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DWT exam 4 > Clin path > Flashcards

Clin path Flashcards

1
Q

osmolarity vs osmolality

A

Both: Concentration of a solute

Osmolarity
* Moles per liter (per volume)
* Calculated: Na, K, Glu, Urea
* 2(Na +K) + glu/18 + BUN/2.8

Osmolality
* Moles per kilogram (per weight)
* Measured: Osmometer

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2
Q

Osmo gap

A

Osmo Gap = Osmolality (measured) – Osmolarity (calculated)
normal gap: -5 - 15

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3
Q

increased osmo gap causes

A

Ethylene glycol
Propylene glycol
Ethanol
Mannitol
Radiographic contrast

An osmotic agent not accounted for in the osmolarity formula

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4
Q

response to hyperosmolality

A

thirst center stim> promote water intake
ADH released> promotes kidneys to absorb water

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5
Q

response to hypoosmolality

A

decreased water intake
increased water secretion

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6
Q

hypovolemia is detected by:

A

kidneys (Juxtagolmerular cells)
* activate renin-angiotensin-aldosterone
* reabsorb Na+, water, secrete K+

carotid sinus baroreceptors
* detect hypovolemia, and ADH > vasoconstriction

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7
Q

hypernatremia and hyperchloremia

A

dehydration
* inadequate water intake
* pure water loss (diabetes insipidus)
* osmotic diuresis (diabetes mellitus)
* hyperaldosteronism
* excess intake (salt poisoning)

glucocorticoids, endotoxins, hypercalcemia

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8
Q

acquired diabetes insipidus

A

dehydration due to water loss > hypernatremia and hyperchloremia
can be caused by glucocorticoids, endotoxins, hypercalcemia

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9
Q

Hyponatremia & Hypochloremia

A

Sodium & chloride loss (anywhere you can lose water)
* GI tract (diarrhea, diuresis)
* Kidneys
* Skin (sweat)

Excess water (heart failure)
Sodium & chloride shifting
* Cell lysis (K+ Leaks out, Na+/Cl- leaks into cell)
* Cavitary (3rd) space (uroabdomen)
* diabetes mellitus

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10
Q

selective hypochloremia

A

vomiting
metabolic alkalosis

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11
Q

selective hyperchloremia

A

Secretional metabolic acidosis
diarrhea
aka hyperchloremic metabolic acidosis

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12
Q

hyperkalemia

A

increased potassium
Increased intake
* IV fluids

decreased renal excretion
* renal failure (anuric or oliguric)
* hypoadrenocorticism (Addisons)
* urinary tract obstruction

postassium shifting
* Metabolic acidosis
* Cell lysis
* Cavitary (3rd) space (uroabdomen)

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13
Q

decreased Na:K ratio

A

less than 27 (decreased Na, increased K)
diseases:
* Hypoadrenocorticism (Addison’s disease, less than 22)
* Renal failure
* Urinary tract obstruction
* Uroabdomen
* Rhabdomyolysis
* Diabetic ketoacidosis
* Diarrhea

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14
Q

biologically active form of Ca

A

free Ca
not bound to protein or anions

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15
Q

Major factors affecting Ca

A

Age: puppies have higher Ca
intestinal absorption: require vit D
resorption from bone
resorption from tubular fluid

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16
Q

Major factors affecting serum P levels

A

renal clearance
intestinal absorption
resorption from bone
shifting from ECF/ICF
Age (younger=higher)

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17
Q

PTH

A

activated by decreased serum Ca levels
causes:
* bone: increase resorption of Ca and P from bone
* increased absorption of Ca and P from intestine
* Kidney: increased resorption of Ca, excretion of P

Net effect: Increase Ca, decrease P

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18
Q

Vitamin D

A

net effect: Increase Ca and P

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19
Q

calcitonin

A

net effect: decrease Ca and P

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20
Q

Hypocalcemia

A

Hypoalbuminemia
Primary hypoparathyroidism
Milk fever
Renal secondary hyperparathyroidism
Nutritional secondary hyperparathyroidism
others

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21
Q

Primary hypoparathyroidism

A

Uncommon
Damage to the gland by trauma, inflammation, surgical removal
* No response to hypocalcemia
* Decreased resorption from bone, decreased intestinal absorption
* Hyperphosphatemia develops and inhibits vitamin D activation > worsening of hypocalcemia

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22
Q

Milk fever (parturient hypocalcemia)

A

Most common in dairy cattle
High calcium diet during the dry period leads to suppression of the parathyroid gland
Sudden demand for Ca in the milk > decrease in serum Ca
Parathyroid gland secretes PTH, but its effects are too slow to mobilize sufficient Ca in time
Continued loss of Ca into milk > severe hypocalcemia and clinical signs
* Recumbency, bradycardia, arrhythmias

Mildly decreased P, mildly increased Mg, and mildly increased glucose also common
Similar conditions can occur in dogs, ewes, and mares

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23
Q

Renal secondary hyperparathyroidism

A

↓Ca
* Decreased renal reabsorption of calcium
* Decreased hydroxylation (activation) of vitamin D
* Increase in P > complexing with Ca (metastatic mineralization)

Parathyroid hyperplasia > increased PTH
↑P due to decreased renal excretion of P

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24
Q

Nutritional secondary hyperparathyroidism

A

Diets with ↓Ca:P
* All meat diets in carnivores
* Excessive grain diets in horses
* High grain/nut diets or lack of UVB source in reptiles

Serum Ca is often WRI, but may be decreased
Decreased Ca stimulated PTH secretion
* Resorption from bone > “rubber jaw”

Serum P may be increased if due to high P diet, but won’t be increased as much as is seen with renal secondary hyperparathyroidism

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25
Q

hypercalcemia causes

A

Young, growing animals
Hyperparathyroidism
Humoral hypercalcemia of malignancy
Vitamin D toxicity
others

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26
Q

Primary hyperparathyroidism

A

Parathyroid adenoma secretes PTH
increased Ca
P may be decreased or WRI

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27
Q

Humoral hypercalcemia of malignancy (HHM)

A

Secretion of PTH-like hormone, PTHrP
Increased Ca
P may be decreased or WRI
Most common neoplasms are lymphoma and apocrine gland anal sac adenocarcinoma (AGASACA)
Others also possible

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28
Q

Vitamin D toxicity

A

rodenticides, supplements, some plants
Vit D: Increase serum Ca and P
mineralization of tissues > death
* if Ca x P >80 mineralization

29
Q

Hyperphosphatemia

A

Hypoparathyroidism
Decreased GFR for any reason
Vitamin D toxicosis
Shift of PO4 from ICF to ECF

30
Q

Hypophosphatemia

A

Equine renal failure
Prolonged anorexia
Milk fever

31
Q

Major factors affecting serum Mg

A

Serum protein concentration
GI absorption
* Rumen in ruminants
* Distal SI and colon in monogastrics
* Enhanced by Vit D
* Inhibited by dietary Ca and PO4

Excretion
* Fecal
* Kidneys
* Mammary gland

32
Q

Hypermagnesemia

A

Decreased urinary excretion
* Renal failure and other causes of decreased GFR (herbivores)

Shift from ICF to ECF
* In vivo hemolysis or delayed RBC separation from serum (except cattle)

Increased PTH: Milk fever

33
Q

Hypomagnesemia

A

Hypoproteinemia
Inadequate GI absorption
* Prolonged anorexia
* Calves on whole milk diet
* Grass tetany

34
Q

Grass tetany

A

Lush pasture with low Mg
Mg needed for PTH function
↓Mg and ↓PTH
May lead to hypocalcemia
Hypocalcemia may not respond to treatment until hypomagnesemia is corrected

35
Q

Hypothalamic-pituitary-adrenal axis (HPAA)

A
36
Q

Hyperadrenocorticism in dogs

A

Clinical signs: PU/PD, Polyphagia, Muscle weakness, pendulous abdomen, Alopecia, thin skin, Hepatomegaly, Panting

Clin path abnormalities:
* Elevated ALP (dogs)
* Stress leukogram
* Isosthenuria/hyposthenuria
* Hypercholesterolemia
* Recurring urinary and skin infections
* Hyperglycemia/concurrent DM

Cushings

37
Q

Types of Hyperadrenocorticism in dogs

A

Pituitary dependent (secondary HAC)
* 80% of canine HAC
* Pituitary microadenoma

Adrenal dependent (primary HAC)
* 20% of canine HAC
* Adrenocortical adenoma or adenocarcinoma
* May produce cortisol precursors (17-hydroxyprogesterone) instead of cortisol

Iatrogenic
* Exogenous glucocorticoid administration

38
Q

Pituitary dependent (secondary HAC)

A

80% of canine HAC
Pituitary microadenoma

39
Q

Adrenal dependent (primary HAC)

A

20% of canine HAC
Adrenocortical adenoma or adenocarcinoma
May produce cortisol precursors (17-hydroxyprogesterone) instead of cortisol

40
Q

Iatrogenic Hyperadrenocorticism in dogs

A

Exogenous glucocorticoid administration

41
Q

hyperadrenocorticism screening tests

A

Urine cortisol-creatinine ratio (UCCR)
Low-dose dexamethasone suppression test (LDDST)
ACTH stimulation test

42
Q

hyperadrenocorticism Confirmatory/differentiating tests

A

Endogenous ACTH (eACTH)
Low-dose dexamethasone suppression test LDDST
High-dose dexamethasone suppression test (HDDST)
Abdominal ultrasound
Head and abdominal CT/MRI

43
Q

Urine cortisol-creatinine ratio (UCCR)

A

Collect urine in the morning at home and measure cortisol and creatinine
Positives
* Very sensitive
* 90% of dogs with HAC will have elevated UCCR
* Easy and inexpensive
* Owners can collect urine at home = less stress to patient

Negatives
* Poor specificity
* 20% specificity
* 80% false positive rate
* Use primarily in patients with only a few signs of HAC
* Use to rule HAC OUT, DO NOT USE to rule HAC in

44
Q

Low-dose dexamethasone suppression test (LDDST)

A

Baseline cortisol measured, dexamethasone administered, cortisol measured again at 4h and 8h
* Use the 8h value to rule in/out HAC
* Use the 4h value to differentiate PDH from AT

Positives:
* Cheaper than ACTH stimulation test
* May differentiate PDH from AT
* High sensitivity

Negatives:
* Lower specificity than ACTH stim test
* High false positive rate
* Best to use with patients who have classic clinical and CBC/chem features of HAC

45
Q

ACTH stimulation test

A

Measure baseline cortisol, give ACTH, measure cortisol again in 1-2h
Positives
* Highest specificity (low false positive rate)
* Does not require all-day hospitalization (test done in 1-2h)
* May be less stressful to patient
* Can identify iatrogenic HAC

Negatives
* Less sensitive than LDDST
* More expensive than LDDST

Use to screen patients that are not the classic presentation
* Less likely to get false positive than with LDDST

Also used to monitor therapy

46
Q

Key points Comparing the screening tests (UCCR vs ACTH stim vs LDDST)

A

UCCR
* High sensitivity
* High negative predictive value
* Poor specificity

ACTH stimulation test
* Most specific test
* High positive predictive value
* Not as sensitive as the others

LDDST
* High sensitivity
* High negative predictive value
* Reliable if clinical signs and clin path data are supportive of HAC
* Specificity is poor if there is non-adrenal illness

47
Q

High-dose dexamethasone suppression test (HDDST)

A

Used to help differentiate PDH from ADH
Only about 14% of the dogs with PDH that don’t suppress at 8h on the LDDST will suppress at 8h on the HDDST

dont really use

48
Q

High-dose dexamethasone suppression test (HDDST)

A

Used to help differentiate PDH from ADH
Only about 14% of the dogs with PDH that don’t suppress at 8h on the LDDST will suppress at 8h on the HDDST

dont really use

49
Q

Endogenous ACTH (eACTH)

A

Single time-point measurement of ACTH
Very sensitive to specimen handling, consult lab for best procedure
Positives
* Good at differentiating PDH from AT

Negatives
* ACTH is very unstable > prone to pre-analytical error and falsely decreased values
* Some assays have a poor detection limit
* Misclassification of HAC type in 15-25% of cases

Use to differentiate PDH from AT ONLY after HAC is ruled in
Do NOT use to screen for HAC

50
Q

Hypoadrenocorticism causes and clinical signs

A

Addisons
Cause:
* >90% Primary: lymphocytic adrenalitis > destruction of all three layers of adrenal cortex > lack of aldosterone and cortisol; “atypical Addison’s disease” is a lack of cortisol only
* Secondary: lack of ACTH > lack of cortisol
* Iatrogenic: chronic corticosteroid treatment > atrophy of pituitary and adrenal glands

Clinical signs:
* Occurs most commonly in** young to middle-aged dogs;** rare in cats
* Lethargy, weakness, vomiting, diarrhea, abdominal pain, anorexia; often intermittent
* Bradycardia, collapse, shock, hypovolemia

50
Q

Hypoadrenocorticism causes and clinical signs

A

Addisons
Cause:
* >90% Primary: lymphocytic adrenalitis > destruction of all three layers of adrenal cortex > lack of aldosterone and cortisol; “atypical Addison’s disease” is a lack of cortisol only
* Secondary: lack of ACTH > lack of cortisol
* Iatrogenic: chronic corticosteroid treatment > atrophy of pituitary and adrenal glands

Clinical signs:
* Occurs most commonly in** young to middle-aged dogs;** rare in cats
* Lethargy, weakness, vomiting, diarrhea, abdominal pain, anorexia; often intermittent
* Bradycardia, collapse, shock, hypovolemia

51
Q

Hypoadrenocorticism clin path abnormalities

A

Azotemia, hyperphosphatemia, inadequately concentrated urine
Hyponatremia, hyperkalemia, Na:K ratio <27
Absence of stress leukogram
+/- hypoglycemia, anemia, hypercalcemia

52
Q

Tests for hypoadrenocorticism

A

Baseline cortisol
* Use to rule OUT hypoadrenocorticism
* Use when there is less suspicion of Addison’s
* A normal baseline cortisol rules out Addison’s
* Decreased baseline cortisol does NOT confirm hypoadrenocorticism

ACTH stimulation test
* Confirmatory test
* Use when there is high suspicion of Addison’s
* Addisonian animals will have a flat ACTH response

53
Q

Normal thyroid pathway

A
  1. TRH stims release of TSH from pituitary
  2. TSH stims thyroid to secrete T4 (and some T3)
  3. T4 has negative feedback on hypothalamus and pituitary
54
Q

tests for hyper/hypothyroid

A

hyperthyroid: TT4, fT4
hypo: TT4, fT4, TSH

55
Q

Hyperthyroidism in cats

A

Cause: Thyroid adenoma (primary hyperthyroidism)
Generally occurs in middle-aged to older cats
Clinical signs:
* Hyperactivity
* weight loss despite normal appetite or polyphagia
* +/- PU/PD, tachycardia, vomiting, patchy alopecia, unkempt haircoat,

Clin path abnormalities:
* mild to moderate increase in ALP, mild increases in ALT, AST
* hypocalcemia and hyperphosphatemia
* +/- azotemia, mild polycythemia, stress leukogram

56
Q

TT4

A

total T4
Increased TT4 = hyperthyroidism
* TT4 in upper half of the reference interval > gray zone (10% of hyperthyroid cats will fall in this area)
* TT4 secretion is pulsatile, can be variable in hyperthyroid cats
* Non-thyroidal illness can falsely decrease values

Use as a screening test to rule out hypothyroidism
* 95% hypothyroid dogs will have ↓TT4
* 20% dogs without hypothyroidism may have ↓TT4 – “euthyroid sick” (false positives for hypothyroid)
* Rarely, autoantibodies may falsely increase TT4

57
Q

fT4

A

free T4
Use when there is clinical suspicion of hyperthyroidism, but TT4 is in the upper half of the reference interval
Non-thyroidal illness can cause false increases
DO NOT USE fT4 ALONE FOR DIAGNOSIS OF HYPERTHYROIDISM

Use equilibrium dialysis fT4 test > not affected by non-thyroidal illness

58
Q

Hypothyroidism in dogs

A

Cause:
* 95% Primary: lymphocytic thyroiditis > follicular destruction
* ≤5% Secondary: structural or biochemical lesion in the pituitary: pituitary tumor/cyst, pituitary hypoplasia, TSH deficiency in giant schnauzers

Clinical signs
* Weight gain without increase in food intake
* Lethargy
* Cold intolerance, heat-seeking behavior
* Dull haircoat, alopecia, hyperpigmentation – without pruritus
* +/- secondary skin disorders: seborrhea, dry coat, pyoderma

Clin path abnormalities
* Hypercholesterolemia (80%) and hypertriglyceridemia
* Mild non-regenerative anemia (30%) or hct in low end of RI
* +/- Increased liver enzymes, increased CK

59
Q

Lymphocytic thyroiditis

A

Hypothyroidism in dogs
Clinical signs develop gradually over years
Lymphocytes and plasma cells produce antibodies directed at thyroglobulin (most common), colloid, TT3, TT4

60
Q

TSH test

A

Theoretically, dogs with primary hypoparathyroidism should have elevated TSH
Only about 2/3 hypothyroid dogs have elevated TSH
Some of these may have secondary hypothyroidism (↓TSH> ↓T4)

61
Q

Diabetes mellitus

A

Clinical signs:
* PU/PD
* Weight loss despite normal or increased appetite
* Decreased appetite
* +/- diabetic cataracts (dogs), recurring skin and urinary infections

Clin path abnormalities
* Dehydration: erythrocytosis, increased Pi, azotemia
* Isosthenuric or minimally concentrated urine, glucosuria, ketonuria
* Hyponatremia, hypochloremia, +/- hypokalemia, +/- hypophosphatemia
* Hypercholesterolemia, hypertriglyceridemia
* Acidosis, increased anion gap (ketoacidosis)
* Hyperosmolality
* Increased hepatic and pancreatic enzyme activities

62
Q

Diagnosis of Diabetes Mellitus

A

Differentiate from other causes of hyperglycemia
Severity of hyperglycemia
* DM typically >250 mg/dL
* Stress/excitement in cats can be >300 mg/dL
* Fast small animals for 12h before blood collection

Urine glucose/ketones
* Glucosuria expected with DM
* Glucosuria possible but unlikely with transient increases
* Ketonuria may be present with DM, but is not expected with stress/excitement

Fructosamine
* Estimate of glucose concentrations over the previous 2-3 weeks
* Will not be increased with stress/excitement

63
Q

Fructosamine

A

Monitoring of insulin therapy
Marked elevation with poor control
Mild elevation with good control
Considerable variability regardless of control
Single blood draw – easier on owner and patient than glucose curve

64
Q

Glucose curve

A

Monitor glucose concentration over an 8, 12, or 24h period – document time and dose of insulin administration and meals
Will detect Somoygi effect with insulin overdosing
Time-consuming, difficult for owner to do, stressful for patients in-hospital > accuracy?

65
Q

Hypoglycemia causes

A
  • Insulin overdose
  • Extreme exertion – hunting dogs, endurance horses
  • Glycogen storage diseases – rare
  • Hepatic insufficiency – should see hypoalbuminemia, decrased BUN, and increased serum bile acids
  • Neonatal (all species)/juvenile (toy breed puppies <6 mo) – fasting or other stressors
  • Bovine ketosis/lactational hypoglycemia
  • Pregnancy – dogs and sheep
  • Sepsis
  • Xylitol toxicosis in dogs
  • Insulinoma – dogs, cats, ferrets
66
Q

Somoygi effect

A

insulin overdosing with rebound hyperglycemia

67
Q

Insulinoma

A

Beta cell tumor > secretes insulin > hypoglycemia
Patients with insulinomas may be euglycemic
Measure serum insulin at a time when patient is hypoglycemic
Increased insulin or insulin WRI with concurrent hypoglycemia > insulinoma
Hypokalemia is also frequently associated with hyperinsulinism

DWT exam 4 (10 decks)

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