What does it do?

A

Alpha-latrotoxin

Causes massive Ach vesicle release at the NMJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

True or false — organophosphates form temporary bonds to the acetylcholinesterase proteins

What is the significance of this?

A

False — they like to form more stable bonds to these proteins. The significance is that you want to treat these patients as early as possible with 2PAM.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why might junctionopathies affect the areas like the face and oral cavity sooner than appendicular musculature?

A

Reduced safety factor of the NMJ at these locations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What neuromuscular condition also affects the autonomic nervous system? Why?

A

Botulism

NMJ blockade also occurs at the other location of the nicotinic acetylcholine receptors — the autonomic ganglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
In what breed of dog does congenital myasthenia spontaneously resolve?
Miniature dachshunds
26
What drug reaction in cats results in myasthenia gravis?
Methimazole
27
Which focal form of myasthenia gravis are cats unlikely to get? Why?
Megaesophagus — the distal 2/3rds of the feline esophagus is smooth muscle
28
What percentage of dogs with acquired MG present with focal signs?
36-43%
29
What percentage of dogs with generalized MG are sero-negative? What are some reasons that a dog could be sero-negative?
2% - all antibody is bound to receptors - antibody is damaged during processing - antibodies are directed against a different target besides the AChR (titin, ryanodin) - pre-treatment with steroids
30
What are the four criteria needed to diagnose a sero-negative myasthenic?
1. Clinical signs consistent with MG 2. Consistent diagnostics (edrophomium / EDX) 3. Resolution of appendicular weakness with acetylcholinesterase drugs 4. At least 2 negative anti-AChR titers
31
What antibiotic classes should be used cautiously in MG patients?
Ampicillin (bc it gets degraded into penicillinamine) Aminoglycosides Lincomycin Polymyxin Tetracyclines
32
What is the mechanism of action for blue-green algae (cyanobacterium) toxicity?
Potent agonist of the nicotinic ACh receptor — causes severe muscle rigidity, recumbency, seizures and death within an hour of exposure
33
Do aminoglycosides cause a pre-synaptic or post-synaptic NMJ blockade?
Both — pre is via blockage of calcium influx and post is by blocking the ion channel within the ACh receptor
34
Ingestion of what growth promoter for ruminants can cause severe LMN signs in dogs?
Lasalocid
35
Describe the clinical signs of black widow envenomation
They develop severe muscle rigidity followed by flaccid paralysis as they run out of ACh. They also have stimulation of their autonomic and sensory systems, which causes intense pain, and salivation, lacrimation, and tachycardia.
36
What type of botulinum toxin typically affects small animals? Large animals?
Small animals — C Large animals — D
37
What class of neuromuscular blocking agents is non-depolarizing? Depolarizing?
Non-depolarizing = curare / curare related agents Depolarizing = succinylcholine
38
Mechanism of action of organophosphate toxicity. What are the three broad groups of signs?
Irreversible binding to acetylcholinesterase - muscarinic overload (SLUDD) - nicotinic overload (weakness, tremors) - CNS overload (restlessness, seizures, coma)
39
What is the main difference between organophosphate and carbamate toxicoses? What are the clinical ramifications of this?
It’s how they bind to the acetylcholinesterase enzyme. Organophosphates do so irreversibly, while carbamates are reversible. Carbamate toxicity has a good prognosis generally, and is relatively easily reversed with atropine.
40
What percent of rattlesnake envenomations resulted in neurotoxicity?
5.4%
41
Coral snake envenomation MOA? What is the median duration of time between bite and onset of signs?
“Curare”-like action of AChR binding. 105 minutes
42
What are five extrinsic factors to determining cerebral blood flow?
1. PaCO2 (higher = higher CBF) 2. PaO2 (lower = higher CBF) 3. Temp (higher = higher CBF) 4. Blood viscosity (lower = higher CBF) 5. Venous drainage
43
Do benzodiazepines increase or decrease CBF? Opioids?
Benzo = Decrease via decrease in oxygen consumption by neurons Opioid = maybe increase due to decreased respiratory drive and associated hypoventilation leading to elevated PaCO2; maybe decrease per Google AI
44
What is normal residual urinary bladder volume?
0.2-0.4 mL/kg
45
What is the name of one of the main receptors involved in transduction of nociceptive stimuli? What can it be activated by?
Transient receptor potential vanilloid subtype 1 (TRVP1) Heat, low pH, ATP, bradykinin, trypsin, prostaglandins, etc…
46
What are the two types of neurons that are primarily responsible for transmitting pain signals? What is different between them?
A-delta and C fibers A-delta fibers are thinly myelinated, faster and transmit sharp / superficial pain, while C fibers are not myelinated, slower and transmit deep pain.
47
What dorsal horn laminae do nociceptive fibers send their central projections to? What type of neurotransmitters do these fibers release at these synapses? What receptors do they bind to?
Laminae I, II and IV Glutamate and neuropeptides, both of which are excitatory Glutamate will bind to AMPA and NMDA receptors, and the neuropeptides will bind to neurokinin 1 & 2 receptors.
48
What types of receptors are located pre and post synaptically at the dorsal grey horn that decrease incoming nociceptive information? By what mechanisms do they inhibit signal transmission pre and post-synaptically?
Opioid receptors Serotonin receptors Alpha 2 adrenergic receptors GABA (B) receptors Pre — decreased neurotransmitter release Post — hyper-polarization of the post-synaptic membrane
49
What are the names of the three “nuclei” in the dorsal grey horn, and what are their respective laminae?
Marginal nucleus — 1 - contributes to spinothalamic Substantia gelatinosa — 2 - sends interneurons to nucleus proprius Nucleus proprius — 3, 4 and 5 - contributes to spinothalamic / spinocervicothalamic
50
Define nociceptive pain, neuropathic pain, hyperalgesia, and allodynia.
Nociceptive pain — “normal” pain arising from stimulation of nociceptors in tissue Neuropathic pain — pain arising from damage or dysfunction of the nervous system, typically chronic Hyperalgesia — increased pain response to a painful stimulus Allodynia — pain response to a non-painful stimulus
51
What is the mechanism of action of butorphanol? Buprenorphine?
Butorphanol — agonist / antagonist (kappa more than mu) Buprenorphine — partial mu agonist
52
Traditionally, which COX is considered constitutive (good) and which one is involved in the inflammatory pathway? Where does COX contribute to the pain pathways?
COX 1 = constitutive COX 2 = inflammatory COX 2 is primarily involved in the transduction portion (peripheral sensitization) of the pain pathway, but may also be involved in central sensitization.
53
Induction of emesis removes what percentage of the total stomach contents?
40-60%
54
What is the difference between the MOAs of amphetamines and methylphenidate?
Amphetamines get taken up into the nerve terminal and stimulate release of norepinephrine and dopamine, while methylphenidate blocks re-uptake of these molecules to keep them in the synapse longer.
55
What are the three broad organ systems affected in caffeine toxicity? What is the main route of exposure in small animals? What is the toxic principle, and what are the 4 MOA?
GI, cardiovascular and neurologic Chocolate ingestion Methylxanthine Phosphodiesterase inhibitor, increased catecholamine release, adenosine antagonism, increased intracellular calcium
56
What are the two main organ systems associated with lead toxicity? Are juveniles or adults more prone to toxicity? Why?
GI and neuro Juveniles because they absorb more lead from their GI tract than adults (40-50% v 5-10%)
57
What are the mechanisms of action of pyrethrin / pyrethroid medications?
Enhanced sodium ion conductance and decreased GABA activity
58
Imidacloprid is an analog to what biochemical substrate?
Nicotine — as such toxicity resembles signs of nicotine toxicity
59
What toxicity can result in a delayed polyneuropathy? What species is this best reported in?
Organophosphates Cats
60
Mechanism of action of bromethalin toxicity? What is the actual toxic metabolite?
Uncouples oxidative phosphorylation, resulting in lack of ATP, which leads to failure of the ATPase ion pumps and subsequent edema development Desmethylbromethalin
61
What are the two clinical presentations of bromethalin toxicity?
- High dose exposure = acute onset of excitation, seizures, tremors - Lower dose exposure = delayed onset (1-7 days) of mixed CNS signs (ataxia, paresis to paralysis, rigidity, mental depression, tremors, +/- seizures)
62
Classic histopathologic finding of bromethalin toxicosis?
Intramyelinic edema, specifically at the interperiod line
63
What are the main clinical signs associated with serotonin syndrome?
- neuromuscular hyperactivity (tremors, myoclonus) - autonomic hyperactivity (mydriasis, tachycardia, hyperthermia) - Altered mental status
64
Mechanism of action of carbon monoxide poisoning? Where are lesions seen in dogs?
Very tight binding of carbon monoxide to hemoglobin Polioencephalomalacia involving cerebral cortex, basal nuclei, substantia nigra and cerebellum — chronic change can also result in peri-ventricular demyelination /white matter necrosis.
65
What is the recurrence rate for IVDH in dogs that receive multisite fenestration v those that do not? Where does recurrence occur most frequently?
Non-fen: 17-19% Fen: 5-7% 87% of recurrences occur at the adjacent site
66
What is a common clinical sign seen in dogs with polymicrogyria? Why? Common breed?
“Cortical” blindness — presumably because this malformation predominantly affects the occipital lobes Standard Poodle
67
True or false — the degree of cerebellar herniation is not associated with the presence or absence of concurrent syringomyelia
True (Mai)
68
What is the EEG definition of status epilepticus?
It’s an epileptiform pattern lasting more than 10 continuous minutes or present in at least 20% of any 60 minute recording. The epileptiform discharges are spikes, sharp waves and combinations of spikes and waves
69
What is this diagnosis? Describe these findings. How do you know the weighting of the right image?
- globoid cell leukodystrophy - diffuse T2W hyperintensity of the white matter (making it iso-intense to grey) and mild T1W hyper-intensity of the corpus callosum. - the right image a pre-T1W image, and you can tell because of the hyper-intensity of the neurohypophysis.
70
There are three abnormalities (at least) in this image. What are they and what is the diagnosis? What can you see on a TRV T2W image?
1. Absent corpus callosum 2. Absent rostral commissure 3. White matter of cerebellum is iso-intense to grey matter This is a dog with GM1 gangliosidosis. A T2W TRV would reveal overt T2W hyper intensity of the white matter and a very small corpus callosum. (Mai)
71
Abnormalities of this structure identified on a midline sagittal brain image have been proposed as a screening tool for this category of diseases? Which one in particular?
Corpus callosum Lysosomal storage diseases Gangliosidoses (Mai)
72
Mucopolysaccharidoses occur secondary to deficiency in the metabolism of what molecule?
Glycosaminoglycan
73
What are three MRI features associated with neuronal ceroid lipofuscinosis?
- severe diffuse cerebral / cerebellar atrophy - contrast enhancement and thickening of meninges - subdural hematoma (Mai)
74
True or false — cerebellar cortical abiotrophy is “a special type of NCL”
True (Mai)
75
What is the diagnosis? Describe the findings? Three breeds this is common in?
L-2 hydroxyglutaric aciduria Diffuse polioencephalopathy with T2W grey matter hyper-intensity / swelling. Affects all cerebral grey matter and basal nuclei. Staffordshire terriers, Westies, and Yorkies (all terriers) (Mai)
76
What is this trying to show? What are other common finding in some of these patients?
T1W hyperintensity of the lentiform nuclei in a patient with HE. Other findings include generalized brain atrophy and extensive bilateral T2W hyper-intensities.
77
True or false — MRI lesions associated with rapid correction of hyponatremia are limited to the pons
False — they are also found in the thalamus, caudate nuclei and grey/white matter junction.
78
What are two breeds of dog predisposed to NLE?
Yorkie Frenchie
79
What condition is this? What breed may be pre-disposed?
Idiopathic hypertrophic pachymeningitis Greyhounds
80
Acute distemper meningoencephalitis affects the ______ matter, and chronic affects the _______ matter.
Acute = grey Chronic = white
81
What infectious CNS organism results in the formation of intracranial pseudocysts? What do these correlate to histopathologically? What is another MRI common pattern for this disease?
Cryptococcus Areas of gelatinous capsular material and fungi, typically within the Virchow-Robins spaces Diffuse meningeal contrast enhancement
82
What are the two general MRI appearances of CNS blastomycosis?
Mass form (single or multifocal) Ventricular / ependymal form
83
What is the origin of T2W hypo-intense rims around the periphery of abscesses?
Paramagnetic free radicals within phagocytic macrophages
84
What side of an intracranial brain abscess is thinner? Why is this important?
Medial side, potentially because the white matter is less vascular. This can be a helpful distinguishing feature from other types of pathology, and also can explain why these can rupture into the ventricular system.
85
What are cross-excitation artifact and cross-talk artifacts? How can they be corrected for?
Cross-excitation = loss of signal due to partial saturation of protons from neighboring slices. Can be addressed by adding an interslice gap or via interleaving. Cross-talk = when two slices overlap (ie if you have multiple slice groups) (see picture), also resulting in partial or complete saturation of spins. Just need to plan slices more accurately if it interferes with anatomy.
86
Why does wrap artifact occur? What direction does wrap artifact occur in? How can you correct for wrap?
Occurs when the FOV is smaller than the area of anatomy being imaged. Normally, in the phase encoding direction. With 3D imaging sequences, it can also occur in the slice encoding direction as well. You can use phase over-sampling techniques, increase the FOV to include more of the anatomy, or align the PE direction with the thinnest part of the anatomy (like right to left in transverse images).
87
Where does Gibbs artifact occur? What are ways to address it? What are two alternative names for this artifact?
Gibbs artifact occurs at high contrast boundaries, and look like a series of alternating dark and bright lines. Worst in the PE direction, and so you can increase the resolution by adding more PE steps (which I think decreases voxel size). Ringing or truncation artifact
88
Where do susceptibility artifacts tend to occur? What type of sequences are the worst in?
At the boundaries of two materials that have very different magnetic susceptibilities (bone / air). Worse in GRE sequences
89
Explain the magic angle effect.
This is an artifact that results in falsely high signal from anatomic structures, predominantly tendons. Tendons have very uniquely aligned protons (due to the arrangement of collagen fibers) — this arrangement normally causes these protons to rapidly dephase, leading to low signal. If these tendons are oriented at a specific angle to the main magnetic field axis, then not as much dephasing occurs, and this allows the tendons to produce signal. The specific angle is 55 degrees (+/- 10). This is most common on sequences with a short TE (shorter the TE, the less time the signal has to be lost) — therefore, it is most obvious on PDW and T1W images, and not present on T2W images.
90
Explain what ADC and FA are? What MRI sequences generate each value?
Apparent diffusion coefficient (DWI)— an index of water diffusibility in a certain region Fractional anisotropy (DTI) — an index reflecting the magnitude of oriented water diffusion (associated with the structural integrity of white matter)
91
What were the four main findings of this paper?
Intratumoral ADC values were higher in meningiomas than HS — tumors with higher cellularity have lower ADC values Peritumoral ADC values were higher in HS than meningiomas — HS causes more disruption of surrounding tissues, leading to more severe edema? Peritumoral FA values were lower in HS than meningiomas — more aggressive tumors infiltrate / destroy surrounding white matter, lessening directional water diffusion here (water can’t follow the normal white matter tracts) HS had meningeal enhancement / mass effect extending into the sulci, while meningiomas did not.
92
What were the main findings of this article?
- HS more frequently had peri-lesional and distant meningeal enhancement - HS had both lepto- and pachymeningeal CE, while meningiomas just had pachy - HS had worse edema - only meningiomas caused adjacent bony changes and were cystic - HS would extend into the sulci more
93
Per Mai, what are some distinguishing MRI features between oligodendrogliomas and astrocytomas?
- astrocytomas are more common the caudal fossa - oligos are more likely to contact the surface - oligos are more likely to cause ventricular distortion - oligos are more likely to have an intraventricular location
94
What the most common locations for choroid plexus tumors?
4th ventricle, then 3rd and then lateral (reverse order)
95
What brain tumor is more common in cats than dogs? What kind of brain tumor have cats not been reported to get?
Ependymoma is more common in cats, and they have not been reported to get choroid plexus tumors.
96
What is the cellular origin of medulloblastomas?
External granular (germinal) layer of the cerebellum
97
Why might intracranial histiocytic sarcomas more be likely to cause herniation than meningiomas?
They grow faster than meningiomas +/- cause more edema.
98
What tumor classically is spread over the cerebral convexities? What is another classic feature of this tumor?
Granular cell tumor Pre-T1W hyperintensity
99
What type of mass is this? How do you know?
This is an osteochondroma. We can tell because of the T2 hyperintense cartilage cap.
100
What three features might help you distinguish a chondroma from a myxoma?
— location: myxomas should be arising from the joint, and will be dorsally / dorsolaterally located, while chondromas often arise above / near the disc space — shape: myxomas commonly have a very lobulated appearance — invasion: myxomas can be locally invasive within the surrounding soft tissues

Specialty Boards Prep (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions