Mini Veterinary School
Teaching case for wanna be veterinarians.
If you enjoy figuring out veterinary medical puzzles, we have a treat for you.
We will give you a chance to test your medical skills.
Answer the questions honestly, and don't peek at the answers.
There is 15 available points if you answer all the questions correctly.
Vinnie Bag of Donuts
We met Vinnie on September 26th. He is a 9yr old neutered male indoor-only Maine Coone who had been overweight all his life.
Presenting complaints:
Weight loss of 3-4 weeks duration.
Complete loss of appetite for three days, vomiting for a day.
Vinnie's Diet : Dry. (Ingredients: http://www.hillspet.com/products/sd-feline-adult-indoor-dry.html)
Symptoms and Examination findings:
Marked depression / loss
of energy
Loss of appetite
Weight loss
Nausea and vomiting
Drooling / hyper
salivation
Moderate Dehydration
Yellowing of the whites of
the eyes and skin
Enlargement on cranial abdominal palpation
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What tests would you order?
a) EKG
b) urinalysis
c) blood test + urinalysis
d) X-ray
e)blood test
Give yourself 2 points if you answered c) blood test + urinalysis and scroll down to read the results.
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WBC
|
12.2
|
4.2 - 15.6 K/uL
|
| |
RBC
|
6.05
|
6.0 - 10.0 M/uL
|
| |
HGB
|
8.1
|
9.5 - 15 g/dL
|
LOW
| |
HCT
|
25.1
|
29 - 45 %
|
LOW
| |
MCV
|
42
|
41 - 58 fL
|
| |
MCH
|
13.4
|
11.0 - 17.5 pg
|
| |
MCHC
|
32.3
|
29 - 36 g/dL
|
| |
% RETICULOCYTE
|
0.3
|
%
|
| |
RETICULOCYTE
|
18
|
3 - 50 K/uL
|
| |
RETICULOCYTE COMMENT
|
A reticulocyte count of greater than 50 K/uL of blood is considered
evidence of bone marrow response to an increased peripheral demand.
Depending on the degree of anemia, a reticulocyte count <50 K/uL may
indicate an inadequate bone marrow response. Serial monitoring of the
erythrogram and absolute reticulocyte count may be useful to evaluate
bone marrow responsiveness over time.
The following chart can be used as a guideline to determine
appropriateness of regenerative response.
Degree of bone marrow response (K/uL):
Mild 50-75
Moderate 75-175
Marked >175
Please note: For information about our new reticulocyte reporting,
please see the Diagnostic Update on Vetconnect.com or call the
internal medicine consulting team at 1-888-433-9987, option 4, option
2.
|
|
NEUTROPHIL SEG
|
85.0
|
35 - 75 %
|
HIGH
| |
LYMPHOCYTES
|
9.0
|
20 - 55 %
|
LOW
| |
MONOCYTES
|
4.0
|
1 - 4 %
|
| |
EOSINOPHIL
|
2.0
|
2 - 12 %
|
| |
BASOPHIL
|
0.0
|
0 - 1 %
|
| |
AUTO PLATELET
|
547
|
170 - 600 K/uL
|
| |
REMARKS
|
NO FELINE HEMOTROPIC MYCOPLASMAS (FHM, formerly Hemobartonella) seen.
IF FHM IS SUSPECTED, THE IDEXX RealPCR FOR FHM IS MORE SENSITIVE THAN
BLOOD FILM REVIEW. UNIT CODE 1717.
SLIDE REVIEWED MICROSCOPICALLY.
|
|
ABSOLUTE NEUTROPHIL SEG
|
10370
|
2500 - 12500 /uL
|
| |
ABSOLUTE LYMPHOCYTE
|
1098
|
1500 - 7000 /uL
|
LOW
| |
ABSOLUTE MONOCYTE
|
488
|
0 - 850 /uL
|
| |
ABSOLUTE EOSINOPHIL
|
244
|
0 - 1500 /uL
|
| |
ABSOLUTE BASOPHIL
|
0
|
0 - 100 /uL
|
| |
FREE T4 (ng/dL)
|
0.6
|
0.7 - 2.6 ng/dL
|
LOW
| |
FREE T4 (pmol/L)
|
7.7
|
9.0 - 33.5 pmol/L
|
LOW
| |
ALK. PHOSPHATASE
|
498
|
0 - 62 U/L
|
HIGH
|
|
ALT (SGPT)
|
37
|
28 - 100 U/L
|
|
|
AST (SGOT)
|
38
|
5 - 55 U/L
|
|
|
CK
|
158
|
64 - 440 U/L
|
|
|
GGT
|
2
|
0 - 6 U/L
|
|
|
AMYLASE
|
1295
|
520 - 2060 U/L
|
|
|
LIPASE
|
21
|
10 - 195 U/L
|
|
|
ALBUMIN
|
3.4
|
2.3 - 3.9 g/dL
|
|
|
TOTAL PROTEIN
|
7.1
|
5.9 - 8.5 g/dL
|
|
|
GLOBULIN
|
3.7
|
3.0 - 5.6 g/dL
|
|
|
TOTAL BILIRUBIN
|
6.3
|
0.0 - 0.4 mg/dL
|
HIGH
|
|
DIRECT BILIRUBIN
|
6.0
|
0.0 - 0.2 mg/dL
|
HIGH
|
|
BUN
|
20
|
15 - 34 mg/dL
|
|
|
CREATININE
|
1.3
|
0.8 - 2.3 mg/dL
|
|
|
CHOLESTEROL
|
146
|
82 - 218 mg/dL
|
|
|
GLUCOSE
|
103
|
70 - 150 mg/dL
|
|
|
CALCIUM
|
9.7
|
8.2 - 11.8 mg/dL
|
|
|
PHOSPHORUS
|
4.2
|
3.0 - 7.0 mg/dL
|
|
|
TCO2 (BICARBONATE)
|
17
|
13 - 25 mEq/L
|
|
|
CHLORIDE
|
116
|
111 - 125 mEq/L
|
|
|
POTASSIUM
|
4.7
|
3.9 - 5.3 mEq/L
|
|
|
SODIUM
|
153
|
147 - 156 mEq/L
|
|
|
A/G RATIO
|
0.9
|
0.4 - 0.8
|
HIGH
|
|
B/C RATIO
|
15.4
|
|
|
|
INDIRECT BILIRUBIN
|
0.3
|
0 - 0.3 mg/dL
|
|
|
URINALYSIS ADD-ON
|
Test
|
Result
|
Reference Range
|
|
|
COLLECTION METHOD
|
NOT GIVEN
|
|
|
|
COLOR
|
DARK YELLOW
|
|
|
|
CLARITY
|
TURBID
|
|
|
|
SPECIFIC GRAVITY
|
1.036
|
|
|
|
GLUCOSE
|
NEGATIVE
|
|
|
|
BILIRUBIN
|
3+
|
|
HIGH
|
|
KETONES
|
NEGATIVE
|
|
|
|
BLOOD
|
3+
|
|
HIGH
|
|
PH
|
6.5
|
|
|
|
PROTEIN
|
|
|
|
|
WBC
|
0-2
|
0 - 5 HPF
|
|
|
RBC
|
20-30
|
0 - 5 HPF
|
HIGH
|
|
BACTERIA
|
NONE SEEN
|
HPF
|
|
|
EPI CELL
|
1+ (1-2)
|
HPF
|
|
|
MUCUS
|
NONE SEEN
|
|
|
|
CASTS
|
NONE SEEN
|
HPF
|
|
|
CRYSTALS
|
|
OTHER
|
AMORPHOUS DEBRIS
PRESENT
|
|
|
|
UROBILINOGEN
|
NORMAL
|
|
|
|
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With what you know so far about Vinnie and with these lab results do you suspect that he has:
a) kidney infection
b) thyroid disease
c) pancreatitis
d) liver disease
e) liver disease and anemia
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Diagnosis
Elevated alkaline phosphatase, a liver enzyme indicative of damage of the cells surrounding the bile ducts.
Elevated bilirubin is a marker of jaundice (yellowing of skin and gums), but unfortunately it takes a marked elevation and advanced disease for the skin to become obviously yellow.
Bilirubin in blood ( bilirubinemia) and
Bilirubin in urine ( bilirubinuria) confirm that Vinnie was suffering from hepato-biliary disease. In cats, unlike dogs, any bilirubin in the urine is abnormal.
Anemia ( low Red Blood Cells) are indicated by low Hematocrit ( HCT similar to PCV) and HGb ( hemoglobin)
There are other causes
of elevated alkaline phosphatase : such as rapid bone turn-over in young growing patients,
as well as elevated bilirubin : hemolysis
you can read about here ---> http://www.vetmed.wsu.edu/cliented/lab.aspx
In determining the likely origin of elevated tests we look at the "whole picture"--the entirety of all the tests and the clinical picture of the patient, to arrive at the most likely cause.
If you said d) liver disease (hepatopathy), give yourself 2 points
if you said e) liver disease (hepatopathy) and anemia give yourself 4 points
The liver is an organ with hundreds of jobs. Some of the more important ones are
- Production of bile needed to digest fat, and storing it in the gall bladder.
- Production of vital proteins- albumin and clotting factors. Conversion of hormones.
- Storage of glycogen ( a starchy form of sugar) and converting it back into sugar when the need for energy arises.
- Storage of red blood cells and iron for hemoglobin, and clearance/ recycling of worn out red blood cells.
- Packaging of amino- acids (building blocks of proteins), fatty acids, triglycerides, cholesterol.
- Bacteria of the bowels produce ammonia as they break down proteins, which the liver converts into a less toxic substance called urea ( BUN) which is excreted by the kidneys in the urine.
- Clearing blood of toxins, drugs and anesthetics
- Storage of fat soluble vitamins: A, D, E, K.
- Filtering bacteria from the small intestines
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What test would you order at this point?
a) x-ray
b) ultrasound with ultrasound-guided fine needle aspirate (FNA)
c) barium study
d)exploratory abdominal surgery
e) ultrasound
avetsguidetolife.blogspot.com
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If you said ultrasound, give yourself 2 points
if you said ultrasound with ultrasound-guided FNA, give yourself 4 points
Vinnie’s ultrasound ruled out many underlying illnesses while confirming our suspicion of an
enlarged liver. Unlike an Xray which shows outlines of organs, an ultrasound can image soft tissue organs in three dimensions enabling us to see the texture and dimensions of all soft tissue organs--liver, kidneys, spleen, pancreas, intestines, lymph nodes, adrenal glands, as well as to evaluate organs in motion ( which is especially important for studies of the heart). An Xray would have just shown us that Vinnie's liver was enlarged, bout would not enable us to know the condition of the rest of the organs. This test is not uncomfortable and does not require anesthesia.
A fine needle aspirate (FNA) was performed with ultrasound guidance. This is a noninvasive test in which liver cells are harvested with a syringe and examined on a slide. The technique, known as cytology is not as conclusive as histopathology or biopsy, because we examine individual cells and are unable to see how they are arranged. Although not without limitation, cytology unlike biopsy does not require general anesthesia thereby involving much less risk, as well as costs.
Cytology confirmed
hepatic lipidosis ( steatosis) -infiltration and distention of liver cells with large fat vacuoles (the foamy cells seen are vacuolated hepatocytes)
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If Vinnie could only have ONE thing, what is the single most important treatment Vinnie must have to overcome his disease?
a) antibiotics and anti-inflammatory drug injections
b) IV fluids and nausea drugs
c) herbs and supplements to help his liver
d) implantation of a feeding tube for aggressive nutritional support
e) liver transplant
----------------------------------------------------------------------------------------------------------------------------------
Treatment
Vinnie was hospitalized and was given intravenous fluids and medications to control nausea. The medications he was given are listed below with links for more thorough understanding and reasoning behind each
A feeding tube was implanted in his esophagus, which enables aggressively feeding him in spite of him not being interested in eating at all. The feeding tube also enables easy administration of his medications. It is difficult, if not impossible, to force- feed these patients adequate calories and nutrients to reverse the disease without a feeding tube.
Feeding:
Each day the owner places a can of Science Diet A/D in a blender and blenderize it into a slurry which is easy to administer through the tube.
http://www.hillspet.com/products/pd-feline-ad-caninefeline-critical-care-canned.html
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If you answered feeding tube give yourself 5 points.
Without aggressive nutritional support it is difficult , if not impossible, to force-feed these patients adequate calories and nutrients to reverse the abnormal metabolic cycle.
Considering how Vinnie looked a couple of weeks ago, we are pleased with his progress. He is acting more and more like himself every day. Yesterday his mom said he begged for treats for the first time in a long time.
Hepatic lipidosis (HL) is one of the most common of all cat liver
diseases, affecting cats of any age, breed and sex. Overweight cats are at increased risk of
developing HL. Rapid weight loss, loss of appetite, starvation and catabolism are
the initiating cause of fat infiltrating the liver.
Similar disease is seen in birds, rabbits, mustelids
(mink, ferrets), as well as people in whom it is known as Non-alcoholic fatty liver disease
(NAFLD).
Anorexia (loss of appetite) can be caused by changes in
diet, stress, and the underlying disorders listed below. Inflammatory bowel disease (IBD) is frequently associated with hepatic lipidosis.
Other liver disorders:
|
Small intestinal diseases:
|
Cholangiohepatitis
|
Eosinophilic enteritis
|
Choledochitis
|
Lymphocytic/plasmacytic enteritis
|
--extrahepatic bile duct obstruction
|
Chronic bowel obstruction
|
Chronic suppurative hepatitis
|
Salmonella enteritis
|
Portosystemic vascular anomaly
|
|
Bile duct adenocarcinoma
|
Renal disorders
|
Hepatic lymphosarcoma
|
Chronic FUS
|
Neoplasia (non-hepatic):
|
Pyelonephritis
|
Urinary bladder
|
Chronic interstitial nephritis
|
--transitional cell carcinoma
|
Hyperthyroidism
|
Metastatic carcinoma
|
Severe Anemia
|
Intestinal adenocarcinoma
|
Pyometra
|
Intestinal lymphosarcoma
|
Cardiomyopathy
|
Pancreatitis
|
Central neurologic disease
|
Diabetes mellitus
|
|
In many cases no underlying cause can be identified and then
the disorder is called idiopathic hepatic lipidosis.
Since we found no underlying cause for Vinnie's hepatic lipidosis, his form of liver disease is termed idiopathic hepatic lipidosis.
The rapid development of hepatic lipidosis in obligate carnivores during
fasting could be related to depletion of arginine (an amino acid/ building
block of proteins) and the loss of muscle mass due to reliance on
gluconeogenesis (http://en.wikipedia.org/wiki/Gluconeogenesis ) for blood sugar provision during food
deprivation. Other explanations are
altered omega-6 to omega-3 fatty acid ratio and oxidative stress. Mobilization and accumulation of fat in the liver impairs liver function until the liver fails.
If not recognized promptly
and treated aggressively, the patient would progress to stupor, seizures, coma,
internal bleeding and death.
Fortunately for us Vinnie
is getting better. As of yesterday he is no longer nauseous and is beginning to
show interest in treats. We are hoping to be able to remove the esophageal
feeding tube within a few weeks.
Once he is eating voluntarily we will feed him a meat- only diet, free of grains; especially avoiding the genetically modified corn, whose safety studies leave me entirely unimpressed.
In fact, these exact histopathological findings are reported in the majority of the rats in this study on Bt corn ( Mon 863), Table 7: Liver Vacuolization 17/20 male control rats 20/20 male rats fed this genetically modified corn, 18/20 female rats fed control corn and 20/20 female rats fed the gentically modified corn.
Results of a 90-day safety assurance study with rats fed grain from corn rootworm-protected corn
B. Hammond a,*, J. Lemen a, R. Dudek a, D. Ward a, C. Jiang a, M. Nemeth a, J. Burns b
Clearly this variety of corn with or without genetic modification causes liver changes in mammals. It is impossible to tell how much the genetic modification itself contributes to liver toxicity of this corn with a group this small. And I find it curious that in this experiment 80 rats were fed the genetically modified variety but results are only published for 40--this renders any statistical analysis invalid.
Additionally liver toxicity on the nuclear cellular level leading to alteration of protein expression, related to splicing structures in rodents is associated with genetically modified soybeans as extensively documented by Manuella Malatesta.
A long-term study on female mice fed on a genetically modified soybean: effects on liver ageing.
Source
Dipartimento di Scienze Morfologico-Biomediche, Sezione di Anatomia e Istologia, University of Verona, strada Le Grazie 8, 37134, Verona, Italy. manuela.malatesta@univr.it
Abstract
Liver represents a suitable model for monitoring the effects of a diet, due to its key role in controlling the whole metabolism. Although no direct evidence has been reported so far that genetically modified (GM) food may affect health, previous studies on hepatocytes from young female mice fed on GM soybean demonstrated nuclear modifications involving transcription and splicing pathways. In this study, the effects of this diet were studied on liver of old female mice in order to elucidate possible interference with ageing. The morpho-functional characteristics of the liver of 24-month-old mice, fed from weaning on control or GM soybean, were investigated by combining a proteomic approach with ultrastructural, morphometrical and immunoelectron microscopical analyses. Several proteins belonging to hepatocyte metabolism, stress response, calcium signalling and mitochondria were differentially expressed in GM-fed mice, indicating a more marked expression of senescence markers in comparison to controls. Moreover, hepatocytes of GM-fed mice showed mitochondrial and nuclear modifications indicative of reduced metabolic rate. This study demonstrates that GM soybean intake can influence some liver features during ageing and, although the mechanisms remain unknown, underlines the importance to investigate the long-term consequences of GM-diets and the potential synergistic effects with ageing, xenobiotics and/or stress conditions.
Since no epidemiological studies have been published to date comparing cats eating GMO- corn and soybeans with non-GMO- corn and soybeans, the precautionary principle dictates avoiding corn and soy in cat foods.
We hope you did well on the quiz and enjoyed the learning experience.
Give yourself an A if you scored 15 points, a B if you scored 11, a C if you scored 10 or less.
Feel free to ask questions or leave comments, if you like.
References:
Treatment for Severe Feline Hepatic Lipidosis
Sharon A. Center, DVM, DACVIM College of Veterinary Medicine, Cornell University