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clin path > exam 2 things to remember > Flashcards

exam 2 things to remember Flashcards

1
Q

chronic lymphocytic leukemia

A
  • over 30,000
  • CML- rare, CLL common- small and well differentiated
  • clinical signs: asymptomatic lymphocytosis +/- anemia and thrombocytopenia
  • increase in small lymphocytes on bone marrow
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2
Q

acute leukemia

A
  • see blasts in blood
  • short survival time
  • differentiate from stage V lymphoma
  • clinical signs: anemia, thrombocytopenia
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3
Q

myeloproliferative leukemia

A

-granulocytic, erythroid, megakaryocytic

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4
Q

lymphoproliferative leukemia

A

-lymphoblastic, lymphocytic, plasma cell (multiple myeloma)

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5
Q

multiple myeloma

A
  • Bence-Jones proteins in urine
  • > 20% plasma cells in bone marrow
  • monoclonal/biclonal gammopathy
  • lytic lesions in bone marrow
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6
Q

BUN

A
  • used to assess GFR

- in ruminants correlate changes in BUN with changes in CREA and USG to predict renal disease

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7
Q

increased BUN

A
  • increased protein in upper GI (upper GI bleed), increased production
  • decreased GFR
  • renal reabsorption varies with rate of flow through tubules
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8
Q

decreased BUN

A
  • decreased urea production by liver: portosystemic shunt, decreased protein in diet, intestinal loss of protein (PLE), hepatic insufficiency
  • renal causes of decreased BUN: decreased water resorption in PCT, increased GFR, increased tubular flow (osmotic diuresis, less concentrated urine)
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9
Q

Creatinine

A
  • muscle mass matters
  • filtered by glomeruli and excreted, not reabsorbed or changed by kidney
  • excellent indicator of GFR
  • increased creatinine= decreased GFR, possibly altered nephron function
  • decreased creatinine- not clinically significant
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10
Q

SDMA

A
  • only IDEXX, excreted almost exclusively by kidneys, not impacted by extrarenal factors, early indicator of kidney disease
  • used for monitoring and management
  • if SDMA increased and creatinine is normal, rule out all other causes of decreased GFR besides renal failure
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11
Q

causes of pre-renal proteinuria

A
  • physiologic: hypertension, fevers, seizures, exercise

- increase small proteins in blood: hemoglobin, myoglobin, para-proteins (Bence Jones)

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12
Q

causes of renal proteinuria

A
  • Glomerulonephritis

- tubular proteinuria- acute renal disease/ Fanconi syndrome

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13
Q

Post-renal proteinuria

A
  • hemorrhage

- inflammation

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14
Q

UPCR

A
  • normal: <5
  • tubular or glomerular: >.5
  • glomerular: >1.0= most severe, only time you will see hypoalbuminemia
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15
Q

isosthenuria

A

-1.008-1.012

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16
Q

pre-renal azotemia

A
  • before kidneys (blood, liver, GI)
  • increase in BUN +/- increase in CREA, increase in SPG, P & Mg
  • Ddx: decreased renal bloodflow–> decreased GFR, dehydration
  • Ddx: increased urea production: upper GI bleed
  • dehydrated animal with normal renal function: decreased urine function, increased urine spg (concentrated)
  • dehydration or bleeding
  • increased urea production- due to increased amino acids, decreased rumen motility or upper GI bleed
  • increased creatinine due to muscle or in neonatal foals
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17
Q

Renal azotemia

A
  • increased BUN, CREA, decreased specific gravity
  • isosthenuria
  • increased water loss
  • check analytes: increase P, Ca varies based on- species, cause, or age, increased PTH, decreased phosphorus in chronic, and increased potassium in acute, metabolic acidosis, Na-CL usually normal, decreased in chronic
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18
Q

post-renal azotemia

A
  • after kidneys (ureter, bladder, urethra)- increase in BUN, CREA, variable specific gravity
  • obstruction of urinary outflow distal to nephron
  • uroabdomen
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19
Q

Glomerulonephropathy

A
  • hypoalbuminemia
  • proteinuria
  • evidence of renal insufficiency (?)
  • nephrotic syndrome= protein losing nephropathy, leads to abdominal effusion
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20
Q

acute renal failure

A
  • usually good BCS
  • anorexia, V+, D+, halitosis
  • renal: oliguric–> anuric
  • neuro: depressed to non-responsive, seizures
  • etx: toxic, ischemia, infeciton
  • decreased GFR, azotemia- FAST
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21
Q

chronic renal failure

A
  • usually old cats
  • poor BCS, dehydration, anorexia, V+, D+, halitosis, polyuria, depressed, hypertension
  • non-regenerative anemia, azotemia, hyperphosphotemia, hypokalemia, metabolic acidosis–> more severe at end stage, isosthenuria
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22
Q

uroabdomen

A
  • males
  • trauma, chronic urethral obstruction
  • abdominal effusion: increased K, decreased sodium and Cl in serum
  • increased Na and CL in urine
  • urea and K in plasma
  • bloodwork: decreased sodium, increased potassium, decreased chlorine, increased BUN
  • increased CREA in plasma
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23
Q

Birubinuria

A
  • orange urine
  • some normal in hypersthenuric dog
  • hyperbilirubinemia- cholestasis, hemolysis, fever, prolonged fasting (esp in horses)
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24
Q

Maldigestion

A
  • exocrine pancreatic insufficiency
  • voluminous, poorly formed stool, flatulence, malodorous
  • decrease in weight
  • chronic biliary obstruction
  • increase in serum bile acids
  • TLI test
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25
Q

Malabsorption

A
  • intestinal disease
  • voluminous, poorly formed grey feces, weight loss
  • hypoproteinemia
  • protein losing enteropathy
  • intestinal lymphoma
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26
Q

TLI

A
  • test for exocrine pancreatic insufficiency
  • dogs: > 5ug/L=normal
  • <2.5 ug/L= EPI
  • grey zone= 2.5-5 ug/L
  • cats= <8 ug/L= EPI
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27
Q

vitamin B and folate

A
  • both decreased= generalized malabsorption
  • folate decreased, B12 normal= proximal SI defect
  • folate normal, B12 decreased- distal SI defect
  • cats: EPI may result in decreased IF release which leads to decreased B12- do TLI to determine if generalized malabsorption or EPI, intestinal disease may accompany EPI
  • dogs: stomach also secretes some IF, B12 levels slightly decreased
  • increased folate, decreased B12= bacterial overgrowth
  • decreased folate or B12= PLE, increased fecal alpha-1 protease inhibitor, decreased albumin and globulin
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28
Q

albumin binds Ca

A

-decreased albumin= apparent hypocalcemia

29
Q

fructosamine increases with:

A

-hyperglycemia, diabetes mellitus

30
Q

regulation of calcium

A
  • increased by: PTH, vitamin D (calcitriol)

- decreased: calcitonin

31
Q

What changes would you see in calcium and phosphorus in renal disease?

A

-decreased calcium, increased phosphorus

32
Q

Calcium

A
  • hypoalbuminemia= hypocalcemia
  • acidosis: increased ionized calcium
  • alkalosis= decreased ionized calcium
33
Q

common causes of hypocalcemia

A
  • renal disease: no vit D activation by kidney
  • ethylene glycol
  • pancreatitis: Ca 2+ binds necrotic fat
  • eclampsia
  • sepsis
34
Q

uncommon causes hypocalcemia

A
  • hypoparathyroidism: No PTH
  • nutritional secondary hyperparathyroidism
  • intestinal malabsorption
  • fleet enemas
  • citrate tox
  • hypomagnesia needed for PTH production and release
  • massive tissue degeneration
  • hypercalcitonism
35
Q

hypercalcemia

A
  • hypercalcemia of malignancy
  • granulomatous inflammatory disease
  • renal disease
  • idiopathic
  • vitamin D toxicosis
  • Addison’s
  • primary hyperparathyroidism
  • renal disease in horses
36
Q

regulation of phosphorus

A
  • decrease- PTH and calcitonin

- increase- vitamin D

37
Q

hypophosphatemia

A
  • metabolic acidosis
  • osmotic diuresis
  • primary hypoparthyoidism
  • hypercalcemia of malignancy
  • vitamin D deficiency
  • chronic renal failure in horses
  • increased phosphorus and decreased calcium- leads to mineralization
38
Q

hyperphosphatemia

A
  • decreased GFR
  • ruptured bladder
  • vitamin D toxicosis
  • acidosis
  • excessive intake
  • primary hypoparathyroidism
39
Q

hypokalemia

A
  • chronic renal failure

- cats and cows in chronic renal failure

40
Q

hyperkalemia

A
  • oliguria/anuria

- renal failure/ end stage chronic renal failure

41
Q

sodium and chloride

A
  • normal in most cases of renal failure
  • hyponaturemia and hypochloremia- sometimes in chronic renal failure expecially in horses and cows
  • uroabdomen
42
Q

When would you find metabolic acidosis?

A

in severe renal disease

43
Q

glucose regulation

A
  • insulin: decrease blood glucose
  • glucocorticoids: increase blood glucose
  • catecholamines- increase blood glucose
  • glucagon- increase blood glucose
  • growth hormones- increased blood glucose
44
Q

-hypoglycemia

A
  • apparent–> failure to remove serum from clot within 30 mins
  • increased insulin levels: insulinoma (hypoglycemic with high insulin), overdose
  • liver disease
  • sepsis
  • ketosis/pregnancy toxemia
  • neonatal/juvenile
  • starvation/ malabsorption/exertion
  • neoplasia
  • xylitol/ackee fruit
45
Q

hyperglycemia

A
  • glucocorticoids
  • catecholamines
  • diabetes mellitus
  • eating
  • pancreatitis
  • hormone imbalance
  • ethylene glycol toxicosis
  • cattle: proximal duodenal obstruction, milk fever
46
Q

hypomagnesemia

A
  • loss through- GI (malabsorption and diarrhea), kidney
  • dietary deficiency in ruminants
  • diabetes mellitus
  • hypercalcemia
  • hyperaldosteronism
  • third space syndromes
  • hypokalemia
  • impaired PTH production
47
Q

hypermagnesemia

A

-compromised renal function

48
Q

diabetes mellitus

A
  • dehydration
  • glucosuria, ketonuria, osmotic diuresis
  • low urine spg, electrolyte loss
49
Q

leakage enzymes

A
  • released with cell injury

- AST,ALT, CK, SDH, GLDH

50
Q

induced enzymes

A
  • produced with cell injury

- ALP, GGT

51
Q

CK

A
  • muscle specific

- increase with muscle damage: IM injection, necrosis, trauma, exercise, downers, anorexic cats

52
Q

AST

A

-liver and muscle, look at CK and ALT

53
Q

CK and AST

A
  • CK increases rapidly during injury, once resolves goes back to normal in 48 hs
  • AST lasts longer
54
Q

ALT

A
  • liver specific

- with super severe muscle damage can somewhat increase ALT

55
Q

myoglobin

A

-released by dying muscle

56
Q

hepatocellular injury

A
  • look at leakage enzymes: ALT, AST, SDH, GLDH
  • old dogs: chronic hepatitis
  • young dogs: portocaval shunt
  • measure bile acids
57
Q

hepatic necrosis

A
  • diffuse: increase in leakage and induced enzymes and bile acids
  • focal: usually no lab changes
58
Q

cholestasis

A
  • ALT and GGT
  • cholangitis, bile duct obstruction, hepatic lipidosis (biopsy to diagnose)
  • increase in total bilirubin
  • cats= GGT for cholestasis, ALT for hepatic lipidosis
59
Q

liver function test

A
  • removed by liver: bilirubin, cholesterol, ammonia, exogenous stuff- failing liver can’t remove this
  • liver makes: albumin, urea (BUN), cholesterol, coag factors: if failing–> decreases
  • bilirubin: increases with RBC destruction and blockage of bile flow
  • bile acids:increase in deviation of portal circulation and liver damage, decrease: in hepatocyte uptake and cholestasis
60
Q

liver failure

A
  • leakage–> normal/increased
  • induced: moderately increased
  • bilirubin: increased
  • ammonia: increased
  • what liver makes: decreased
61
Q

chronic hepatitis

A
  • leakage enzymes increased
  • induced enzymes increased
  • bilirubin is normal to increased
  • bile acids increased
  • loss of function
62
Q

portosystemic shunt

A

-will see microcytic anemia, increased bile acids

63
Q

cardiac

A
  • myocardial cell injury: ALT, CK, troponin
  • functional proteins: naturetic peptides
  • BNP increase in production with ventricular hypertrophy, tachycardia, hypoxia, expanded fluid volume, decreased renal clearance of peptide
64
Q

pancreas

A
  • amylase levels> 3-4x upper end of normal suggest pancreatic injury
  • lipase >2x upper end of normal suggests pancreatic injury, exception: dogs on steroids
  • TLI to detect EPI- dogs- dexamethosone will increase increase TLI
  • PLI to detect pancreatitis- can be increased due to anticonvulsants
  • with pancreatitis: hyperglycemia, hypocalcemia, increase in liver enzyme
65
Q

secondary hyperlipidemia

A
  • hypothyroidism
  • diabetes mellitus
  • hypoadrenocorticism
  • pancreatitis
  • hepatic disease
  • nephrotic syndrome- hypocholesterolemia, PLE
66
Q

hypolipidemia

A
  • liver failure
  • maldigestion/absorption
  • PLE
  • starvation
67
Q

PLE

A

-decrased protein and cholesterol

68
Q

PLN

A

-decreased protein, cholesterol normal

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