Kobi's blood test, urine anaysis, histopathology report


Blood test 16.05.2011

PLT Flags: MIC
WBC: 4.3 10^3/mm^3 (2.5 - 5.5)
RBC: 5.21 10^6/mm^3 (6.50 - 12.0) LOW
HGB: 10.8 g/dl (15.0 - 18.0) LOW
HCT: 34.2 % (40.0 - 60.0) LOW
PLT: 350 10^3/mm^3 (300 - 900)
MCV: 66 Ám^3 (45 - 65) HIGH
MCH: 20.8 pg (15.0 - 20.0) HIGH
MCHC: 31.6 g/dl (30.0 - 34.0)
RDW: 12.3 % (14.0 - 17.0) LOW
MPV: 8.2 Ám^3 (6.7 - 11.1)

DIFF:
%LYM: 12.4 % (12.0 - 50.0) #LYM: 0.5 10^3/mm^3 (0.3 - 1.3)
%MON: 9.6 % (0.0 - 6.0) HIGH #MON: 0.4 10^3/mm^3 (0.0 - 0.2) HIGH
%GRA: 78.0 % (15.0 - 80.0) #GRA: 3.4 10^3/mm^3 (0.4 - 2.0) HIGH

ALB 42 G/L
ALP 218 U/L
ALT 151 U/L
AMY 25 U/L
TBIL 4 UMOL/L
BUN 24.5 MMOL/L
CA 2.45 MMOL/L
PHOS 2.42 MMOL/L
CRE 84 UMOL/L
GLU 8.0 MMOL/L
NA+ 153 MMOL/L
K+ 4.9 MMOL/L
TP 65 G/L
GLOB 22 G/L

QC OK
HEM 0 LIP 3+ ICT 0


Urine analysis 16.05.2011

Dip Stick:
GLU= Neg
BIL= Neg
KET= Neg
S.G= 1.015 S/G 1.014
BLD= +++
pH= 6.5
PRO= +++
UBG= Norm
NIT= Neg
LEU= Neg


Kobi's histopathlogy report (put to sleep 16.08.11)

Post-Mortem Tissues from a Ferret: 11 samples received; 11 sections evaluated on 3 slides.

Heart (slide 2). Myocytes are equivocally broad and show mild to moderate anisokaryosis. Multifocally, especially in the ventricular subendocardium and in the centre of the ventricular muscle, there are irregular wedges of fibrosis associated with loss of myocytes and attenuation of residual myocytes.

Lung (slide 1). Generally, the lung appears well-aerated; however, a minority of alveoli and bronchioles contain luminal proteinaceous fluid, and some affected alveoli also contain low numbers of macrophages with brown granular pigment (haemosiderophages, "heart failure cells''). In several foci, in alveolar lumens beneath the pleura, there are clusters of foamy macrophages (endogenous lipid pneumonia; Insignificant). A tiny focus of parenchymal osseous metaplasia is also present.

Pancreas (2 sections, slide 3) with Duodenum and Lymph Node. The larger section of pancreas is focally multinodular and expanded to approximately 8 - 10 mm in diameter. The expansile

Liver and/or Adrenal Gland (3 sections, slides 1, 2 and 3). In one section with portal tracts and bile ducts (definitive liver) and two other sections that resemble liver, normal hepatic acinar architecture is difficult to discern. The samples consist instead of nodular aggregates, cords and sometimes islands formed from simple to bilayered polygonal cells with a strong resemblance to hepatocytes (but also resembling cells in the adrenal cortical masses, described below). Supporting stroma is delicate and vascularized, resembling irregular sinusoids. Some sinusoids show cavernous dilatation and congestion. The presumed hepatocytes have variable amounts of eosinophilic cytoplasm and somewhat variably sized, oval, nuclei. Nucleoli are sometimes seen. Mitotic figures are rare at approximately 1 per 10 high-power (400x) fields. The cells sometimes appear to interlace with possibly normal hepatocytes near one margin, but no definitive normal borders are visible.

Kidney (slide 1). Multiple radiating wedges of fibrosis extend from the medulla to the cortex, and all enclosed glomeruli and tubules appear sclerotic or attenuated. There is a scattered infiltrate of small mononuclear leucocytes. In adjacent areas, some tubules contain proteinaceous fluid. The inner medullary interstitium (renal crest) appears expanded by fibrosis, and ducts in this area sometimes lack epithelium.

Presumed Urinary Bladder (slide 2). This section is histologically compatible with urinary bladder, although dilated anterior urethra cannot be ruled out. The mucosa appears normal. The smooth muscle tunics appear thick, with wide myocytes that show hyaline to fibrillar sarcoplasm (hypertrophy).

Adrenal Gland (2 sections, slices 2 and 3). Two definite sections of adrenal gland are similar on histology. Cortical architecture is locally disrupted by zones of haemorrhage with cellular debris (necrosis). Partly replacing the cortex are irregular cords, trabeculae and solid sheets of polygonal to spindled cells with eosinophilic cytoplasm and variably sized but usually medium-large, oval nuclei with prominent nuclei. Mitotic figures are 1 per 10 high-power (400x) fields. The lesion is associated with light proliferation of a background of spindle cells (presumably smooth muscle cells). Some polygonal cells breach the capsule and extend into adjacent adipose tissue and others penetrate the medulla. At the junction of the cortex and medulla in one section, there is a local deposit of amorphous eosinophilic material (presumptive amyloid). This gland also shows a few small, discrete cortical nodules of vacuolated cells (probably cortical nodular hyperplasia) and a few cortical clusters of plasma cells and lymphocytes.

MORPHOLOGICAL DIAGNOSES:

1. Heart: Cardiomyopathy -- hypertrophic, moderate, with multifocal fibrosis
2. Lung: Oedema -- multifocal, mild, with haemosiderophages ("heart failure cells")
2b. Lung: Endogenous Lipid Pneumonia
3. Pancreas: Islet Cell Carcinoma
3b. Pancreas: Pancreatic Nodular Hyperplasia
4. Liver: Hepatocellular Tumour (suggested well-differentiated Hepatocellular Carcinoma; ddx: metastatic adrenal cortical carcinoma)
5. Kidney: Nephritis -- interstitial, chronic, marked, with renal crest necrosis
6. Urinary Bladder: Muscular Hypertrophy -- diffuse, moderate
7. Adrenal Gland: Adrenal Cortical Carcinoma(s)
7b. Adrenal Gland: Amyloidosis, presumptive, with focal adrenalitis

COMMENTS:

This ferret died with serious lesions in virtually all of the submitted tissues, any of which might have contributed to clinical illness.

The heart shows hypertrophic cardiomyopathy with focal fibrosis, resembling resolved infarcts. Cardiomyopathy is common in middle-aged and older ferrets. The pulmonary oedema with haemosiderophages strongly suggests right-sided congestive heart failure.

The lung also shows endogenous lipid pneumonia, a common and clinically insignificant finding in mustelids, but which might have caused an abnormal, spotted appearance to the lungs at necropsy.

As you correctly suspected, the pancreas contains an islet cell carcinoma. According to most sources, pancreatic islet cell tumours are the commonest neoplasms of ferrets. They arise mostly from the beta cells and secrete insulin, hence their popular name of "Insulinoma". They can be benign or malignant, but as this example is invasive, it is clearly a malignancy. Clinical signs of insulinomas are referable to hypoglycaemia. Peak prevalence of these tumours is between 4 and 7 years old and there is no sex predilection, although there is a suggestion that neutered animals are more frequently affected than intact ones.

The pancreas also shows marked nodular hyperplasia; a benign change that is common in the pancreas of middle-aged and older carnivores, including ferrets. This harmless lesion is an incidental finding.

This ferrets liver contains a tumour that most closely resembles a primary hepatocellular malignancy (hepatocellular carcinoma). The cells in the adrenal cortical carcinoma also have a hepatoid appearance, and it is difficult to distinguish them on histology -- the possibility that some of the liver nodules might be metastases from the adrenal tumour(s) is not completely ruled out. Hepatocellular tumours are rarely reported in ferrets and other mustelids, although we have seen occasional cases. They have potential for metastasis and also for rupture, leading to abdominal haemorrhage.

Interstitial nephritis is a very common lesion in middle-aged to older ferrets. If the sample submitted is representative of both kidneys, then this ferret was probably in or approaching renal failure. As with most chronic lesions, the initiating cause is no longer visible.

Hypertrophy of the muscle of the urinary bladder might reflect partial outflow obstruction by the reportedly enlarged prostate.

The two sections of adrenal gland both contain an adrenal cortical carcinoma. These are common tumours in ferrets, and in spite of their designation as malignancies based on cytology and local invasiveness, the vast majority apparently do not metastasize or else metastasize late in the course of disease. As mentioned above, I cannot completely exclude metastasis to the liver in this case, based on very similar appearance of the adrenal tumour cells to liver cells, but in my opinion, the liver tumour is likely to be a separate entity. In ferrets, adrenal cortical carcinomas generally produce sex hormones (primarily oestrogens) rather than cortisol. Associated clinical syndromes include prostatic squamous metaplasia (possibly relevant here) and endocrine dermatopathy.

Thank you for the additional verbal history for this case. I apologize for the slightly delayed report.