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Doctor of Veterinary Medicine (Work in progress) > Veterinary Medicine - Endocrinology > Flashcards

Veterinary Medicine - Endocrinology Flashcards

1
Q

Hypothyroidism - What are the 2 main etiologies and what are their prevalence?

A

Lymphocytic Thyroiditis (50%)

Idiopathic Follicular Atrophy (50%)

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2
Q

Hypothyroidism - Common dermatological findings

A

Truncal bilateral symmetric alopecia

Myxedema (Classic “Sad Face”)

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3
Q

Hypothyroidism - Possible neurological findings

A

Cranial nerve deficits (Trigeminal Facial Vestibulocochlear )

Peripheral neuropathy (Can present up to Quadriparesis)

Seizures (Due to hyperlipidemia and hyperviscosity syndrome)

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4
Q

Hypothyroidism - What is the prevalence of weight gain?

A

Only 40% of cases

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5
Q

Hypothyroidism - Possible ocular findings

A

Lipid keratopathy

Keratoconjunctivitis Sicca (Concurrent with Lympocytic thyroiditis)

Retinal detachment (Hyperviscositiy syndrome)

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6
Q

Hypothyroidism - Possible cardiological findings

A

Bradycardia, Weak pulse, AV-Block

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7
Q

Hypothyroidism - Classic lab findings

A

Hypertriglyceridemia\ Hypercholesterolemia (75-90% of cases)

Mild non-regenerative anemia

Mild increase - ALP AST ALT CK

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8
Q

Hypothyroidism - What is the Prevalence of Dermatological Signs?

A

60-80% of cases (Most common sign!)

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9
Q

Hypothyroidism - What causes mild increase in liver enzymes? What enzyme increases the most

A

Vacuolar Hepatopathy

ALP > AST ALT

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10
Q

Hypothyroidism - In what percent of cases is TSH not above the threshold?

A

30% of cases

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11
Q

Hypothyroidism - What are 2 possible explanations for low T4 and normal TSH in a lethargic dog?

A

Hypothyroidism with normal TSH (30% of cases)

Euthyroid sick syndrome (decrease in T4 due to another illness)

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12
Q

Hypothyroidism - What 2 drugs can cause a decrease in T4?

A

Glucocorticoids

Phenobarbital

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13
Q

Hypothyroidism - Why do anti-thyroglobulin antibodies can interfere with thyroid panel interpretation? What is the solution?

A

Sometimes antibodies are formed against T4 as well - Which are then read as T4 on the thyroid panel - causing a false increase

Use Free-T4

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14
Q

Hypothyroidism - What are the 2 tenets of treatment monitoring? Explain

A

T4 levels - 4-6 hours after administration of Levothyroxine - Indication of absorption and possible overdosing

TSH levels - Checks the actual efficacy of the treatment

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15
Q

Hyperthyroidism - Commonly caused by…? Usually UniBilateral?

A

Thyroid Adenoma, Bilateral

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16
Q

Hyperthyroidism - Easy thing to do on physical examination when suspecting the disease?

A

Thyroid slip - Palpate along the trachea (90% of Cases - enlargement of thyroid gland)

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17
Q

Hyperthyroidism - Possible GI clinical signs

A

Polyphagia

Vomiting

Diarrhea

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18
Q

Hyperthyroidism - Possible urinary tract related clinical sign

A

PuPd

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19
Q

Hyperthyroidism - What is the most common CBC finding? In what percentage of cases?

A

Erythrocytosis (50%)

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20
Q

Hyperthyroidism - What is the most common panel finding? In what percentage of cases?

A

Increased liver enzymes (90%)

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21
Q

Hyperthyroidism - What is the drug of choice for conservative treatment? What are the indications?

A

Methimazole

Patient won’t undergo definitive treatment (Surgery Radioactive iodine)

Pre-op (Stabilize the patient Reduce the size of the gland)

Patient with concurrent diseases (i.e. CKD)

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22
Q

Hyperthyroidism - What is the definitive treatment?

A

Radio-Iodine (If available - Best)

Thyroidectomy

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23
Q

Cushing’s Disease - Most common etiology for the disease

A

Pituitary Dependent Hyperadrenocorticism (PDH) - Adenoma of the hypophysis (75% of Cases)

Adrenal tumor (25%)

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24
Q

Cushing’s Disease - Common clinical signs

A

Panting

Polyphagia

PuPd

Pendulus abdomen (“Pot Belly”)

Cranial organomegaly

Dermatological findings: Symmetric truncal alopecia Hypotrichosis, Hyperpigmentation, Comodons, Calcinosis Cutis, Skin infections

Urinary tract infections

CNS signs (In cases of macroadenomas in PDH)

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25
Q

Cushing’s Disease - Why do patients sometimes present with central neurological signs?

A

Macroadenomas in the hypophysis

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26
Q

Cushing’s Disease - Common complications

A

PTE

UTI

Urinary calculi

Skin infections

Gallbladder mucocele

Diabetes Mellitus

Hypertension

Central neurological signs

Metastasis (In cases of adrenal tumor)

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27
Q

Cushing’s Disease - Common CBC findings

A

Stress Leukogram

Erythrocytosis

Thrombocytosis

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28
Q

Cushing’s Disease - Common panel findings

A

Increase in ALP (C-ALP + Cholestasis due to Vacuolar Hepatopathy)

Increased liver enzymes

Hypercholesterolemia

Hypertriglyceridemia

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29
Q

Cushing’s Disease - Common UA findings

A

Decreased USG (Isosthenuria)

Proteinuria

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30
Q

Cushing’s Disease - Common US findings

A

Diffusely hyperechoic liver (Vacuolar hepatopathy)

PDH - Normal to bilaterally enlarged adrenal glands

AT - Adrenal mass \ Enlarged adrenal gland while the other adrenal gland is smaller than normal

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31
Q

Cushing’s Disease - Most specific diagnostic screening tool?

A

ACTH Stimulation test

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32
Q

Cushing’s Disease - LDDST - If any suppression is detected - Can the location of the pathology be determined?

A

Yes - PDH

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33
Q

Cushing’s Disease - LDDST - If no suppression is detected - Can the location of the pathology be determined?

A

No - Can be either AT or PDH

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34
Q

Cushing’s Disease - 2 Options for medical treatment for PDH

A

Trilostane (Inhibition of cortisol synthesis)

Lysodren (Adrenolytic)

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35
Q

Cushing’s disease - What is the indication for radiotherapy

A

PDH with Macroadenoma - to lessen CNS signs only!

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36
Q

Cushing’s Disease - Signalment and Prognosis

A

Middle age - Old dogs (>6)

MST ~2 Years

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37
Q

Cushing’s Disease - Common concurrent disease diagnosed along with it in cats is…?

A

Diabetes Mellitus

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38
Q

Cushing’s Disease - Most sensitive diagnostic screening tool?

A

Urine Creatinine Cortisol Ratio

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39
Q

Cushing’s Disease - ACTH Stimulation test is more sensitive for PDH AT? Why?

A

PDH

AT can lose their receptors for ACTH and become autonomous, therefore producing a false negative result

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40
Q

Cushing Vs. Addison - Age of onset

A

Cushing - Middle age - Old

Addison - Young - Middle age (But can be at any age)

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41
Q

Addison’s Disease - What Is usually affected first - Glucocorticoid or Mineralocorticoid secretion?

A

GC first (Atypical Addison’s disease)

2nd - Mineralocorticoid (weeks - months later)

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42
Q

Addison’s Disease - Clinical Signs

A

Atypical Addison’s:
Lethargy
Anorexia
Vomiting
Diarrhea
Hematochezia
Melena
Hematemesis

Addisonian crisis:
Hypovolemic Shock
Collapse
Seizures (Hypoglycemia)
Bradycardia (Hyperkalemia)
Regurgitation (Megaesophagus) - Rare

43
Q

Addison’s Disease - CBC Findings

A

Eosinophila

Lymphocytosis
*Alternatively - Lack of stress leukogram in a sick animal

Hemoconcentration (Dehydration)
*Alternatively: Mild non-regenerative anemia Regenerative anemia in cases of GI ulcers

44
Q

Addison’s Disease - Panel Findings

A

Hyperkalemia & Hyponatremia

Low Sodium Potassium ratio (<26)

Azotemia (Urea > Creatinine due to significant pre-renal element GI bleeding, AKI due to hypovolemia also possible)

Hypoglycemia (30%)

Hypocholesterolemia (GI loss and decreased absorption)

Hypoalbuminemia +- Hypoproteinemia (PLE)

Increase in liver enzymes (Hypoxia)

45
Q

Addison’s Disease - DDs for low sodium : potassium ratio

A

Addison’s Disease

AKI

Urinary tract block

Uroabdomen

Certain GI parasites (e.g. Trichuriasis)

Effusions Repeated chylothorax drainage

46
Q

Addison’s Disease - Possible findings in thoracic X-Rays

A

Microcardia

Megaesophagus (Rare)

47
Q

Addison’s Disease - Possible abdominal US findings

A

Normal to decreased size of adrenal glands

48
Q

Addison’s Disease - Diagnosis

A

ACTH Stimulation Test

49
Q

Addison’s Disease - Treatment (Addisonian crisis situation)

A

Fluids +- Dextrose in case of hypoglycemia

Treat Hyperkalemia (Bicarbonate Dextrose +- Insulin Calcium gluconate)

Glucocorticoid & Mineralocorticoid supplementation:
Dexamethasone (Doesn’t interfere with ACTH Stimulation)
Hydrocortisone IV (GC + MC)
Prednisone PO + Fludricortisone PO (when starts to recover)

Treat GI Ulcers AKI

50
Q

Addison’s Disease - What are the 2 long term treatment options

A

1) Fludrocortisone (Glucocorticoid + Mineralocorticoid activity)

50% of dogs will need addition of GC (Prednisone)

2) DOCP (Only Mineralocorticoid) + Prednisone

51
Q

Diabetes Mellitus - Insulin dependent disease in dogs and cats?

A

Yes to both

Dogs start as ID because of autoimmune insulinitis (Diabetes type 1) and decrease in insulin production), Cats start as non-ID (Diabetes type 2) but due to amyloid deposition and destruction of beta-cells -> Becomes ID

52
Q

Diabetes Mellitus - Etiologies

A

Hereditary Genetic (Dogs)

Pancreatitis (Dogs and Cats)

Obesity

Acromegaly (25% of DM cases in cats)

Pregnancy

Cushing’s Disease (Common concurrent disease in cats)

53
Q

Diabetes Mellitus - What are the 3 hallmark clinical signs

A

Polyphagia

Weight loss

Pu\Pd

54
Q

Diabetes Mellitus - Common ocular related finding in dogs

A

Cataract

55
Q

Diabetes Mellitus - Common neurological sign in cats

A

Peripheral neuropathy (Plantigrade walk on hindlimbs)

56
Q

Diabetes Mellitus - Diagnosis

A

History and classic clinical signs + Hyperglycemia & Glucosuria

*Hyperglycemia and glucosuria in cats can be not as specific as it can also happen in times of stress

Fructosamine

HbA1c

57
Q

Diabetes Mellitus - Common CBC Findings (Trick question)

A

None

58
Q

Diabetes Mellitus - Common Panel Findings

A

Hyperglycemia

Hypercholesterolemia

Hypertriglyceridemia

Increased liver enzymes (ALP > ALT) - due to Vacuolar Hepatopathy

59
Q

Diabetes Mellitus - Why is it important to do a urinalysis in an animal suspected of DM? What are the possible findings?

A

UTI - Common
(Due to the urine is being more dilute and neutrophil dysfunction)

USG - can be normal or only slightly low (due to glucosuria)

Bacteria

Proteinuria

RBC

WBC

60
Q

Diabetes Mellitus - What are the 3 tenets of treatment?

A

Insulin

Diet (Cats - High protein content, Dogs - High fiber content)

Exercise

61
Q

Diabetes Mellitus - What is the main problem we want to monitor and avoid during treatment that can lead to hospitalization

A

Hypoglycemia

62
Q

Diabetes Mellitus - Monitoring options

A

Monitor clinical signs! Decrease in Pu\Pd, Polyphagia, Weight gain

Freestyle libre

Glycosylated Hb

Fructosamine

Continuous Blood Glucose Curve

63
Q

Diabetes Mellitus - Fructosamine measures mean glucose of the past…?

A

2 Weeks

64
Q

Diabetes Mellitus - Glycosylated Hb measures the mean glucose of the past..?

A

3 Months

65
Q

Diabetic Ketoacidosis - Basic pathogenesis (3 elements)

A

Lack of insulin secretion (DM Type 1)

Anorexia Low caloric intake

Increased secretion of diabetogenic hormones (e.g. Glucagon, Cortisol)

66
Q

Diabetic Ketoacidosis - Common causes

A

Inflammation Infections:
Periodontitis
UTI
Pneumonia
Pancreatitis
Pyometra

Endocrinopathies:
Cushing Acromegaly

Pregnancy\Diestrus

67
Q

Diabetic Ketoacidosis - Clinical signs

A

Lethargy

Depression

Anorexia

Vomiting

Pu\Pd

Hypovolemic shock (e.g. Tachycardia, Tachypnea, Hypothermia, Prolonged CRT etc.)

Kussmaul respirations

68
Q

Diabetic Ketoacidosis - After the Patient is Fully Stabilized - What is our Next Big Goal?

A

Find the Predisposing Disease! (i.e. Infections)

69
Q

What electrolytes are most affected in DKA? How are each affected?

A

Hyponatremia - Blood Glucose draws fluids from the interstitium and dilutes the sodium

Hypokalemia - Vomiting / Insulin administration / Osmotic diuresis due to glucosuria and ketonuria.

Hypophosphatemia - Osmotic diuresis / Insulin administration

Hypomagnesemia - Insulin administration

70
Q

Diabetic Ketoacidosis - Treatment

A

Fluids

Anti-emetics

Analgesia (if indicated)

antibiotics (a lot of DKA cases are due to infectious processes, such as UTI)

Electrolyte supplementation (Potassium, Phosphate that were lost due to osmotic diuresis)

Insulin:
1) Start with Regular Insulin IMCRI. Blood Glucose levels should be decreased no more than 50 mg\dL\hour

2) When Blood Glucose levels drop below 250 mg\dL - administer fluids + Dextrose in addition to regular insulin. If BG levels drop below 150 mg\dL - Only supply animal Dextrose and cease Regular Insulin.

3) When the animal starts to recover, is well hydrated and eats on its own - Try switching to Insulin SC (e.g. NPH for dogs\Glargine for cats) after each meal)

71
Q

DKA - What is a big clue that a patient is suffering from Hypomagnesemia?

A

Hypokalemia that doesn’t normalize despite supplementation

72
Q

Diabetes Mellitus - An animal diagnosed with DM presents with unbalanced glycemic control (i.e. Hyperglycemia). What are you’re next steps?

A

Verify with the owners:
1) Proper Insulin administration and storage

2) Feeding according to guidelines (e.g. Proper diet suited for DM, fixed meal times and no snacks in between (Easier in dogs.

If owners are operating according to instructions - check for and treat pathologies that can lead to Insulin-resistance (e.g. Infection\Inflammation such UTI, Pancreatitis, Concurrent Endocrinopathies such as Cushing, Acromegaly, Hyperthyroidism, Neoplasia Pregnancy, Diestrus).

73
Q

Acromegaly - Signalment and Etiology

A

middle-age to Old cats

Pituitary Neoplasia

74
Q

Acromegaly - Clinical Signs

A

Enlarged Mandibles (Prognatism)

Enlarged paws

Organomegaly

75
Q

Acromegaly - Diagnosis

A

1) IGF-1 levels - Increased - Can also be increased in Diabetes Mellitus

2) Brain imaging - CTMRI - Pituitary Tumor

76
Q

Acromegaly - Treatment

A

Somatostatin analogues

77
Q

Hypoparathyroidism - Treatment

A

Acute seizuring - Calcium Gluconate IV

Long term:
1) Vitamin D analogous - For life

2) Calcium supplements - until ionized calcium levels reach low-normal to normal levels, then slowly taper off.

78
Q

Hypoparathyroidism - What is a classical clinical sign that can manifest at the time the dog is brought to the clinic? Explain

A

First-time seizure at the vet clinic

Stress => Panting => Blood becomes slightly more alkalemic => Ionized calcium binds to albumin => Less ionized calcium is available at the blood stream than usual => Seizure

79
Q

Hypoparathyroidism - Prognosis

A

Excellent. Normal life expectancy.

80
Q

Hyperparathyroidism - Clinical signs

A

Anorexia

Lethargy

Vomiting

Diarrhea

Pu\Pd

Stranguria, Pollakiuria, Hematuria (Due to Ca-Ox uroliths UTI)

Tremors

81
Q

Hyperparathyroidism - Important DD for hypercalcemia with high PTH that must be ruled out

A

Lymphoma

82
Q

Hyperparathyroidism - Prognosis

A

Very good. A high chance to be completely cured with definitive treatment

83
Q

Hyperthyroidism - Prognosis

A

Generally good, MST - 3-5 Years

84
Q

Hypoparathyroidism - Clinical signs

A

Restlessness

Muscle fasciculations

Tremors

Involuntary muscle contractions

Seizures

Behavioral changes

Coma

Cataracts

85
Q

Hypoparathyroidism - Signalment

A

Young - middle age female dogs

86
Q

Hypoparathyroidism - Diagnosis

A

Low total & Ionized calcium

Low PTH \ Inappropriately low (could be still in the normal range) in the face of hypocalcemia

87
Q

Hypoparathyroidism - Panel findings

A

Low total calcium

Low ionized calcium

Hyperphosphatemia

88
Q

Hyperparathyroidism - Signalment

A

Middle age - Old dogs

89
Q

Hyperparathyroidism - Lab & Imaging findings

A

Panel:
High total & ionized calcium
Hypophosphatemia.

UA: Isosthenuria, Possible signs of UTI (WBC, RBC, Proteinuria), Ca-Ox crystals

Cervical US: Enlarged parathyroid glands

90
Q

Hyperparathyroidism - Treatment

A

Treatments for hypercalcemia:
Fluids
Furosemide
Steroids
Bisphosphonates
Calcitonin.

Definitive treatments for Hyperparathyroidism:
Surgical removal of the parathyroid

Glandular ablation by radiofrequency or ethanol injection.

*Subsequent hypocalcemia Post-op is common - ongoing treatment is necessary (Vitamin D analogous, Calcium supplements)”

91
Q

Primary Hyperaldosteronism - Signalment

A

Old cats (75% of cases above the age of 11 years)

92
Q

Primary Hyperaldosteronism - Etiology

A

Adrenal Adenoma/ Hyperplasia / Carcinoma (Can be bilateral)

93
Q

Primary Hyperaldosteronism - Clinical signs + Lab finding

A

Hypertension:
Ocular (Blindness / Hemorrhage / Retinal Detachment)
Epistaxis
CNS Signs
Worsening of Cardiac (Murmur / Gallop) and Kidney disease (Azotemia / PUPD).

Hypokalemia: Muscle weakness / Paresis / Neck ventroflexion / Plantigrade walk.

In addition to Hypokalemia, Metabolic Alkalosis can also be seen due yo excess H+ secretion in the kidneys.

94
Q

Primary Hyperaldosteronism - Diagnosis

A

Hypertension

Hypokalemia.

Ultrasound - Adrenal mass (False negative is very possible if micronodular hyperplasia).

Gold standard: High Aldosterone (or even normal) in the face of high BP and hypokalemia

95
Q

Primary Hyperaldosteronism - Treatment

A

Medical:
Spironolactone (Aldosterone antagonist)
Amlodipine
Potassium supplements
Low-sodium diet.

Surgery: Adrenalectomy (Treatment of choice)

96
Q

Idiopathic Hypercalcemia - Common Signalment & How to Diagnose

A

Young - middle aged cats

High ionized Ca+
normal PTH
No Malignancy (Neoplasia) or other causes found

97
Q

At what calcium levels can you start to see clinical signs of hypocalcemia (total and ionized calcium)

A

Total calcium - <6 mg\dL.

Ionized calcium - <0.6 mg\dL.

98
Q

What is the main panel finding in SIADH?

A

Hyponatremia

99
Q

Hyperthyroidism - Signalment, Common history/clinical signs

A

Cat - 10 y.o.and older.

Weight Loss

Polyphagia

Pu\Pd

Vomiting

Diarrhea

Tachycardia

Tachypnea

Hyperthermia

Dermal Changes

Behavioral Changes (Either More Aggressive or Calmer).

Target organ damage from hypertension (E.g. blindness from retinal detachment, CNS signs, L-CHF)

100
Q

Hyperthyroidism - Common sequela(s) if left untreated

A

Retinal detachment -> Acute Blindness

CKD

Heart disease

CNS signs (e.g. Stroke)

Cachexia

101
Q

Hyperthyroidism - After starting treatment - which organ requires monitoring?

A

Renal Function

102
Q

Hyperthyroidism - Common lab findings / diagnostics

A

Erythrocytosis

lymphocytosis

Hypocholesterolemia

Electrolyte Changes (Vomiting / Diarrhea)

Slight liver enzyme elevation

Low CK (Sarcopenia).

UA: Proteinuria

103
Q

Hyperthyroidism - What are the 4 Treatment Options

A

Radioactive Iodide (I131) - If available - treatment of choice

Surgery

Methimazole

Low iodine diet

104
Q

Hyperthyroidism - Prognosis

A

Good to Excellent (~5 years in old Cats) - Depending on method of treatment

Doctor of Veterinary Medicine (Work in progress) (17 decks)

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