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Endocrinology Flashcards

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1
Q

What is the stimulus for insulin release

A

rising blood glucose levels (after eating a carbohydrate-rich meal)

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2
Q

What are the 2 effects of insulin

A

1) Body cells take up more glucose
2) Liver takes up glucose and stores it as glycogen \

*Blood glucose levels declines to a setpoint, stimulus for insulin release diminishes

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3
Q

Is insulin anabolic or catabolic

A

anabolic- increases storage of glucose, FA, and amino acids

suppresses all forms of energy production (fat lipolysis, FA oxidation, gluconeogenesis, glycogenolysis)

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4
Q

Is glucagon anabolic or catabolic

A

catabolic- increases mobilization of glucose, FA, amino acids

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5
Q

How do cataracts develop in dogs with diabetes mellitus

A

glucose converted to lactic acid (anaerobic glycolyic pathway

glucose converted to sorbitol and fructose where it cant diffuse out of the eye

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6
Q

What three ways do recurrent infections occur in patients with diabetes mellitus

A

1) Decreased blood flow due to microangiopathies and atherosclerosis
2) Abnormal neutrohpil chemotaxis
3) Impaired cell-mediated response

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7
Q

T/F hepatomegaly is a symptom of diabetes mellitus

A

T - without insulin you get hyperglycemia, hyperlipidemia, ketones, increased gluconeogenesis, increased glycogenolysis

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8
Q

What is the renal threshold of glucose to get glucouria in dogs

A

180 mg/dl

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9
Q

What is the renal threshold of glucose to get glucouria in cats

A

250 mg/dl

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10
Q

What are the 5 clinicopathologic changes in patients with Diabetes mellitus

A

1) Hyperglycemia
2) Glucosuria
3) Elevated cholesterol
4) Elevated liver enzymes
5) minimally concentrated urine (osmotic diuresis)

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11
Q

What three ways are responsible for elevated blood cholesterol in patients with diabetes mellitus

A

1) Lack of Insulin- fat metabolism derangement
2) Impaired Lipoprotein lipase (clears VLDLs and chylomicrons)
3) Impaired LDL receptor- clears LDLs (cholesterol)

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12
Q

What portion of the adrenal gland cortex produces mineralocorticoids (aldosterone and RAAS) ?

A

Glomerulosa (outermost layer of adrenal cortex)

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13
Q

What portion of the adrenal gland cortex produces glucocorticoids (cortisol)

A

Fasciculata (middle layer of adrenal cortex)

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14
Q

What portion of the adrenal gland cortex produces androgens

A

Reticularis (innermost layer of adrenal cortex)

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15
Q

What portion of the adrenal gland produces Epinephrine, Norepineohrine, and Dopamine

A

the medulla

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16
Q

Adrenal glomerulosa produces ______

A

Mineralocorticoids (aldosterone and RAAS)

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17
Q

Adrenal fasciculata produces _______

A

Glucocorticoids (cortisol)

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18
Q

Adrenal reticularis produces _______

A

Androgens

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19
Q

What enzymes do Zona Glomerulosa and Fasciculata have

A

Glomerulosa: Aldosterone Synthase for Aldosterone production

Fasciculata: 17-a hydroxylase for cortisol, DHEA, and Androstenedione production

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20
Q

What initiates the first step of steroid synthesis

A

Endogenous ACTH

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21
Q

What does the hypothalmus release in the hypothalamic-pituitary-adrenal axis

A

CRH (corticotropin releasing hormone)

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22
Q

What does the pituitary release in the hypothalamic-pituitary-adrenal axis

A

ACTH (Adrenocorticotropic hormone)

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23
Q

What does the adrenal gland release in the hypothalamic-pituitary-adrenal axis

A

cortisol

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24
Q

What is a result of an adrenal gland tumor

A

1) high amounts of cortisol
2) one adrenal gland enlarged, one is atrophied
3) Low ACTH

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25
Q

What is the result of a pituitary tumor releasing excess ACTH

A

1) high amounts of cortisol
2) Both adrenal glands become hyperplastic
3) excessive ACTH

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26
Q

What is a result of iatrogenic Cushing’s

A

1) Suppression of pituitary ACTH by exogenous steroid (Low ACTH)
2) only atrophy to zona fasciculata atrophy
3) Low cortisol (but not glucocorticoid)

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27
Q

Two Results of Typical Addisons

A

1) Low Cortisol (immune destruction of zona fasciculata)
2) Low Mineralocorticoids (immune destruction of zona glomerulosa)
3) High ACTH

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28
Q

What is the Result of atypical Addison’s

A

1) Low Cortisol only (immune destruction of zona fasciculata)
2) High ACTH

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29
Q

Is cortisol anabolic or catabolic

A

catabolic
-increases glucose for energy
-Breaks down protein
-Liberates lipids for b oxidation

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30
Q

What vascular effect does cortisol deficiency have

A

hypotension

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31
Q

What vascular effect does cortisol excess have

A

hypertension

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32
Q

What effect does cortisol have on the immune system?

A

excess leads to immunosuppression
-Inhibits phospholipase A2, which prevents the formation of important inflammatory products as this enzyme forms Arachidonic acid which later forms leukotrienes, prostaglandins, thromboxane, and prostacyclins through COX

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33
Q

What areas does cortisol excess cause alopecia in?

A

Perineum
Caudal thighs
Lateral thorax and abdomen

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34
Q

What is the cause of calcinosis cutis

A

Cushings Disease (excess cortisol)

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35
Q

Does cortisol excess of deficiency result in PU/PD?

A

They both do! through different mechanisms

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36
Q

What are the GI symptoms of addisons (cortisol deficiency)

A

vomiting and bloody diarrhea through the lack of GI mucosa maintenance

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37
Q

What CBC results are seen in Cushings

A

Stress Leukogram
-Neutrophilia- prevents migration out of circulation
-Lymphopenia- immune suppression
-Eosinopenia - immune suppression

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38
Q

What CBC results are seen in in Addisons

A

Lack of Stress Leukogram
Anemia

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39
Q

What biochem results are seen in Cushings

A

1) increased in ALP/GGT that are larger than ALT and AST
2) Increased cholesterol (increased lipolysis)
3) Increased glucose (mild) - increased gluconeogenesis and glycogenolysis

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40
Q

What biochem results are seen in Addisons

A

1) Increased ALT
2) Decreased Cholesterol (less GI uptake)
3) Decreased glucose mild(decreased gluconeogenesis/glycogenolysis)
4) Increase K* (less mineralocorticoids)-not atyical Addisons
5) Decrease Na+ (less mineralocorticoids) - not atypical Addisons

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41
Q

What urinalysis results are seen in Cushings

A

Decreased USG (ADH inhibition)
Proteinuria (multifactorial)
Bacteriruia without pyuria (immunosuppression)

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42
Q

What urinalysis result is seen in Addisons

A

Decreased USG due to decreased mineralocorticoids (not in atypical addisons disease)

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43
Q

Does thyroid hormone bind to receptors on membrane or in the nucleus

A

receptors in nucleus, forms a hormone-receptor complex to initiate gene transcription or inhibition

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44
Q

What hormone is released from the hypothalamus in the thyroid axis?

A

Thyrotropin-releasing hormone (TRH)

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45
Q

What hormone is released from the anterior pituitary in the thyroid axis?

A

Thyroid stimulating hormone (TSH)

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46
Q

What hormone is released from the thyroid in the thyroid axis?

A

T4 and T3

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47
Q

What are the 2 stimuli for the hypothalmus to release Thyrotropin-releasing hormone (TRH)

A

Stress and Cold

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48
Q

A disproportionate dwarf is a result of ______

A

lack of thyroid hormone

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49
Q

A proportionate dwarf is a result of ______

A

lack of growth hormone

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50
Q

Why do you see tachycardia and hypertension +/- arrhythmias and murmurs in cats with hyperthyroidism

A

Beta-adrenergic receptor numbers and affinity are unregulated to increase cardiac output

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51
Q

What are the cardiovascular effects of hyperthyroidism in cats

A

tachycardia and hypertension
+/- arrhythmias and murmurs

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52
Q

What are the CNS effects of cats with hyperthyroidism

A

nervousness, hyperactivity, aggression

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53
Q

What are the CNS effects of dogs with hypothyroidism

A

*Demyelination and decreased action potential
-mental dullness
-Decreased reflexes
-Forelimb and/or limb paresis
-Cranial nerve deficits
-Tragic face

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54
Q

What might be noticable about a hyperthyroid cat’s haircoat

A

It will be unkept
T3/T4 moves hair from the telogen to anagen phase
CNS effects and less grooming might also be a factor

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55
Q

What might be seen in a hypothyroid dog’s haircoat

A

hair gets stuck in telogen (resting) stage
alopecia in areas of wear
lack of regrowth after clipping
hyperpigmentatio

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56
Q

Hyperthyroid cats have extra oxygen consumption and increased cariac output leading to increased renal blood flow and what symptoms

A

1) Muscle wasting
2) Fat loss
3) Tachypnea
4) PU/PD

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57
Q

Hypothyroid dogs have what changes in their weight?

A

They gain weight

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58
Q

What biochem abnormalities is seen in hypothyroid dogs

A

increased cholesterol due to disrupted cholesterol synthesis and degradation

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59
Q

What biochem abnormalities is seen in hyperthyroid cats

A

Increased BUN
Increased glucose (mild)
Increased liver enzymes (ALT>ALP)

due to liver hypoxia from increased O2 consumption

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60
Q

What urinalysis abnormalities will be seen in cats with hyperthyroidism

A

Decreased USG (Increased cardiac output leads to increased renal blood flow and medullary washout)

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61
Q

Where is calcitonin produced and what does it result in?

A

C cells of the thyroid (parafollicular cells)
tones down calcium when it is high

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62
Q

what kind of cells produce parathyroid hormone

A

chief cells of the parathyroid gland
function to increase calcium levels

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63
Q

Vitamin D results in increases of ________

A

Ca2+ and PO4

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64
Q

What are the 10 differentials for hypercalcemia

A

GOSH DARNIT
1) Granulomatous (fungal)
2) Osteolytic
3) Spurious
4) Hyperparathyroidism (adenomas or hyperplasia)
5) Vitamin D Toxicosis
6) Addisons Disease
7) Renal secondary hyperparathyroidism (decreased Vit D production and Phosphorus retention)
8) Neoplasia
9) Idiopathic
10) Toxin

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65
Q

What factors cause spurious hypercalcemia

A

-Lipemia
-Hemolysis (sample handling)
-Hemoconcentration
-Hyperalbuminemia
-Acidosis
-Young animals

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66
Q

How does renal disease lead to hypercalcemia

A

Renal secondary hyperparathyroidism
-Decreased Vit D production leading to increased PTH
-Phosphorus retention (kidney dysfunction)

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67
Q

Total calcium is often elevated in renal disease but ionized calcium is often _________

A

normal or decreased

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68
Q

What are the two most common tumors causing hypercalcemia

A

Lymphoma
Apocrine gland adenocarcinomas of the anal sac

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69
Q

What common toxins can cause hypercalcemia?

A

Day-blooming jessamine (Cestrum diurnum)
Vitamin D

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70
Q

Excessive volume excretion of urine

A

Polyuria

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71
Q

Pollakiuria

A

excessive frequency/urgency of urination

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72
Q

Dysuria

A

difficult or painful urination

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73
Q

excessive frequency/urgency of urination

A

Pollakiuria

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74
Q

slow, painful urination, caused by muscular spasms of the urethra and bladder

A

Stranguria

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75
Q

excessive volume of drinking

A

polydipsia

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76
Q

What volume determines an animal is polyuric?

A

if they produce more than 50ml/kg/day of urine
*not feasible to determine

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77
Q

What volume determines an animal is polydipsia?

A

if they drink more than 60-80 ml/kg/day of water

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78
Q

Secondary (compensatory) polydipsia

A

excessive drinking that occurs as a result of primary polyuria
majority of case
peeing too much, compensate by drinking more water

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79
Q

What are your 4 differentials for osmotic diuresis for PU/PD patients

A

1) Diabetes mellitus- excess glucose overwhelms renal reabsorption
2) Post-obstructive diuresis- blocked tom, urea cant get out and accumulates until the obstruction is relieved, also some damaged tubular cell
3) Chronic kidney disease- less urea and sodium reabsorbed. also lost of medullary gradient
4) Fanconi Syndrome- tubular defects prevent various solute reabsorption including glucose and sodium

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80
Q

What are your 5 main categories of differentials for PU/PD animals

A

1) Central diabetes insipidus
2) Primary polydipsia
3) Primary nephrogenic diabetes insipidus
4) Secondary nephrogenic diabetes insipidus
5) Osmotic diuresis

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81
Q

What are your major rule out for Secondary nephrogenic diabetes insipidus

A

1) Addisons
2) Cushings
3) Hyperthyroidism
4) Pyometra
5) Hypercalcemia
6) Drugs
7) Medullary washout
8) Hepatic insuffiency
9) Pyelonephritis
10) Hypokalemia

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82
Q

How does Cushings result in PU/PD

A

excess glucocorticoids interferes with ADH rceptors and ADH release

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83
Q

What three ways does Addisons cause PU/PD?

A

1) lack of mineralocorticoids (no aldosterone leading to Na+ wasting)
2) Osmotic agent
3) Medullary washout

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84
Q

How does hyperthyroidism result in PU/PD cats?

A

being in a hypermetabolic state leads to increased blood flow to the kidney and decreased time for sodium reabsorption, creating a decreased osmotic gradient leading to increased PU/PD

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85
Q

What is often the chief complaint in pyometra cases

A

PU/PD.
E coli endotoxins interfere with ADH receptor (secondary NDI)

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86
Q

T/F hypercalcemia causes PU/PD

A

interference with function of ADH receptors and tubular cells

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87
Q

What are the causes of primary polydipsia (brain causes)?

A

-Hyperthyroidism
-Hyperadrenocorticism
-Hepatic Disease
-Learned behavior- psychogenic polydipsia

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88
Q

Primary polydipsia leads to __________ which leads to eventual _______ _________

A

Primary polydipsia leads to overhydration which leads to eventual medullary washout

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89
Q

What is the result of no ADH

A

Water channels do not get inserted into the distal tubules leading to no water absorption and diuresis

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90
Q

If urine is hypersthenuric (Dog > 1.030/35 & Cat > 1.040/45) then are they PU/PD?

A

No they are not. they can concentrate their urine

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91
Q

At what USG, should you do a workup for PU/PD?

A

urine that is minimally concentrated, isosthenuric, or hyposthenuric
Dog: < 1.030
Cats: < 1.040

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92
Q

Dog with history of PU/PD. Urinalysis, CBC, Biochem, and imaging is normal. ACTH stim rules out hyperadrencorticism. nx bile acids What are the next steps

A

Use the dreaded modified water deprivation test to diagnose psychogenic polydipsia, medullary washout, or central diabetes insipidus

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93
Q

How does the modified water deprivation test work

A

*rule out absolutely everything before performing
1) Hospitalize and withhold water until 5% dehydrated
-if USG > 1.030- psychogenic polydipsia
2) If USG <1.030- Give ADH
-if USG > 1.030 - Central Diabetes Insipidus
-If USG < 1.030- medullary washout or NDI

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94
Q

How does hepatic insufficiency lead to PUPD

A

direct brain effects on the thirst center
impaired urea production
impaired cortisol metabolism

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95
Q

Where and how does Furosemide act

A

it acts to inhibit NaCl reabsorption in the thick ascending limb of the loop of Henle

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96
Q

A patient presents with weight loss. What should you first ask about?

A

If they have polyphagia or anorexia

Polyphagia: Inadequate Intake, Hypermetabolism, Nutrient loss

Anorexia: Primary, pseudoanorexia, primary gi, non GI

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97
Q

Patient with Weight Loss and Polyphagia
You determine the patient is not being fed enough
What do you consider as diagnosing?

A

-Insufficient quantity of food
-Poor food quality
-Increased exercise and demand
-Growing animal
-Pregnancy

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98
Q

Patient with Weight Loss and Polyphagia
You determine the patient is being fed enough
What could be occurring

A

1) Hypermetabolism (Hyperthyroidism, Fever, Neoplasia, Pregnancy, Lactation)
2) Nutrient loss
a) Glucose- Spill-over from DM, cant absorb in Fanconi
b) Protein- GI (PLE, parasite maldigestion, mabsorption), kidney (protein losing nephropathy), skin (severe burns, open abdomen), third space (osmotic pressure- cardiac disease, portal hypertension)
c) Fats- GI

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99
Q

Pseudoanorexia

A

Weight loss with anorexia that is due to issues with:
-teeth (dental dz)
-Mucosa (abscess, neoplasia, ulcerations)
-Bone (fracture, neoplasia)
-Joint (osteoarthritis, polyarthritis)
-Muscle (myopathy)
-Nerves (trigeminal nerve)

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100
Q

What are broad reasons that a patient might be anorexic

A

1) Hunger center- CNS disorders
2) Pseudoanorexia- due to teeth, mucosa, bone, joint, muscle, nerves
3) Primary GI- Intolerance (allergy), inflammation (IBD), infection, obstruction (Mechanical or functional) , GI neoplasia (lymphoma, adenocarcinoma, leiomyosarcoma, mast cell tumor)
4) Secondary GI - organ system disease, metabolic (diabetes, hyperthyroidism, Addisons) systemic neoplasia

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101
Q

What are the different waves of diagnostics for a complaint of weight loss

A

1) History of appetite, Physical exam, intake relation to weight, minimum database, fecal

2) Based on the first wave: Total T4 and FeLV/FIV in cat, Texas GI panel, chest and abdominal films

3) Barium series (rarely done), ultrasound, endoscopy, abdominal exploratory

4) Last resort- CT or MRI scan to rule out central disease

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102
Q

How do you calculate RER

A

RER= 70 * BW(kg)^0.75

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103
Q

What are your differentials for weight gain with increased food intake and polyphagia

A

Hyperadrenocorticism
Insulinoma
Growth Hormone
Pregnancy
Drugs

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104
Q

What are your differentials for weight gain with normal or decreased appetite/intake

A

Hypothyroidism (Dogs)
Central Disease
Characteristics: Female, Neutering, Breed, owner related
Edema, Ascites, intra-abdominal masses, organomegaly

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105
Q

What are your waves of diagnostics for a complaint of weight gain in an animals

A

1) History of appetite, Physical exam, Calculate intake, Minimum database

2) Thyroid panel (dog), Adrenal testing for Cushings

3) CT or MRI scan

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106
Q

Are males or female dogs more prone to diabetes mellitus?

A

Females are twice as affected as males

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107
Q

When do most dogs present for diabetes mellitus

A

Between 7-9 years (middle aged)

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108
Q

What breeds of dogs are predisposed to diabetes mellitus

A

Keeshond *
Beagles
Miniature Schnauzers
Miniature Pinschers
Cairn Terriers

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109
Q

Are males or female cats more prone to diabetes mellitus?

A

Males are twice as likely as females

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110
Q

T/F Diabetes mellitus has a breed predilection in cats

A

False

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111
Q

What are the similarities between dogs and cats with diabetes mellitus

A

Both are
1) PU/PD
2) Polyphagia with weight loss
3) Fasting hyperglycemia
4) Glucosuria
5) Prone to infections

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112
Q

Is dog diabetes mellitus due to a lack of insulin or insulin resistance

A

Type I: lack of insulin from immune-mediated beta cell destruction

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113
Q

Is cat diabetes mellitus due to a lack of insulin or insulin resistance

A

Type 2: Insulin resistance (relative lack of insulin)

114
Q

What is significant about the clinical signs of dogs with diabetes mellitus

A

they can develop cataracts due to the lack of insulin

115
Q

What is significant about the clinical signs of cats with diabetes mellitus

A

They might have Frosty paws or develop neuropathies (plantigrade stance)

Profound stress (epi induced) hyperglycemia

116
Q

How do the dietary requirements of dogs with diabetes mellitus differ from cats with diabetes mellitus

A

Dogs: Need complex carbs

Cats: Need high protein diet, carbs need to be avoided

117
Q

Why is hyperglycemia and glucosuria not significant for a diabetes mellitus diagnosis in cats?

A

Because they can have a profound stress hyperglycemia that can be up to 350 mg/dL and the spill over is 250mg/dL

118
Q

How can you differentiate chronic hyperglycemia from acute hyperglycemia in cats for diabetes mellitus diagnosis?

A

Fructosamine test

119
Q

What three ways can insulin resistance develop in cats?

A

1) Glucose toxicity (chronic hyperglycemia impairs function of beta (less release) and peripheral cells (glucose transport down-regulation) leading to more hyperglycemia)

2) Beta cell destruction (chronic hyperinsulinemia destroys the beta cell thus reducing insulin production)

3) obesity induced insulin resistance (both dog and cat) circulating fatty acids induces insulin resistance in the peripheral tissues

120
Q

What hormones interfere with the normal amount of insulin (resulting in insulin resistance)

A

1) Epinephrine (infections/inflammation)
2) Cortisol (infections/inflammation, Cushings, Steroids)
3) Progesterone (pregnancy)
4) Growth hormone (acromegaly)
5) Glucagon (glucagon-secreting tumors)
6) Thyroid hormone (hyper AND hypothyroidism)
7) Obesity induced- multifactorial

121
Q

How might a patient present if they have undiagnosed Diabetes mellitus

A

-PU/PD
-Polyphagia with weight loss
-Fasting hyperglycemia with glucosuria
-Infections
-Cataracts (dog)
-Neuropathies/plantigrade stance (cat)
-Frosty paws (cat)

122
Q

What is special about the insulin you give for Diabetic ketoacidosis patients

A

GIVE IM (q2-4 hours) or IV as a CRI
-regular insulin (Humulin- R or Novalin-R)

123
Q

What insulin do you give dogs with DM and at what dosing frequency

A

-Intermediate action insulin - lente (Vetsulin)
Given SQ twice a day

124
Q

Lente / Vetsulin

A

Insulin used for Dogs
Intermediate Duration
Crystalline
Given SQ twice daily

125
Q

Regular insulin / Humulin-R / Novalin-R

A

Insulin used for DKA patients
Short Duration
Crystalline
Given IM (q2-4hrs) or IV as CRI

126
Q

What is the go to insulin for cats in the management of DM

A

Glargine (Given SQ twice daily)

127
Q

Glargine or Detemir

A

Insulin for Cats
Long duration
Analog
Given SQ twice daily

128
Q

Why are oral hypoglycemics that reduce peripheral insulin resistance and increase insulin secretion not useful in dogs?

A

The dogs have no b cells to produce the insulin

129
Q

Why are oral hypoglycemics that reduce peripheral insulin resistance and increase insulin secretion not useful in cats?

A

fill in later

130
Q

What diet considerations should you take when managing a dog with DM

A

Complex carbs and fiber
regular or moderate exercise

131
Q

What diet considerations should you take when managing a cat with DM

A

Protein, low carbs

132
Q

What should you do at recheck appointments of patients with DM

A

Urine dipstick, spot glucose, or fructosamine (cats)

Minimum database for concurrent disease

Glucose curve (to assess insulin duration, effectiveness and glucose nadir)

133
Q

When should the appropriate blood glucose nadir be in a glucose curve?

A

At 6 hours post-injection

134
Q

What should the appropriate time duration of insulin be?

A

About 12 hours (to decrease and return back to appropriate blood glucose levels

135
Q

What should the appropriate effectiveness of insulin be (glucose range)

A

Dogs: 80 - 200 mg/dl
Cats: 80 - 300 mg/dl

136
Q

What should the appropriate glucose nadir be at?

A

80-100 mg/dl

137
Q

What are the features of an appropriate glucose curve?

A

1) Appropiate time of nadir (at 6 hours)
2) Appropriate duration of curve (12 hours)
3) Glucose range of 80 to 200 (dogs) or 300 (Cats)
4) Nadir Range at 80 - 100mg/dl

138
Q

At what insulin dose might dogs and cats develop insulin resistance?

A

Dogs: > or equal to 1.5 units/kg/dose

Cats: > 5 units/dose

139
Q

What are the two likely patients presenting with Diabetic Ketoacidosis (DKA)

A

Previously undiagnosed diabetics
Unregulated diabetics

140
Q

Describe the pathogenesis of DKA

A

the body perceives starvation
lipolysis to liberate free fatty acids leading to increased uptake of circulating fatty acids into the liver where beta oxidation occurs
acetone, b-hydroxybutyrate, and acetoacetate leads to acidosis (Lethargy, anorexia, vomiting)

141
Q

A patient presents with hx of PU/PD, polyphagia with weight loss, lethargy, anorexia, vomiting, dehydration, and hypovolemia

Clinpath abnormalities: Acidosis, hyperglycemia, Azotemia, increased liver enzymes, Hyponatremia, Hypochloremia, hyperkalemia, glucosuria, and ketonuria

What is the diagnosis

A

Diabetic ketoacidosis

142
Q

What additional tests might you perform to diagnose DKA

A

1) Venous blood gas: for electrolytes (Na, K, Cl), Acid-base status (pH), Perfusion (lactate), degree of hyperglycemia (glucose), degree of dehydration (cretinine)

2) Urine dipstick: confirms glucosuria and ketonuria

143
Q

What are the treatment goals of DKA

A

Steps
1) Restore fluid and electrolytes
2) Correct acidosis
3) Provide regular insulin (IM or CRI)
4) Provide glucose
5) Identify trigger

144
Q

How does giving fluids help initially with DkA

A
  • Corrects dehydration and Improves perfusion, decreasing acidosis
    -Corrects electrolyte abnormalities as it replaces Na+ and Cl-, also decreases potassium, phosphorus, and magnesium
145
Q

Why shouldnt you give regular insulin in a DKA patient

A

because it will not be well absorbed in a dehydrated patient

146
Q

What is the most common trigger for DKA

A

urinary tract infection

also dental abscess, pancreatitis, pneumonia

147
Q

What a potential triggers for DKA

A

anything that results in insulin resistence
-Epinephrine (infections/inflammation)
-Cortisol (infections/inflammation or steroids or Cushings)
-Progesterone (pregnancy)
-Growth hormone (acromegaly- cats)
-Glucagon (glucagon-secreting tumors- v rare)
-Thyroid hormone (hyper and hypo)
-Obesity

148
Q

What are you next steps for determining the trigger for DKA

A
  • Acquire a Minimum Database
  • Urine culture for UTI
  • Abdominal ultrasound
    -Abdominal or Thoracic radiographs
149
Q

Cervical ventroflexion in a DKA patient is a result of

A

Muscle weakness from being hypokalemic

150
Q

Hemolysis in a DKA patient is a result of

A

Hypophosphatemia

151
Q

What 5 things should you monitor in a patient with DKA

A

1) Cervical ventroflexion or muscle weakness (potassium decrease)
2) Hemolysis (phosphorus)
3) Mentation change (cerebral edema)
4) pH change- worsening acidosis

152
Q

What are the typical presenting problems in patients with Addison’s Disease

A

1) PU/PD
2) collapse

153
Q

What age is Addisons typically diagnosed in dogs?

A

often young to middle aged dogs (around 2 years)

154
Q

Are patients with Addisons typically male or female

A

Female

155
Q

What breeds are predisposed to Addison’s disease

A

-Standard Poodle
-Portugese Water dog
-Labrador Retriever
-Bearded Collie

156
Q

What are the diagnostic findings of a patient with Addisons

A

USG: low (PU/PD)
CBC: lack of a stress leukogram, anemic once rehydrated
Pre-Renal Azotemia
Decreased glucose
Decreased cholesterol
Decreased Na and Cl - lack of aldosterone

157
Q

What are the clinical signs associated with Addisons Disease

A

Cortisol: Waxing/waning illness, lethargy, anorexia, weight loss, vomiting, diarrhea, regurgitation?, slightly thin, abdominal pain, blood/melena on rectal, bradycardia despite hypotension, shock from hypotension

Aldosterone: PU/PD, shock due to hypovolemia

158
Q

What you expect to see in the UA of a patient with Addisons

A

Only abnormality is a low urine specific gravity due to aldosterone deficiency

159
Q

What would you expect to see in the CBC of a patient with Addisons

A

-Lack of Stress Leukogram
-anemia (decreased erythropoiesis and/or GI blood bloss and/or anemia of chronic disease)

160
Q

What would you expect to see in the biochem of a patient with Addisons

A

Increased: Azotemia (BUN, Creatinine, P), Potassium, Calcium, +/- elevated liver enzymes

Decreased: Glucose, Cholesterol, Sodium/chloride, Bicarbonate, +/-

161
Q

What three characteristics are unique about the EKG findings of a patient with Addisons

A

-No P-wave
-Wide QRS complex
-Spiked T wave (can be inverted)

from hyperkalemia

162
Q

Why do patients with Addisons have an EKG with No P wave, Wide QRS complex, and a spiked T wave

A

hyperkalemia (although not all patients with hyperkalemia have this)

163
Q

What layers of the adrenal glands are impacted in a patient with typical Addisons

A

both the zona glomerulosa and fasiculata

164
Q

What else might be on your differentials for a patient with atypical Addisons (vomiting, diarrhea, painful abdomen, normal Na+ and K+)

A

-GI foreign body
-Pancreatitis
-Acute hemorrhagic diarrhea syndrome (AHDS)

165
Q

What ratio of sodium to potassium should you consider for typical Addisons?

A

Na:K < 28:1 - Consider typical Addisons
Na:K < 25:1- Highly suspicious for typical Addisons
Na:K < 21:1 - Slam dunk for typical Addisons

*Does not rule out atypical Addisons because you dont get the electrolyte abnormalities

166
Q

How do you get a definite diagnosis of Addisons Disease?

A

ACTH Stimulation Test

Pre: Low cortisol
Give eACTH: High Cortisol
Post: Low cortisol

167
Q

What is a good screening test for Addisons Disease

A

Baseline Cortisol
-If <2: Do ACTH Stim for definite diagnosis
-If >2: Not Addisons, sufficient cortisol test

good for ruling out Addisons but not good the definite diagnosis

168
Q

What is the importance of giving fluids in an Addisonian emergency

A

Its important for hypovolemic shock
-Restores NaCl levels
-Helps dilute K+
-Helps correct acidosis

169
Q

What should you give in an Addisonian emergency to replace glucocorticoids

A

Dexamethasone only
only one type of glucocorticoid prior to ACTH Stimulation test
All other glucocorticoids cross-react with the cortisol assay (leading to false negative)

170
Q

Calcium gluconate

A

given to Addisonian patients in an emergency
doesnt change the hyperkalemia levels but it prevents the entry into the heart

171
Q

Bicarbonate use in Addison emergency

A

allows the entry of potassium into the cell to correct hyperkalemia

172
Q

Do patients on DOCP require prednisone?

A

Yes

173
Q

Prednisone

A

exogenous glucocorticoid that can be dosed physiologically for the maintenance of Addison patients
Owners must increase dose before stressful events

174
Q

Desoxycorticosterone pivalate (DOCP)

A

an injectable mineralocorticoid that is given once every 25 days
patients receiving it still need to get prednisone

175
Q

Florinef (Fludrocortisone)

A

a mineralocorticoid oral medication that is given daily
50% do not need prednisone, start all on prednisone and discontinue if PU/PD/polyphagia is severe

176
Q

Are the majority of Cushing cases PDH or Adrenal Tumors

A

Pituitary Dependent (PDH)

177
Q

Name the disease: high ACTH and high cortisol

A

Pituitary Dependent Cushings

178
Q

Name the disease: low ACTH and high cortisol

A

Adrenal Dependent Cushings

179
Q

Name the disease: low ACTH and low cortisol

A

Iatrogenic Cushings

atrophy of the adrenal gland, if stopped giving, go into Addisonian Crisis

180
Q

Do small dogs typically get pituitary dependent or Adrenal dependent Cushings?

A

Pituitary dependent

181
Q

Do large dogs typically get pituitary dependent or Adrenal dependent Cushings?

A

Adrenal tumors

182
Q

What are the clinical signs of Cushings

A

PU/PD
Polyphagia
Panting
Weight gain
Alopecia
Potbelly
Hepatomegaly
Muscle wasting (apaxial)
lameness and weakness

183
Q

What should you do as your initial diagnostics if you suspect Cushings?

A

Minimum database (CBC, biochem, urinalysis)
Urine culture (more prone to UTI)
Check systemic blood pressure for hypertension as excess cortisol can create hypertension

184
Q

What urinalysis findings might you find in a patient with Cushings

A

Minimally concentration (>1.012 - 1.025)
Isosthenuric (1.008 - 1.012)
Hyposthenuric (<1.008)

Proteinuria

Urinary Tract Infection (Bacteriuria without pyuria- cortisol prevents neutrophil egress from vessels to the site of infection

185
Q

What CBC findings will you see in a patient with Cushings

A

A Stress Leukogram

186
Q

What biochem findings will you see in a patient with Cushings

A

Hyperglycemia (mild)
Hypercholesterolemia
Elevated liver enzymes (ALP>ALT)

187
Q

What liver enzyme will be raised the most in Cushings?

A

ALP

188
Q

Name the 3 diagnostic screening tests for Cushings

A

Used to screen the patient. Is this Cushing’s disease or not?

1) Urine-cortisol:creatinine ratio
2) ACTH Stimulation
3) Low-dose dexamethasone suppression test

189
Q

Name the 3 diagnostic discriminatory tests for Cushings, determining what form

A

1) High-dose dexamethasone suppression test (HDDST)
2) Endogenous ACTH (eACTH)
3) Imaging (ultrasound, CT, MRI)

190
Q

Is the urine cortisol:creatinine ratio test highly sensitive or specific?

A

highly sensitive: a negative test is more reliable.
Use it to rule out HAC

191
Q

ACTH stimulation test

A

Synthetic ACTH given, and increased cortisol should be released
Only test for iatrogenic Cushings
Only test for monitoring Cushing treatment
Only test for Addisons

1) Collect blood at 0 hrs (measure cortisol)
2) Give synthetic ACTH IV
3) Collect blood at 1 hour (measure cortisol)

*If below normal post-ACTH range (>18) then they are not Cushings
*If it is above, it is Cushings but we cannot determine the etiology

192
Q

Low dose dexamethasone suppression test

A

A screening test for Cushings. Dexamethasone suppresses ACTH secretion and therefore cortisol in a normal dog for 8 hours
One test can determine if they are Cushings and if it is PDH
Stressed or patients with co-morbidities can result in false positives
1) Collect blood at 0 hours (measure cortisol)
2) Give dexamethasone IV
3) Collect blood at 4 hr (measure cortisol)
4) Collect blood at 8 hours (cortisol)

*If 8 hour value is less than 1.4 or 50% then it is not Cushings
*If it is, look at 4 hours, if it is suppressed then it is PDH. If it is not suppressed then it is either PDH or AT.

193
Q

You perform a LDDS. There is suppression (<50%) at both 4hr and 8hr. What is the interpretation?

A

The patient does not have Cushings

194
Q

You perform a LDDS. There is no suppression (<50%) at both 4hr and 8hr. What is the interpretation?

A

The patient has Cushings but you cannot determine if it is Pituitary dependent or an adrenal tumor

195
Q

You perform a LDDS. There is suppression (<50%) at both 4hr but not at the 8hr point. What is the interpretation?

A

The patient has pituitary dependent Cushing’s
This outcome is a discriminatory test

196
Q

You perform a LDDS. There is suppression and then escape. What is the outcome

A

The patient has pituitary dependent Cushing’s
This outcome is a discriminatory test

197
Q

Endogenous ACTH assay

A

Used as a discriminatory test for Cushings.
-Low: AT- suppressed
-High: PDH
single blood draw.
Most reliable if it is high because it is a labile hormone

198
Q

Endogenous ACTH assay is most reliable when it is___________

A

high. it is extremely labile

199
Q

High-dose dex suppression test

A

a discriminatory test for Cushings
Large amount of dexamethasone will suppress ACTH production by even stubborn pituitary tumors by 8 hours
Adrenal tumors never suppress
PDH tumors suppress (70%)

200
Q

What will the adrenal glands look like on ultrasound if there is a pituitary tumor

A

both of the adrenals will be enlarged

201
Q

What will the adrenal glands look like on ultrasound if the patient has an adrenal tumor

A

one will be enlarged, and one will be atrophied

202
Q

Upon ultrasound for suspected Cushings, you notice that both of the adrenals are enlarged. What is the diagnosis

A

Pituitary tumor

203
Q

Upon ultrasound for suspected Cushings, you notice that one of the adrenals is enlarged, while the other is atrophied. What is the diagnosis

A

Adrenal tumor

204
Q

Upon ultrasound for suspected Cushings, you notice that both of the adrenals are atrophied. What is the diagnosis

A

Iatrogenic Cushings

205
Q

Trilostane

A

a 3-b-hydroxysteroid dehydrogenase inhibitor that interferes with steroid production.
For tx of PDH Cushings
Fewer side effects
Reversible

206
Q

What medication can you give for Pituitary Dependent Hyperadrenocorticism

A

Trilostane

207
Q

What two ways can you treat PDH Cushings

A

1) Stereotactic Radiosurgery
2) Trilostane

208
Q

T/F Trilostane can be used to tx adrenal tumor Cushings

A

it may not control

209
Q

What two ways can you treat adrenal tumors?

A

1) Trilostane (may not control)
2) Adrenalectomy

210
Q

What should you consider when performing a unilateral adrenalectomy

A

The other adrenal gland is atrophied so there could be an Addisonian Crisis

211
Q

Are females or male cats more susceptible to feline hyperadrenocorticism

A

Females

212
Q

What are the differences between Cushings in dogs and cats

A

Cats- very uncommon
fragile skin syndrome
Concurrent diabetes mellitus - 85%
PU/PD and ALT from diabetes
ALP often normal because not steroid-induced isoenzyme
tx with bilateral adrenalectomy or trilostane

213
Q

Is there polyphagia or anorexia with CKD

A

anorexia

214
Q

What are the physical exam findings of a feline patient with hyperthyroidism

A

-Growling and pacing around the room
-Dilated eyes
-Nodules in the cervical area
-High heart rate
-Gallop rhythm
-Left systolic murmur
-Panting
-Thin
-Rough, unkempt haircoat
-Weight loss with polyphagia
-PU/PD

215
Q

What single test should you perform if PU/PD is on the problem list

A

a urinalysis

216
Q

What CBC findings will you see in a cat with hyperthyroidism

A

-Stress leukogram
-Slightly increased PCV

217
Q

What biochem findings will you see in a cat with hyperthyroidism

A

Increased ALT (especially), ALP, and AST
Hyperglycemia
Increased BUN

218
Q

What is the first test you should do if you suspect hyperthyroidism for cats

A

Total T4
-Positives are reliable but there are some false negative

219
Q

99% of the time, is hyperthyroidism a result of thyroid adenomas or adenocarcinomas

A

thyroid adenomas

bilateral 70& of the cases

220
Q

What is the summary of all findings with cats with hyperthyroid

A

-Weight loss
-Polyphagia
-PU/PD
-Hyperactivity
-GI signs
-Skin changes
-Respiratory
-Apathetic

-Thyroid slip
-Gallop rhythm/murmur
-hypertension
-retinal petechiae
-Detached retinas

-Increased ALT
-Increased PCV
-Elevated BUN
-Decreased USG

221
Q

What disease can mask the signs of CKD

A

Feline Hyperthyroidism

222
Q

Is total T4 or free T4 more sensitive

A

Total T4- it is a good screening test. Good for ruling out- positives are reliable (some false negatives)

223
Q

Nuclear Scintigraphy

A

Method for diagnosing hyperthyroidism in cats
uses Technetium and compares radioactivity compared to the salivary glands
compares bilateral vs unilateral

224
Q

What diet should you have a hyperthyroid cat on?

A

A diet that is deficient in iodine

225
Q

What drug is used to treat hyperthyroidism in cats?

A

Methimazole: blocks thyroid synthesis

226
Q

What is methimazole used to treat

A

hyperthyroidism in cats - blocks thyroid synthesis

227
Q

Methimazole

A

tx hyperthyroidism in cats - blocks thyroid synthesis

Pros: Non-invasive, Inexpensive, Reversible

Cons: Pill cat, doesnt cure, Adverse effects (hepatotoxicity, bloo dyscrasias, GI signs, facial excoriation)

228
Q

What are the adverse signs of Methimazole that you should watch for

A

GI upset
Facial excoriation
Blood dyscrasias (anemia, thrombocytopenia, neutropenia)
Hepatotoxicity

Monitor T4, Kidney function (BUN, creatinine, USG), Complete blood count, liver enzymes

229
Q

I-131 treatment

A

SQ injection for permanent treatment of hyperthyroidism
Selects abnormal cells
Expensive
Do methimazole challenge prior to I-131 to assess renal function
isolation for long time

230
Q

Describe of I-131 treatment works

A

Atrophy of healthy cells due to lack of TSH stimulation because of hyperthyroidism
1) SQ injection of I-131
2) Healthy (atrophied) cells do not take up the I-131
3) Adenoma cells take up the I-131
4) Abrupt stop of T4 from the adenoma
5) The healthy cells will return to normal in 1-6 months as they are stimulated by TSH

231
Q

What are the 3 possible complications with thyroidectomy

A

1) Transient or permanent hypothyroidism
2) Laryngeal paralysis
3) Hypoparathyroidism leading to hypocalcemia (muscle tremors, facial pruritus, seizures)

232
Q

How do you treat hypertension and hypertensive retinopathies due to hyperthyroidism

A

Give Amlodipine (Calcium channel blockers)

233
Q

Amlodipine

A

A calcium channel blocker that is used to treat hypertension and hypertensive retinopathies

234
Q

What two ways does primary hypothyroidism occur in dogs?

A

1) Lymphocytic thyroiditis (against thyroglobulin)
2) Idiopathic atrophy

235
Q

How does euthyroid sick syndrome occur

A

Suppression of T4 by other conditions such as concurrent illness, many medications (steroids), Cushing’s disease

236
Q

What dog breeds have a predilection for hypothyroidism

A

Doberman, Golden Retriever, Labrador, Dachshund, Schnauzer, Great Dane, Cocker

237
Q

How might a hypothyroid dog present?

A

Lethargy
Mental dullness
Weight gain/obesity

Dermatologic lesion (alopecia, seborrhea, pyoderma)

Hypercholesterolemia

238
Q

What two clinical signs common to the other endocrinopathies that hypothyroid dogs do not have

A

PU/PD
Polyphagia

239
Q

What skin abnormalities is seen in hypothyroid dogs

A

fluffy, puppy coat
alopecia in areas of wear
shaved area with no growth
hyperkeratosis in inguinal and axillary regions

240
Q

What disease do you see the tragic face in?

A

Hypothyroidism from facial nerve paralysis and decreased reflexes

241
Q

Does megaesophagus go away when completing the treatment of hypothyroidism in dogs?

A

NO

242
Q

What diseases might be tied to hypothyroidism but it isnt determined due to breed predispositions?

A

1) Megaesophagus
2) Laryngeal paralysis
3) Von Willibrand factor deficiency
4) Infertility

243
Q

What are the only findings from the minimum database that you will see in a hypothyroid dog

A

CBC: Mild, non-regenerative anemia
Biochem: High amounts of cholesterol

244
Q

What is the first test you should perform if you suspect hypothyroidism in dogs?

A

Total T4 and eTSH

245
Q

TgAA assay

A

Thyroglobulin autoantibody
present in 50-60% of hypothyroid dogs
Suggest the presence of autoimmune thyroiditis

*Does not predict the current or even future hypothyroidism

246
Q

Is TT4 or Free T4 more sensitive for the testing of hypothyroidism

A

fT4

247
Q

What would you expect tT4, fT4 and TSH to be in a patient with primary hypothyroidism

A

tT4: Low
fT4 : Low
TSH: High
*but TSH can be normal in 25% of dogs

248
Q

What would you expect tT4, fT4 and TSH to be in a patient with euthyroid sick syndrome

A

tT4: Low
fT4 : normal
TSH: Normal to Decreased

249
Q

What would TSH levels be in a patient that has euthyroid sick syndrome

A

Normal to Decreased

250
Q

What is the best test for hypothyroidism in dogs?

A

Screen with TT4 + TSH (limited thyroid panel)

If suspect still, add fT4 and autoantibodies

251
Q

What should you not do when interpreting a total T4 for hypothyroid dogs

A

Do not interpret it alone

You must have both TT4 (+/- fT4) and TSH because otherwise you cant differentiate true primary hypothyroidism from euthyroid sick syndrome

252
Q

What should you do to treat hypothyroid dogs?

A

Supplement with L-thyroxine (T4), twice daily dose

253
Q

What is the response time to L-thyroxine?

A

Activity level: 2 weeks
Haircoat, body weight, bloodwork abnormalities: 6-8 weeks
Neurologic signs- months
Megaesophagus: may not resolve

254
Q

How should you monitor a patient after treatment with L-thyroxine

A

after 6-8 weeks of therapy
take a 4-6 hours post-pill sample
maintain in high normal or slightly increased range

255
Q

What should you consider if there is a high total calcium but ionized calcium is low to normal (with azotemia present

A

Chronic kidney disease

256
Q

What are your 4 differentials for high calcium and phosphorus

A

1) Renal disease
2) Addisons
3) Vitamin D toxicosis
4) Osteolysis

257
Q

What do you suspect with calcium is high and phosphorus is low

A

Primary hyperPTH
Neoplasia

258
Q

What should you consider if a patient has
-High total calcium and ionized calcium
-Low Phosphorus

A

-LN aspirate or rectal exam (Lymphoma/AGASACA)
-Cervical ultrasound (Hyperparathyroidism)
-PTH panel (Hyperparathyroidism)

259
Q

What results would you expect to see in a patient with primary hyperPTH

A

tCa2+: High
iCa2+: High
PTH: High
PTHrp: 0
P: Low

260
Q

What results would you expect to see in a patient with lymphoma or AGASACA

A

tCa2+: High
iCa2+: High
PTH: Low
PTHrp: High
P: Low

261
Q

Is PTH of a patient with lymphoma or AGASACA low or high

A

Low

262
Q

Is PTH of a patient with Vitamin D toxicosis low, high, or normal

A

Low to normal - there is already high calcium so no stimulus

263
Q

What are the two most common diseases with increased total calcium

A

1) Secondary Renal Hyperparathyroidism (has normal to low iCa2+)
2) Neoplasia

264
Q

What are 5 therapy optins for hypercalcemia

A

1) Sodium diuresis (competes with Ca2++ reabsorption)
2) Furosemide (Inhibits Ca2+ reabsorption in the thick ascending loop of Henle)
3) Glucocorticoids: inhibits GI absorption, bone reabsorption, increases calciresus (Get aspirates and biopsies first)
4) Bisphosphonate: inhibits osteoclast function
5) Salmon calcitonin

265
Q

What else can cause the parathyroid to become hyperplastic that is not primary hyperPTH

A

Secondary to Renal disease

266
Q

How can you differentiate renal hyperparathyroidism from primary hyperparathyroidism

A

Calcium (ionized) will be low to normal

267
Q

What is the therapy for primary hyperparathyroidism

A

Surgical removal
Try to leave at least one of the 4 parathyroid gland
Recurrence is more likely if there is hyperplasia

268
Q

How do you manage a patient that just had its parathyroidglands removed

A

Monitor calcium (Usually declines within 1-7 days)
Supplement with vitamin D and calcium (often for life)

Look out for hypocalcemia signs (Muscle tremors, facial pruritus

269
Q

Of the two synthetic mineralocorticoids available, which one must always be supplemented with prednisone?

A

DOCP

Desoxycorticosterone (DOCP) only has mineralocorticoid properties. Patient receiving DOCP must receive prednisone. About 50% of patients receiving fludrocortisone require prednisone, but the other 50% of patients can be successfully treated with fludrocortisone alone.

270
Q

Which insulin is used for diabetic ketoacidosis?

A

Regular insulin is the insulin of choice for a patient with DKA. It should be given as intermittent intramuscular (IM) injections or IV as a constant rate infusion while the patient is dehydrated and not eating. Sometimes we will use subcutaneous injections before we transition to intermediate acting insulin but only if the the patient is eating and drinking. You can also go directly from IM or IV regular insulin to intermediate-acting insulin once the animal is eating and drinking on its own.

271
Q

When should you measure insulin?

A

To diagnose an insulinoma

You should never measure insulin as part of a diabetic or acromegalic workup. The only time we measure insulin is if the glucose is low and we suspect an insulinoma. A diagnosis of insulinoma is made when the fasted glucose is low at the same time that the insulin level is high, since that is inappropriate. When a patient is hypoglycemic, insulin secretion should be shut down.

272
Q

You should not run a HDDS (a discriminating test) before running a screening test like LDDS.

Explain why the results can make it hard to differentiate between a normal patient and one with PDH.

A

You have to think about the theory behind the HDDs. The theory is that even though a pituitary dependent tumor might not suppress with a low dose of steroids, it could suppress for 8 hours with even higher doses. It might even suppress at 4 hours and stay suppressed at 8 hours.

But remember that a normal dog will suppress at 8 hours with the low dose of steroids, which means it will ALSO suppress with high dose of steroids.

That means that the results for both a normal dog and a PDH dog that suppresses at both 4 and 8 hours will have the same curve. Therefore, if you do a HDDS test first, you can’t differentiate between a normal dog and one that has PDH.

273
Q

What species is a thyroid panel for?

A

Dogs

274
Q

“Tim”, 12 yr old, MC, DSH

Tim has a recent history of PU/PD. His blood glucose is 310 and he has trace glucose in his urine.

What do you recommend next?

A

This is the ideal situation to run a fructosamine since it will help you difference chronic hyperglycemia from epinephrine-induced hyperglycemia. It is not safe in this situation, given the barely detectable glucosuria, to start insulin. Better to wait for 24 hours for a test that helps you feel more confident in your diagnosis. Retesting the urine may or may not change the result. We do not measure insulin levels in our diabetic patients, so please don’t select insulin levels for any answers on this exam!

275
Q

“Michael”, 5 yr old, MC, Keeshond

Michael has been diagnosed with DKA and you are treating him with fluids and insulin. This morning his PCV is 25% (low).

What would you like to measure next?

A

Phosphorus

276
Q

“Boggy”, 2 yr old, MC, lab

Boggy presents to your emergency clinic with acute onset of vomiting, diarrhea, and abdominal discomfort. You suspect Addison’s, but on his venous blood gas, his potassium and sodium are normal.

What are the possible differentials diagnoses? Select all that apply.

A

Atypical Addisons
Pancreatitis
GI foreign body

277
Q

“Lila”, 12 yr old, FS, mixed breed dog

Lila has hair loss on her sides and thinning skin. She presents with lethargy, anorexia and a single episode of vomiting.

Of the possible diagnoses listed below, which one is the most likely?

A

The clinical signs of hair loss along her trunk should make you think Cushing’s or hypothyroidism. The thinning skin points to Cushing’s.

But, more important is the patients with pituitary-dependent Cushing’s or adrenal, or hypothyroidism are not sick!

Addisonian patients are sick but they don’t have thinning skin or an endocrine alopecia pattern.

A patient with iatrogenic Cushing’s will have the clinical signs of Cushing’s, but if the exogenous steroid is abruptly stopped, they will develop an Addisonian crisis (which is atypical since electrolytes are normal) and present with GI signs and shock. Remember the cortisol allows us to respond to stress, including raising blood pressure during stressful events, so you don’t need a mineralocorticoid deficiency to present in shock.

278
Q

“Liddy”, 3 yr old, FS, Westie

Presents in an Addisonian’s crisis with a potassium of 6.8 (high).

Your supervising clinician recommends giving insulin and dextrose. Why?

A

Insulin will cause glucose uptake into the cells. Glucose uptake is a co-transporter with potassium, which helps move potassium from the bloodstream into the intracellular space where it normally resides. Don’t forget to provide glucose when giving insulin!

Addisonian patients have normal or decreased glucose, not hyperglycemia.

Addisonian patients mild hypercalcemia, not hypocalcemia.

Although shifting K+ into the cells may help somewhat with the acidosis, it is not the primary goal of insulin and glucose as the acidosis is almost always corrected with fluid administration.

Insulin-glucose therapy does not impact the sodium levels.

279
Q

“Daschell”, 3 yr old, MC, Portuguese water dog

You suspect atypical Addison’s and perform a baseline cortisol (screening test for Addison’s). The value is 1.5 (low).

What is your next best step?

A

Perform an ACTH stim

280
Q

Would you use DOCP in atypical Addison

A

NO

281
Q
A

Clinical Science (5 decks)

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