#plasmacytic

[phoenixofmetal]

A semi-low effort shitpost featuring Hasumet, my Necron character, fleeing from the second greatest bane of her existence: the humble plasmacyte

[audley-and-cherry]

Today's goal is to finish the base colors on the first phase of the Crustcron army (and especially my kill team).

Here are the 9 I have left:

A handful of Immortals, 2 plasmacytes, a technomancer, and a plasmancer.

Now for a break before the Immortals' weapons!

[archmagemeow]

Ms. Cherry 🍒, My Ten-Year-Old Blind & Toothless Cat

Ms. Cherry is a ten-year-old blind & toothless cat with an autoimmune disease called Lymphocytic-plasmacytic cholangiohepatitis. This autoimmune condition primarily affects her liver & bile ducts. She is on a liver supplement & steroid to help manage her symptoms.

She is a spunky gal who adores being outside & feasting as often as she can; she is a fiend for a good chewy snack!

Besides her lack of vision, teeth, & normally functioning liver & bile ducts, she is as happy as can be!

She is my study buddy, too. She adores a quaint & cozy spot in my lap during my study sessions.

I highly encourage those, who can afford to both emotionally and financially, to adopt a medically complex senior cat to help give them loving homes! 🏠 🤎

[premiummeats]

applied the shades and the tesseract glow to my necron warriors (and also their pet scarab swarms) and also the plasmacyte cause i didn't really know when to do him. for my first minis that i've both put together and painted, i think they came out pretty all right, although i'll probably think of something to do with the guns they've got, cause right now they're a bit bland. with how tight some of the angles are to get a paint brush in, if i ever pick up more warriors (i know i will), i might try painting them before even assembling, just so i can drive myself even more crazy trying to get everything the way i'd want them.

[pamprinninja]

My spouse is now a fully-fledged Necron Phaeron; and I could not be prouder of them!

(Seriously, though; it’s been a real pleasure, watching them pick up new techniques and sharpen their brush skills at warp speed. I can’t wait to see what they do next!)

Started my journey into Warhammer painting after getting a kit for Christmas. I thought i'd show off a few of the figures I've painted.

(please be nice, I'm so new to miniature painting)

I love these lil Necron dudes. I'm told using all metallic paint was the equivalent of learning to swim in the deep end. 🤷 I'm also hearing using a cold palette is unusual, too. 🫠 Maybe I'm doing it wrong?

[raweggshaver]

After a very long break from warhammer I decided to kitbash some plasmacytes for My Sire's necron kill team. I hope you enjoy them as much as I do

Camera sucks so sorry about the blur but I promise you they are very cool

(P.S. any of the not obviously gw grey plastic are things I found while working at a hospital that made me go "this kinda looks like a thingy-ma-bob and I stole it" anyways I'm excited to prime them)

[waluigis-cock]

I finally decided on a paint scheme for my necron army, and I'm really happy with how it turned out. I only have a few models painted, started with scarabs to figure out what I want to do, then did a plasmacyte to round it out since it has some features shared with scarabs and infantry

[omgkhazadum]

some newly finished dudes

some cryptothralls and canoptek plasmacytes

[sara-paints]

I remember when I started this project of getting my Necrons up to date for 10e, I made a promise to myself that I wouldn't rack up a brand new Pile of Shame. But between my old models, a few new models, and having the 3D printer working overtime, I'm quickly getting one anyway.

Anyway, I have the requisite 3 Skorpekh destroyers and a Plasmacyte, which makes the last models I needed to play Combat Patrol. I also printed 4 Cryptothralls because my Lychguard and possibly my Warriors are going to need Murder Buckets to keep them safe.

[boyzpaint]

🔥Ruthless necron plasmacyte. Ready to incinerate you!!!

[crypticspyder]

Been painting a Plasmacyte for my necrons and im pretty happy with the glow! Working on the OSL now, and I’ll probably highlight the edges of the purple a bit, and maybe shade the leadbelcher more, or paint over some with a thinned black. Not sure!

[banshee-king]

I have to say the Necrons update for 9th ed was honestly such a huge disappointment for me.

Warriors got a new weapon… but it has the same profile as the Immortals’ Gauss Blaster, only difference being 12” Assault 2 vs 30” Rapid Fire 1. So it’s good against exactly the same target (same Strength, AP, and Damage) but at a shorter range. Necrons only have 2 Troops choices, which are barely different to each other. Immortals are just slightly better Warriors. After Gauss weapons lost their anti-vehicle ability, Necron Troops now had 3 similarish anti-infantry weapons for their 2 near identical Troops units. So GW updates Warriors and gives them… a slightly weaker Immortal gun. The redundancy is painful.

Necrons get two news units in the form of Skorpekh and Ophydian Destroyers… which get this, have the same weapons. Both units have Hyperphase reap-blades and Hyperphase threshers. It also gets worse because 1 model for every 3 MUST have the reap-blade. It’s a unit of 3 or 6 models, with 2 or 4 wielding threshers and 1 or 2 wielding reap-blades. There are literally no options whatsoever.

The Canoptek Doomstalker is added as a new anti-tank unit… except it has the same main cannon as the Doomsday Ark but with shorter range. Same Type, Strength, AP, Damage and both units have a similar defensive profile, just slightly different. It’s the Warrior problem all over again.

Flayed Ones got an update too, but only to their looks and their price tag. They got 0 new weapons and are bloody overpriced for 5 infantry models.

For Kill Team Necrons got the worst of any faction so far, no new unit just an upgrade sprue that’s worse than what the T’au got. The Apprentek is at least something, but I couldn’t care less for the Plasmacytes and other cosmetic options. Like 50% of their upgrade sprue feels like a waste of space.

It’s like GW is allergic to giving Necrons more weapons. Necrons before the update were already suffering from a lack of units/wargear/variety compared to other factions. All this new redundancy isn’t helping.

I wish that Warriors instead got a melee weapon so they could actually make use of Strength and Attack buffs and actually function differently to Immortals. I wish the Canoptek Doomstalker was more like a mortar or something and could fire at units it can’t see behind cover. I wish that the Necrons Kill Team update added to the Flayed Ones, gave us Flayed Lord or something, gave them more weapons as well. It’s so frustrating because all this money and attention was obviously spent on them, but it feels so inefficiently used.

At least the Necrons books are good. =/

[audley-and-cherry]

Chipping away at the Crustcrons.

I fell a little short of this morning's goal of getting the remaining base colors down on two warriors, two Deathmark, and two Plasmacytes, but I'm not unhappy with my progress.

I have a contender for favorite Necron with this Deathmark's excellent face!

[careforcritters]

Vet Med in Warrior Cats: Respiratory part 2: Nasal Disease (What’s up with Runningnose?)

disclaimer

Runningnose is a shadowclan medicine cat introduced in The Prophecies Begin. The other cats often joke that he is “a medicine cat who can’t even cure his own cold”. One possible explanation for his frequently runny nose is that he may have lymphocytic-plasmacytic rhinitis (LP rhinitis). This is an immune mediated disease that could be caused by frequent irritation, allergies, or a previous nasal infection, but the definitive cause is unknown. Cats with this disorder have frequent nasal discharge and sneezing and a reduced appetite, but no systemic symptoms. LP rhinitis can’t be treated with antimicrobials. Since it is an immune mediated disease, it can only be managed by drugs that modulate the body’s immune response (which is an explanation for why Runningnose could not cure his running nose). In a veterinary clinic, cats with LP rhinitis would be given steroids such as prednisolone or cyclosporine. Antibiotics like azithromycin are needed only if there is a secondary bacterial infection present. Other management practices like humidifying the air and avoiding airway irritants like dust and smoke can help reduce the severity of disease. Unfortunately Runningnose wouldn’t have much control over that. 

Another possible, but less likely cause, for Runningnose’s ailment is nasopharyngeal polyps. Polyps are benign, granulomatous masses that begin growing in the auditory tube and can travel down to the nose and throat. Polyps cause mucoid nasal discharge, but they can also cause more serious signs as they grow, such as difficulty swallowing, change in vocal sounds, and a respiratory noise called “stertor”, which is low pitched snoring sound during expiration caused by partial obstruction of the airway. Because of this, polyps can become deadly if not treated. In a veterinary office, a polyp can be easily identified and removed using gentle traction under general anesthesia. Provided a cat would be able to reach its paw into another cat’s mouth and retract the soft palate, they may be able to remove a polyp by hooking its claw onto the base of the polyp and pulling slowly and gently. Anesthesia would be preferred, but since these cats remove limbs with no sedation this wouldn’t be as painful.

Cryptococcus is a fungus that causes granulomatous disease in cats. Clinical signs of crypto include mucoid or hemorrhagic (bloody) nasal discharge and sneezing, and sometimes a “roman nose” facial deformity (which is basically a bump along the bridge of the nose due to the space occupying granulomatous mass in the nasal cavity). Crypto is treated by removing the fungal plaques and giving antifungal medication, usually fluconazole. 

Finally, another option for Runningnose’s runny nose is Feline Herpes Virus. I covered FHV in the first respiratory section, but essentially Herpes is basically ubiquitous in feral cat populations. Adult cats that become infected usually aren’t seriously ill or have lower airway signs, however the virus damages the upper respiratory tract which can allow for secondary bacterial invaders to cause more serious illness. The most common clinical signs include mucopurulent nasal and ocular discharge, sneezing, nasal congestion, conjunctivitis, and ocular ulcers. Runningnose is described as having “rheumy” eyes in The Ultimate Guide (2013), which could be taken to mean that he has ocular discharge. FHV is relatively self limiting and will resolve on its own without treatment, however the virus remains latent in the trigeminal ganglia and other peripheral neurons, meaning that when a cat becomes infected they stay infected for life. Usually, this doesn’t cause problems. However, when a cat is stressed, Herpes will recrudesce and cause the cat to show symptoms and shed the virus. If Runningnose is constantly very stressed (which is pretty believable) it is possible that his Herpes infection is always relapsing. Poor thing. 

sources

https://www.vet.cornell.edu/departments-centers-and-institutes/cornell-feline-health-center/health-information/feline-health-topics/nasopharyngeal-polyps

https://www.merckvetmanual.com/respiratory-system/respiratory-diseases-of-small-animals/rhinitis-and-sinusitis-in-dogs-and-cats

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8066322/

https://veterinarypartner.vin.com/default.aspx?pid=19239&id=4951824

[lupinepublishers]

Lupine Publishers|Case Report of Multiple Myeloma Presenting with Unique Skin Manifestation with Literature Review

Abstract

Multiple myeloma (MM), although a rare disease, is the second most common hematologic malignancy. MM is associated with significant morbidity due to its end-organ destruction. It is a disease of the older population and advancements in the diagnosis, monitoring, and treatment of MM are of the utmost importance as the general population lives longer due to other improvements in health care. Herein, we present an interesting case of MM presenting with initially skin manifestation which unfortunately is associated with a poor prognosis due to a relationship indicating higher tumor burden. Despite being on multiple treatment, our patient continued to progress with her disease.

Introduction

Multiple myeloma (MM) accounts for approximately 2% of all malignancies and 13% of hematological malignancies worldwide [1]. MM is the second most common hematologic malignancy [1] and it is a neoplasm of clonal plasma cells which originate from the B-cell lineage and develop after lineage commitment in the bone marrow of progenitor cells [9]. Cutaneous involvement in patients with multiple myeloma is rare and it usually represents of a poor prognosis. Cutaneous involvement indicates an increased tumor burden. The most common cause of cutaneous involvement is due to direct extension from underlying bone lesions of MM or solitary plasmacytoma of bone [2]. It is very rare to have primary cutaneous plasmacytoma [3].

Case Presentation

We present the case of a friendly Caucasian American 70-yearold female with no significant PMH who initially presented to Ruby Memorial Emergency Department in November 2015 with persistent back and left side pain. At that time, she began to notice weakness and some numbness in lower extremities and along with the increasing low back pain decided to seek medical attention and presented to the hospital. On admission, CT thoracic spine (11/16/15) revealed a T5 wedge compression deformity. CT lumbar spine revealed degenerative changes with diffuse osteoporosis. MRI thoracic spine (11/17/15) revealed a T5 burst fracture with retropulsion, focal kyphotic deformity, severe central canal stenosis, possible pathologic fracture deformity, And possible cord contusion at T5. CBC on admission revealed WBC 5.1 with normal differential, Hgb 11.5 with MCV 105.3 and platelet count 170,000. BMP normal, creatinine 0.75, corrected calcium 10.2. Subsequently, she underwent a posterior spinal fusion T3-T8, left costotransversectomy with left pedulectomy and subtotal corpectomy (excision of tumor) via transpedicular approach with placement of anterior cage, T5 laminectomy, and T6-7 partial laminectomy. Pathology revealed a tumor composed of sheets of atypical plasmacytoid cells positive with immunostain for CD138 and negative for pancytokeratin, CD20, and CD3. Insufficient tissue remained for kappa and lambda ISH. The finding was consistent with plasma cell neoplasm. SPEP revealed an M spike seen in the gamma, consistent with monoclonal gammopathy. Random UPEP/ IFE revealed a monoclonal lambda protein without detectable associated IgG, IgA or IgM heavy chain. In December, SPEP/IFE revealed an IgG Lambda monoclonal protein (5.95 g/dL). Free light chain ratio 0.013 (Kappa 0.80 mg/dL, Lambda 60.50 mg/dL). Quantitative IgG 5950 g/dL. Hgb 9.4 with MCV 98.5. Creatinine 0.62. Corrected serum calcium 11.2. Albumin 2.0. Beta 2 microglobulin 4.25. Skeletal survey reveals diffuse osteolytic process with multiple calvarial, vertebral body and rib lesions identified. T3-T8 posterior spinal fusion for pathological T5 compression fracture noted. She had a bone marrow biopsy/aspirate which revealed 47% lambda restricted plasma cells, with marked atypia including a plasmablastic morphology. Preliminary FISH results indicate multiple trisomies, 1q21 gain, del (13q14) and a non-standard IGH rearrangement-t(8;14). Hyperdiploidy detected. She was diagnosed with IgG Lambda Multiple Myeloma. ISS Stage II, DS IIIA. Soon thereafter, she was started on a bortezomib-based triplet regimen - bortezomib, cyclophosphamide, dexamethasone (CyBorD). She completed 4 cycles. In April 2016, SPEP/IFE revealed an IgG Lambda monoclonal protein - not quantified. Quantitative immunoglobulins: IgG 1013 mg/dL. Free light chain assay revealed a ratio of 1.169 (kappa 2.98 mg/dL, Lambda 2.55 mg/ dL). CBC normal. Hgb 13.2. Serum creatinine 0.59. Serum calcium 9.7 (corrected). Serum albumin 3.0 g/dL. Beta 2 microglobulin 2.65 mcg/mL. Skeletal survey demonstrated new evidence of L5 pathological compression fracture. A repeat bone marrow biopsy revealed a variably cellular marrow (10-50%). Maturing trilineage hematopoiesis noted. No atypical plasma cell infiltrate (<5% by CD138 ICH). Cytogenetics normal. Unable to run FISH. At the end of the month, her regimen switched to Lenalidimide/Dexamethasone and she completed 4 cycles. In August, she began maintenance therapy with Lenalidomide at 10 mg daily. She then presented with multiple skin papule skin lesions (Figure 1) mostly on her gluteal region. In January 2017, she had a left gluteal skin biopsy consistent with plasma cell neoplasm with high grade features (plasmablastic differentation) In February 2017, SPEP/IFE revealed a IgG Kappa monoclonal protein (not quantified). IgG level 2303 mg/dL. Free light chain assay reveals a ratio of 1.31 (Kappa 12.63 mg/dL, Lambda 9.62 mg/dL). She completed radiation therapy to left gluteal skin - received 30 Gy/15 fractions. SPEP/IFE revealed a IgG Kappa monoclonal protein (not quantified). IgG level 2357 mg/dL. Free light chain assay reveals a ratio of 1.47 (Kappa 12.20 mg/dL, Lambda 8.32 mg/dL). In March 2017, she was started on Pomalidomide/ Dex. Unfortuatnely she was found to have progression of her disease noted. She was then started on Daratumumab which she could not tolerate and was then started on Carfilzomib/Dex. She has received multiple radiation therapy to her left gluteal region, mid back and left upper lip with significant resolution in all areas. In February 2017, she was admitted to Ruby with worsening pain and lesions located in her lower extremities and edema (Figure 1). Peripheral duplex was obtained and blood cultures to rules out a venous clot and infection respectively. A biopsy was obtained (Figure 2) which showed cutaneous involvement of her multiple myeloma. Radiation Oncology was consulted, and she was started on palliative radiation for 5days which initially improved her pain and swelling. Unfortunately, her lesions continue to arise with intermittent, short lived responses to systemic therapy. Her lesions now too widespread for continued radiation therapy. She noticed lesion in her scalp. She continues to follow up in clinic where she was started on single agent Doxil 40 mg/m2 every 4 weeks. Sadly, she continues have progressive cutaneous disease around the flank, abdomen, and bilateral thighs.

Discussion

We present an interesting case of cutaneous involvement of multiple myeloma where although the patient has been on multiple therapies continues to progress in her disease. Her case is interesting from other presentations in that they don’t usually do not describe the course of regimen used in treatment. The standard of care of cutaneous involvement revolves controlling the origin of the disease. One specific treatment that we tried was localized radiation. There is not much data or past literature discussing the use of radiation or its efficacy. Unfortunately for our case, the treatment only helped briefly. Most common involvement for MM is soft tissue involvement of the upper airway and oral cavity. They usually consist of firm, erythematous, nontender nodules involving the neck, ears, shoulders, axillae, chest, abdomen, and dorsum of the hands [11]. The first reported case of skin involvement in a person with MM was presented by Bruno Block in 1910. He described a patient who had small reddish macules that evolved into brown reddish papules and nodules with scale crusts. Histologically these lesions showed epidermal necrosis. He eventually had disease in pleura, stomach, and heart and passed away two years later [3]. A review of literature reveals that there are over 100 described cases. The age ranges from 36 to 81 with a median of 60 years old. Numeric date was available for 87 cases and 63 of them were male and 24 were female [4]. Cutaneous involvement of MM may appear in area of the skin, but it has been reported most commonly on the trunk and abdomen. Skin lesions is commonly described as papules or nodules that measure 1-5 cm in diameter with firm consistency, smooth surface, and a red or violaceous color [5]. Some authors reported that cutaneous involvement of MM only occurs when the tumor mas burden is over 2-3 kg [6]. Cutaneous involvement in patient with MM and extramedullary plasmacytoma generally appears late during the disease. On average, death occurred within 12 months after the diagnosis. Autopsy of these patients reveal extensive plasmacytic infiltration of multiple organs [7].

A review of the cases of MM involving the skin revealed that 40 cases were IgG, 21 cases were IgA, and 9 cases were IgD. The risk of cutaneous involvement by MM is not associated with a particular class of myeloma immunoglobins. Histopathologically, the lesions of MM involving the skin show 2 patterns: nodular and diffuse interstitial [6]. (Figure 2, 3). The worldwide incidence of myeloma is 86,000 cases annually. Mortality rate in MM is high with a median survival of 50-55 months and 63,000 deaths being reported worldwide each year [8]. Significant advances have been made in understanding multiple myeloma (MM) and its precursor diseases. These advances include the gain in knowledge in the underlying pathophysiology, Food and Drug Administration (FDA) approvals of novel therapies with meaningful efficacy and the science in underlying disparities in patients with MM [9].

Author would like to thank Dr. Mortazavi and Arham Miah for their support.

Parametrium to be excised x—x: as necessary from the caudal edge of the cervix.

[agbpaints]

Skorpekh destroyers and the weird friend that gives them sketchy drugs.