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Exam 3 (Starts w/ Endocrine) Flashcards

1
Q

Adrenal Anatomy

A

Outside
o Zona glomerulosa – salt – ALD
o Zona Fasciculata – sugar – glucocorticoids
o Reticularis – sex – androgens
Medulla

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2
Q

Affects of Cortisol

A

o Gluconeogenesis/Glycogenolysis

o Maintenance of vascular tone

o Stimulation of erythropoiesis
o Anti-inflammatory
o Adaptation to stress

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3
Q

ALD; regulation, release, primary function

A

Regulated by
* Renin-angitotensin aldosterone system

Released due to
* Hypovolemia
* Hyponatremia
* Hyperkalemia

Primary Function
* Increase Na & Cl reabsorption
* Increase K & H+ secretion

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4
Q

Hypoadrenocorticism (Addison’s) Causes

A

Primary
* Immune mediated destruction of adrenal gland
* Iatrogenic destruction

Secondary
* Rare
* Decreased ACTH due to pituitary lesion

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5
Q

Hypoadrenocorticism (Addison’s); Types

A

Typical
* Electrolyte abnormalities
* Supplementation of cortisol (glucocorticoid) & aldosterone (mineralcorticoid) needed

Atypical
* No electrolyte abnormalities
* Signs of cortisol deficiency only
* Supplementation of cortisol only
* May have normal/partial/no ALD production

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6
Q

Hypoadrenocorticism (Addison’s); Signalment

A
  • Young to middle aged females
  • Standard poodles (doodles)
  • Lots of other breeds at risk
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7
Q

Hypoadrenocorticism (Addison’s); Clinical Signs

A

Acute
* Addisonian crisis
* Present recumbent & in shock

Chonic
* Waxing & waning GI signs
* Chronic PU/PD, lethargy, weightloss

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8
Q

Hypoadrenocorticism (Addison’s); Lab Values

A

CBC
* No stress leukogram
* Eosinophilia
* Lymphocytosis
* Non-regenerative anemia

UA
* Isosthenuria even w/ dehydration (can be hidden by dehydration)

Chem
* Hyponatremia, hyperkalemia, azotemia, hyperphosphatemia (common)
* Hypercalcemia
* Hypoalbuminemia
* Hypoglycemia
* Hypocholesterolemia
* Elevated liver enzymes

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9
Q

Cortisol Vs ALD Deficit

A

Cortisol
* V/D
* Hypoglycemia
* Maintenance of vascular tone

ALD
* PU/PD
* Hyperkalemia
* hyponatremia

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10
Q

Hypoadrenocorticism (Addison’s); Diagnosis

A

Na:K ratio
* K<27 w/ typical addison’s
* NOT HELPFUL in atypical Addison’s

Baseline Cortisol
* <2 – need ACTH stim test
* >2 not Addison’s

ACTH Stim
* Give cosyntropin (ACTH) IV ->
* Measure cortisol 1 hr post administration ->
* Normal animals will have elevated cortisol value 

* Post stim cortisol <2 = Addison’s

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11
Q

Hypoadrenocorticism (Addison’s); Treatment

A

Acute
* IV fluids & symptomatic care
* If you don’t have results of stim right away, give dexamethasone
* Once Na levels are steady, give mineralcorticoid

Chonic
* 0.1-.025mg/kg/d Oral prednisone (glucocorticoid)
* DOCP IM or SQ every 25d (mineralcorticoid)
* Daily Oral Florinef (glucocorticoid & mineralcorticoid)

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12
Q

Hypoadrenocorticism (Addison’s); Monitoring & Prognosis

A

Monitoring
* Monitor electrolytes (due to mineralcorticoid)
* Decrease pred dose if seeing PU/PD, polyphagia, elevated liver enzymes
* Increase pred if seeing GI signs

Prognosis
* Good
* Need lifelong treatment
* Meds are expensive

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13
Q

Hyperadrenocorticism (Cushing’s); Causes, Clinical Signs

A

Causes
o Pituitary gland tumor (ACTH) (small dogs)
o Adrenal gland tumor (Cortisol) (large dogs)
o Treatment w/ steroids
o Most are PDH

Clinical Signs
o PU/PD
o Polyphagia
o Panting due to weakness of diaphragm
o Alopecia
o Recurrent UTIs
o Weakness & muscle wasting
o Abdominal distension
o Dyspnea due to pulmonary thromboembolism
o Neuro signs due to tumor compression on brain

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14
Q

Hyperadrenocorticism (Cushing’s); Ways to Diagnose

A
  • CBC/Chem
  • UA
  • Imaging
  • Urine cortisol/creatinine ratio
  • ACTH stim test
  • Low Dose Dex Suppression Test
  • Endogenous ACTH
  • Abdominal ultrasound
  • CT/MRI
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15
Q

Hyperadrenocorticism (Cushing’s); Expected CBC/Chem, UA, Imaging

A

CBC/Chem
* Stress leukogram
* Thrombocytosis
* Increased ALP
* Hypercholesterolemia
* May have increased ALT & glucose

UA
* Isosthenuria (1.007 – 1.012)
* Proteinuria
* UTIs

Imaging
* Hepatomegaly
* Mets in lungs from adrenal carcinoma (rare)

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16
Q

Urine cortisol/creatinine ratio

A

Negative rules out Cushing’s
* First pee in the am before any “stress”
* Shows elevated cortisol but not “why”

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17
Q

ACTH Stim test For Cushing’s

A
  • Only test usable for iatrogenic cause of Cushing’s
  • Does not differentiate PDH & ADH
  • Post cortisol value >21ug/dL -> most likely cushings
  • Normal result doesn’t rule out Adrenal dependent
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18
Q

Low Dose Dexamethasone Suppression Test For Cushing’s

A
  • Differentiates between ADH & PDH
  • Does not diagnose iatrogenic
  • cannot suppress ADH

8hr
* >1.4ug/dL = Cushings
* cortisol <50% baseline but greater than lab cut off = PDH

4hr
* if cortisol below lab cut off or <50% baseline = PDH
AND
* >1.4ug/dL at 8hrs = Cushings

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19
Q

High Dose Deamethasone Suppression Test For Cushing’s

A

expect suppression at both 4hr & 8hr OR or suppression at 4hr & rebound at 8hr

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20
Q

Endogenous ACTH Test

A

Adrenal Tumor
* ACTH suppressd by negative feedback -> low ACTH

Pituitary Tumor
* ACTH levels normal or high

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21
Q

Abdominal Ultrasound & CT/MRI for Cushing’s

A

Abdominal Ultrasound
* Look ay adrenal size

CT/MRI
* Evaluate pituitary
* Look for macroedema

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22
Q

Hyperadrenocorticism (Cushing’s); Reasons to treat or not

A

Treat
* Urinary accidents and nighttime urination
* Excessive appetite driving the owners crazy
* Secondary infections/ Complications
* Concurrent disease such as diabetes mellitus

No
* Cost
* Side effects/risks
* May not prevent secondary complications

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23
Q

Hyperadrenocorticism (Cushing’s); Treatment for PDH

A

Mitotane
* Chemotherapeutic agent

* Adrenolytic – destroys adrenal tissue
* Less expensive & less frequent dose
* Monitor with ACTH stim tests

Trilostane
* Synthetic steroid analog -> prevents formation of cortisol 

* Reversible and dose dependent 

* “user friendly”
* Monitor with ACTH stim testing 
& electrolytes 


Radiation
* Expensive
* Effectiveness varies

Surgery
* Hypophysectomy
* Need to supplement pituitary hormones post
* Need highly skilled surgeon
* Expensive

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24
Q

Hyperadrenocorticism (Cushing’s); ADH Treatment

A

Trilostane or Mitotane
* Both control clinical signs

Surgery
* Adrenalectomy
* May be curative (recommended)

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25
Hyperadrenocorticism (Cushing's); Prognosis
o Pituitary microadenoma – good o Pituitary macroadenoma – poor w/o treatment & fair w/ o Adrenal tumor – good to poor depending on treatment
26
PTH; Where is it made, function in bone, kidney, small intestine
o Made by chief cells in parathyroid glands Bone * Increase resorption of Ca & P -> blood Kidney * Increases Ca resoprtion * Increases P excretion * Stimulates synthesis of Calcitriol Small intestines * Calcitrol induced by PTH increases Ca & P absorption in intestines
27
Calcitriol Function
o Increases absorption of Ca & P from intestines o Increase Ca & P retention in kidneys o More calcitriol -> decreases PTH
28
Calcitonin Function
o Made in parfollicular cells of thyroid o Decrease serum Ca o Opposite effects of PTH
29
Differentials for Hypercalcemia
o HOGS IN YARD Hyperparathyroidism o high PTH, high iCa, decreased P Osteolytic Granulomatous Dz o high calcitriol, increased Ca, maybe increased P Spurious Idiopathic, Iatrogenic Neoplasia o high PTH-rp, high iCa, P & PTH decreased or normal Young Addison’s o high total Ca & P Renal Dz o high total Ca & P Vitamin D Toxicity o high calcitriol, High Ca & P
30
Narrow Down Differentials for Hypercalcemia
Phosphorous Levels * PTH causes low – low/normal P * Calcitriol causes high-high/normal P PTH Levels * High Ca -> low PTH * PTH normal or high -> increased production of PTH
31
Primary Hyperparathyroidism; What is it? Causes, Signalment, Clinical Signs
o Excessive production of PTH by parathyroid glans Causes * Parathyroid adenoma * Parathyroid carcinoma * Parathyroid hyperplasia Signalment * Middle age * Keeshonds, labs, goldens, german shepherds Clinical Signs * Usually not clinical (seem healthy) * If clinical -> PU/PD, lethargy, UTIs, * Chronic eventually leads to renal failure
32
Primary Hyperparathyroidism; Lab Findings, imaging, Diagnosis
Lab Findings * Hypercalcemia * Low-low/normal P * Isosthenuria or hypersthenuria Imaging * Nephrolyths/calculi on rads or ultrasound * Thoracic rads my show mets * Cervical ultrasound or CT shows mass in area of thyroid gland or visible parathyroid glands Diagnosis * Malignancy panel -> elevated PTHrp -> hypercalcemia of malignancy * Elevated iCa + elevated or normal PTH
33
Primary Hyperparathyroidism; Treatment
Treatment * physiologic saline diuresis * Furosemide * Glucocorticoids * Bisphosphonates * Cinacalcet * Surgical removal of affected glands Surgery * Prophylactic calcitrol prior to Sx -> taper over 2-4mo * Ca supplementation post Sx -> taper over 2-4mo * Must keep Ca high enough until parathyroid gland recovers
34
Hypoparathyroidism; Causes, Signalment, Clinical Signs, Diagnosis, Treatment
Causes * Suppressed secretion of PTH due to trauma surgery etc * Atrophy due to sudden correction of chronic hypercalcemia * Iatrogenic due to removal of parathyroid * Immune mediated destruction of parathyroid gland Signalment * Dogs > cats * Females > males * Poodles, mini schnauzers, german sheps, labs, terriers Clinical Signs * Seizures * Facial/paw rubbing/licking/biting * Tetany/muscle spasms * Stiff gait * Anorexia * Lethargy * V/D * Cataracts * Fever * Cardiac abnormalities Diagnosis * Decreased iCa + increased P * Low-low/normal PTH * Decreased calcitriol Treatment * IV Ca gluconate (in emergency) * Calcitriol for life * Oral Ca carbonate until dz is stable
35
Hypocalcemia; Differentials
PEACE PAIN * Phosphate enemas * Eclampsia * Albumin decrease * Chronic renal dz * Ethylene glycol toxicity * PTH deficiency * Acute pancreatitis * Intestinal malabsorption * Nutritional Vit D deficiency
36
T3
o Most biologically active o Enters cell more rapidly o 3-5 times more potent than T4 o most produced by deiodination of T4
37
Thyroid Hormone Production
o Thyroid peroxidase binds tyrosine on thyroglobulins + oxidized iodide -> o iodinated tyrosine -> o T 3 & T4 bind to TG & secreted
38
Primary Hypothyroidism; What is it? Causes, Signalment, Clinical SIgns
o Decreased T3 & 4 Causes * Thyroiditis * Idiopathic thyroid atrophy * Bilateral thyroid neoplasia (rare) Signalment * Borzoi, toy fox terrier, beagle Clinical Signs * Lethargy * Weight gain * Cold intolerance * Symmetric alopecia * Seborrhea * Hyperpigmentation * Rat tail * “sad” expression * weakness / ataxia * seizures / mentation changes * facial nerve paralysis / vestibular dz * bradycardia
39
Hypothyroidism; Diagnosis
* Normocytic, normochromic, non-regenerative anemia * Fasting hypertriglyceridemia & hypercholesterolemia * Increased ALP * Total T4 for screening (can have false +) Diagnostic * Low Free T4 by equilibrium dialysis * High TSH (normal does not rule out)
40
Euthyroid Sick Syndrome
* Underlying illness suppressing thyroid hormone * Decreased total T4 * Normal TSH
41
Effect of Drugs on Thyroid Testing
* Glucocorticoids can decreas TT4, FT4, & TSH * Phenobarbital & TMS can decrease TT4, FT4 & increase TSH
42
Hypothyroidism Therapeutic Trial
* Treat w/ Levothyroxine -> * Wait 4-8wks -> * Assess for improvements of clinical signs -> * Stop supplementation if response seen -> * Return of signs = most likely hypothyroid
43
Treatment for Hypothyroidism
* Levothyroxine (synthetic T4) * Improve activity first 1-2 wks * Weightloss seen in 8 wks * Normal haircoat may take months * Neuro signs improve rapidly but may take 8-12 wks for full recovery
44
Feline Hyperthyroidism; Causes, Clinical Signs
Causes * Overproduction of hormone from thyroid benign adenoma * Malignant carcinoma (rare) * Genetic * Too much idodine * Too little selenium consumption * Toxins in environement * Immune mediated * Infectious Clinical Signs * Weight loss * Polyphagia * PU/PD * Hyperactivity * Vomiting * Anorexia, depression (less common) * May have palpable thyroid mass (thyroid slip) * Poor hair coat * Dehydration * Maybe cervical ventroflexion (weakness) * Cardiac issues * Hypertension & fundic abnormalities
45
Feline Hyperthyroidism; Diagnosis, Treatment, Prognosis
Diagnosis * Increased PCV * Increased ALT * May have azotemia * Isosthenuria * Increased total T4 (definitive) -> * Repeat Total T4 -> * Measure free T4 -> * T3 suppression test -> * Nuclear scintigraphy Treatment * Methimazole (blocks hormone synthesis = significant side effects but reversible unlike other treatment) * Amlodipine for hypertension * Propanolol or Atenolol to reduce tachycardia, arrhythmias, hyperactivity * Surgery * Radioactive iodine * Iodine restricted diet Prognosis * Generally good
46
T3 Suppression Test
* Last resort * T3 should inhibit TSH * Decreased TSH = decreased T4 * After T3 administrtaion -> T4 should decrease 50% -> Hyperthryoid cats don’t really suppress
47
Nuclear Scintigraphy
* Administer radioactive isotope -> * Hyperthyroid have increased uptale -> * Quantify gamma emission * Helps differentiate adenoma from carcinoma
48
Insulin Dependent Vs Non-insulin Dependent Diabetes Mellitus
Insulin Dependent o Autoimmune damage -> o beta cells can’t produce insulin -> o not reversible o dogs o 20% of cats Non-insulin Dependent o Insulin resistance o Beta cell dysfunction o 80% of cats o potentially reversible
49
Diabetes Mellitus; Signalment
Dogs * Females > males * Middle aged * Small breeds & samoyeds Cats * Neutered males * >6yo * Burmese, abssynians, Siamese
50
Diabetes Mellitus; Clinical Signs
o PU/PD o Polyphagia o Weight loss o Many are “well” Diabetic ketoacidosis or Hyperglycemic/hyperosmolar syndrome (rare) * Anorexia * Dehydration * Vomiting * Lethargy
51
Diabetes Mellitus; Diagnosis, Treatment
Diagnosis o Hyperglycemia (don’t confuse w/ stress) o Glucosuria o Elevated ALP (dogs) o hypercholesterolemia o Maybe ketonuria & proteinuria o Maybe elevated fructosamine o Rads & ultrasound to look for underlying cause Treatment o Insulin BID following meal o Oral hypoglycemic agents (not recommended) o Maintain ideal BCS w/ exercise in diets o Increase fiber & decrease sugar & fat for dogs o Increase protein and decrease carbs for cats
52
Diabetes Mellitus; Concurrent Disease & Wether to Test
o Pancreatitis o Exocrine pancreatic insufficiency o Hypothyroid in dogs (wait to test) o Hyperthyroid in cats (assess w/ diabetes diagnosis) o Hyperadrenocorticism (wait to test)
53
Diabetes Mellitus Remission
o Possible w/ insulin, diet, & treatment of concurrent dz o More likely when caught early, older cats, cats w/o peripheral neuropathy o Risk of hypoglycemia if insulin becomes unnecessary o After remission continue low carb diet & weight monitoring
54
Blood Glucose Curve; Basics, Nadir, Duration, Affects on Results
o 7 days after starting insulin for first time, changing dose, or changing type o feed & give insulin as normal -> check BG every 2hrs for 12 hrs Nadir * time & value when BG is lowest (should happen at 6hrs) * want to shift up or down – change dose * if nadir not at 6hrs, change insulin * Target BG is 100-250 Duration * amount of time following insulin where BG<250 Affects Results * Forgetting insulin * Inappetence * Vomiting * Stress hyperglycemia * Somogyi effect
55
Somogyi Effect
o Too much insulin -> o hypoglycemia (<65 or rapid drop) -> o diabetogenic hormones take over -> o rebound hyperglycemia (>300) o misinterpretation
56
Continuous Glucose Mnitoring
o FreeStyle Libre o Button on skin o Lasts up to 14 days o At home use o Measure interstitial BG o Values may be lower than curve -> look at trends o May be hard to keep on patient
57
Amount to Adjust Insulin Dose
Dogs * 10-25% each dose Cats * ½ unit per dose
58
Chronic Monitoring for Diabetes Mellitus
o Repeat BG curve every 7 days until regulated -> o Then in 1 month -> o Then every 3-6mo or clinical signs present o Repeat urine culture every 6mo
59
Serum Fructosamine
o Glucose bound (glycated) proteins made independent of insulin concentrations 
 o Marker of BG concentration over the past 2-3 wks 
 o Trends most useful 
 o Measure when 1st regulated then every 3-6 months 
 o Not affected by stress so helpful in cats especially 
 o Used for fractious or difficult and well-regulated patients
60
Complications of Diabetes Mellitus
Hypoglycemia * Neuro signs * Keep karo syrup on hand to rub on gums * IV dextrose may be needed Cataracts * Dogs * Secondary lens induced uveitis * Can treat w/ surgery Diabetic Neuropathy * Cats * Rear limb weakness * Plantigrade stance * Treat by improving regulation Diabetic Ketoacidosis
61
Diabetic Ketoacidosis; Triggers, Pathophysiology, Lab Values
Trigger * Marked insulin deficiency * Concurrent dz that causes insulin resistance Pathophysiology * Insulin does not help glucose uptake -> * Cells starved and start to use free fatty acids & ketone bodies -> * Ketone bodies overwhelm body’s buffering capacity -> * Acidosis, osmotic diuresis, dehydration Lab Signs * Non-regenerative anemia * Neutrophilia & Heinz bodies * Increased ALP, ALT, cholesterol * Azotemia * Hypokalemia * Hypophosphatemia
 * Hypomagnesemia * Hyponatremia (pseudo) * Hypochloremia
62
Diabetic Ketoacidosis; Treatment, Monitoring, Prognosis
Treatment * Rehydrate w/ isotonic fluids over 24hrs * IV CRI or IM insulin * Monitor BG every 1-2hrs * Monitor K, P, elctrolytes * Check urine ketones every 24hrs Monitoring * BG every 1-2hrs * K, P, electrolytes every 4-6hrs * Urine ketones every 24hrs Prognosis * 70% survive to discharge
63
Central Diabetes Insipidus
* rare * Partial or complete ADH deficiency * decreased ability/inability of the kidneys to conserve water and concentrate urine in response to increases in plasma osmolality -> * Increased plasma osmolality because fluid is lost in excess of solute -> * stimulates thirst * usually hyposthenuric but partial can be isosthenuric
64
Nephrogenic Diabetes Insipidus
* Kidneys not responding to ADH * Receptors not present or not responsive Primary * Congenital defect * Mutation in ADH receptor or aquaporin * hyposthenuria Secondary * Most common * Conditions affecting ADH binding and function in the renal tubules, loss of medullary gradient, or osmotic diuresis
65
Testing for Primary Diabetes Insipidus
Modified water deprivation test * Dangerous & time consuming * Gradually limit water over 3-5d -> * Remove water and monitor weight, PCV, TP, BUN, Na every 1-2hrs -> * Look for 5% dehydration or >1.025 USG * No concentration of urine -> * Try DDAVP administration test Serum Osmolality Testing * Central diabetes insipidus = high-normal * Psychogenic = low-normal Exogenous DDAVP Administration * Increase in USG by 50% Or >1.030 in day 5-7 * = central DI, psyochogenic, or hyperadrenocorticsim
66
Diabetes Insipidus Treatment
Acquired Nephrogenic * Address underlying cause Central * DDAVP lifelong Congenital nephrogenic * low Na diet * thiazide diuretics OR * Allow constant access to water
67
Diabetes Insipidus Prognosis
Acquired Nephrogenic * Dependent on underlying dz Congenital Nephrogenic * Good w/ constant water Central * Dependent on lesion
68
Acromegaly; Cause, Signalment, Clinical SIgns, Diagnosis, Treatment
Cause * Functional adenoma in pars distalis of anterior pituitary -> * Excessive growth hormone -> * Liver produces insulin-like growth factors Signalment * Older * Males > females * Uncontrolled DM w/ weight gain Clinical Signs * Enlargement of extremities, jaw, tongue, forehead * Clubbing of paws * Organ enlargement * Stridor due to growth of soft tissue in mouth and pharyngeal region * Degenerative joint disease * Cardiac signs leading to CHF * Hypertension * CNS signs * Thickening of skin * Renal signs leading to CRF Diagnosis * Test IGF-1 levels (false negatives or positives w/ diabetes) * CT or MRI of pituitary gland Treatment * Sx – Transsphenoidal hypophysectomy * Radiation (long time) * Somatostatin anologs (need more research) * Palliative – high dose insulin & diabetic diet (poor prognosis)
69
Acromegaly in dogs
o RARE o Excessive exogenous progesterone o OR o Excessive endogenous progesterone in cycling older intact females
70
Feline Cushing's; Cause, Signalment, Clinical SIgns, Diagnosis, Treatment
Cause * Rare * Adenoma in pituitary (most common) * Benign functional adenoma in adrenal gland (less likely) Clinical Signs * Clinical signs of diabetes mellitus * Weight loss > weight gain * PU/PD * Polyphagia * Pot belly * Muscle atrophy * Bilateral symmetric alopecia * Predisposed to infections * Fragile skin * Blindness, abnormal behavior (pituitary) * Spines on castrated males (adrenal) Diagnosis * Stress leukogram * Lack of effect of cortisol on ADH secretion/sensitivity * May be Glucosuria * Maybe proteinuria * Low dose dex suppression test is test of choice * High dose to differentiate pituitary from adrenal Treatment * Trilostane (preferred) * Mitotane * Metyrapone * Radiation * Hypophysectomy * Adrenalectomy
71
Primary Hyperaldoseronism (Conn's); Signalment, Cause, Clinical Signs
Signalment * Cats > dogs * older Cause * Adrenocortical carcinoma
 * Adenoma (unilateral or bilateral) * Bilateral nodular hyperplasia Clinical Signs * Hypertension -> organ damage * PU/PD * Muscle atrophy * Arrhythmia * Pendulous abdomen/mass * Blindness (retinal detachment) * Plantigrade stance * Cervical ventroflexion
72
Primary Hyperaldoseronism (Conn's); Lab Findings, Diagnosis, Treatment
Lab * Hypokalemia * Metabolic alkalosis * Azotemia * Increased phosphorus * Increased CK * Hyperglycemia * Hypernatremia Diagnosis * Imaging looking for adrenal mass, metastatis Treatment * Adrenalectomy (complications_ * K supplementation * Spironolactone (blocks ALD) * Amlodipine (hypertension)
73
Insulinoma; Cause, Signalment, Clinical Signs, Diagnosis, Treatment, Prognosis
Cause * Pancreatic beta cell tumors Signalment * Older * Medium-large dogs * Ferrets > dogs > cats Clinical Signs * Hypoglycemia * Overweight * +/- mild hypokalemia * +/- elevated ALP/ALT Diagnosis * Paired insulin & BG levels * Increased insulin despite low BG * Imaging to find mass Treatment * Surgery (difficult to find tumor) * Steptozotocin chemo * Frequent small meals, high protein & fat * Glucocorticoids * Diazoxide * Somatostatin * Glucagon Prognosis * poor

Small Animal Med (10 decks)

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