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Year 1/2 > Support & Movement 2: Clin Path S1 > Flashcards

Support & Movement 2: Clin Path S1 Flashcards

1
Q

FIP findings/differentials

A
  1. HYPERBILIRUBINEMIA
    - Can be from LIVER
  • Can be pre-hepatic
    –> Cholestasis = hepatocytes are swollen and block off canaliculi, causes unconjugated bilirubin to build up in systemic vasculature
  • FUNCTIONAL cholestasis = from INFLAMMATION, which affects ability to transport bile
  • Can be post-hepatic
    –> There’s an obstruction to COMMON BILE DUCT, so bile (which has bilirubin) goes into intestinal tract –> builds up in systemic
  1. NEOPLASIA
    Can RULE OUT NEOPLASIA by doing a SERUM PROTEIN ELECTROPHORESIS (SPE)
    –> Look for monoclonal gammopathy
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2
Q

differentials for hypercalcemia (7)

A
  1. vitamin D toxicity
  2. addison’s disease (low Na and high K, LOW cortisol)
  3. renal disease
  4. osteolysis
  5. neoplasia
  6. granulomatous
  7. idiopathic
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3
Q

differentials for hypoglycemia (4)

A
  1. ARTIFACT
  2. SIRS/SEPSIS (systemic inflammatory response syndrome)
    - from OVERWHELMING inflammatory changes
  3. COUNTER-REGULATORY HORMONES (hormones that make glucose go down)
    - glucagon
    - epinephrine
    - growth hormone
    - glucocorticoid
  4. LIVER FAILURE
    - look for ABC GLUCOSE
    - decreases in albumin, BUN, creatinine, glucose
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4
Q

how does HYPERcalcemia cause PU/PD?

A

increased Ca causes the body to RESPOND LESS TO ADH, and as a result POLYURIA –> POLYDIPSIA

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5
Q

describe the countercurrent exchange mechanism in the kidney (location, overall process)

A

occurs in the LOOP OF HENLE

in ASCENDING loop, ACTIVE REABSORPTION OF Na/Cl INTO MEDULLARY INTERSTITIUM

in DESCENDING loop, PASSIVE REABSORPTION OF WATER INTO MEDULLARY INTERSTITIUM

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6
Q

in glomerular filtration, what STAYS INSIDE OF VESSELS?

A

WBCs, RBCs, LARGE PROTEINS (albumin)

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7
Q

basics of proximal convoluted tubule, loop of henle, distal convoluted tubule, and collecting duct

A

PCT (renal cortex)
- VERY METABOLICALLY active and LIKELY TO BE INJURED IN ACUTE KIDNEY INJURY
- REABSORBS WATER + other solutes in filtrate including water, NaCl, bicarb, etc.

Loop of Henle (renal medulla)
- MEDULLARY INTERSTITUM
- DESCENDING limb = PASSIVE reabsorption of water
- ASCENDING limb = ACTIVE reabsorption of NaCl

DCT (renal cortex)
- REABSORPTION depends on ADH activity, which is determined by the state of the body
- REABSORBS WATER/NaCl, and EXCRETES K

Collecting duct
- where DCTs will CONVERGE
- ADH helps ABSORB WATER and SOMETIMES UREA

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8
Q

what 2 things determine rate of glomerular filtration (GFR)?

A
  1. PRE-RENAL factors
    - blood pressure
    - cardiac output
    - volume of blood
    **IF any of these are decreased, then decreased GFR
  2. NUMBER of nephrons
    - 1 glomerulus/nephron
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9
Q

what products do we expect to build up if glomerulus not filtering blood efficiently? (4)

A

NITROGENOUS WASTE PRODUCTS

(1) Urea
(2) Creatinine
(3) Phosphorus
(4) Hydrogen ions

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10
Q

what determines the tubular flow rate?

A

GFR/glomerular filtration rate, which is determined by…

Blood volume, blood pressure, CO, and number of nephrons

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11
Q

what does LOW urea indicate?

A

the kidneys are DYSFUNCTIONAL

the collecting tubule CANNOT reabsorb urea efficiently, so it’s excreted as waste

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12
Q

what does HIGH urea indicate?

A

DEHYDRATION

the collecting tubule will REABSORB MORE WATER AND UREA in response to ADH

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13
Q

where are juxtaglomerular cells? what do they do?

A

cells in the DCT that help sense BP and activate RAAS to regulate it

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14
Q

proportion of INTRACELLULAR to EXTRACELLULAR fluid?

A

2/3 to 1/3

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15
Q

what 4 components make up EXTRACELLULAR fluid?

A

(1) BLOOD (plasma)

(2) INTERcellular fluid (interstitium

(3) RUMEN (large animal)

(4) TRANSCELLULAR fluid (third space)
- pleural cavity
- abdominal cavity
- pericardial cavity

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16
Q

what does decreased USG indicate?

A

that the KIDNEY TUBULES ARE DAMAGED, renal injury!

17
Q

carotid sinus baroreceptors and osmoreceptors in the hypothalamus

A

carotid sinus baroreceptors = detect BLOOD VOLUME and causes the HYPOTHALAMUS TO MAKE ADH
–> ADH works on DCT and collecting tubule to resorb water

osmoreceptors = IN the hypothalamus, RESPONDS TO HYPEROSMOLALITY (increased Na, among other solutes)
—> Tells body to DRINK MORE and HYPOTHALAMUS TO MAKE ADH

18
Q

5 differentials of HYPERnatremia

A

(1) DEHYDRATION

(2) LOSS OF FREE WATER

(3) LOSS OF FREE WATER&raquo_space; LOSS OF SODIUM

(4) SODIUM TOXICITY (SALT POISONING)

(5) EXCESS ALDOSTERONE (RARE)

19
Q

4 causes of dehydration? what CBC findings indicate dehydration?

A

CBC = erythrocytosis, increased plasma protein, HYPERNATREMIA

(1) NO ACCESS TO WATER

(2) ORAL LESION
–> drinking is painful

(3) ABNORMAL THIRST RESPONSE
–> brain tumor/lesion that PREVENTS thirst response, CANNOT SENSE THIRST

(4) NEUROLOGIC DISEASE
–> progressed so far that animal cannot drink

20
Q

hypernatremia –> loss of free water, which hormone/disease does this involve? 2 differentials?

A

ADH ISSUE! –> CAUSES DIABETES INSIPIDUS

(1) CENTRAL = issue with the HYPOTHALAMUS so that IT DOESN’T RELEASE ADH due to…
- trauma
- congenital
- tumor

(2) NEPHROGENIC = usually ACQUIRED issue where the DCT/COLLECTING TUBULE DO NOT RESPOND TO ADH, and caused by…
1. E. coli
2. Steroids
3. HYPERcalcemia
4. Persistent HYPOkalemia
5. Kidney disease

21
Q

hypernatremia –> loss of free water&raquo_space; loss of free sodium 2 differentials?

A

(1) osmotic diarrhea
(2) osmotic diuresis

22
Q

why is it important to treat hypernatremia SLOWLY?

A

if giving too many fluids too soon, can rush into cells and cause them to SWELL/LYSE/DIE

23
Q

3 differentials for NON-RENAL DISEASE causes of DECREASED USG

A

(1) DECREASED Na/Cl, medullary interstitial and washout
- FLUID therapy

  • Loop diuretics
  • LACK of aldosterone (Addison’s disease)
  • Kidney disease
  • DIURESIS from DISEASES LIKE…
    –> DIABETES MELLITUS
    –> INCREASED MANNITOL

(2) DECREASED urea
- PORTOSYSTEMIC SHUNT/HEPATIC FAILURE
–> liver usually converts ammonia –> urea

  • LACK of aldosterone (addison’s)

(3) DIABETES INSIPIDUS
- CENTRAL = congenital, trauma, tumor causing hypothalamus to NOT make ADH

  • NEPHROGENIC = ACQUIRED that causes DCT/collecting tubule not to RESPOND to ADH, 5 causes…
    (1) E. coli
    (2) Steroid use
    (3) Kidney disease
    (4) LACK of aldosterone (Addison’s)
    (5) PERSISTENT HYPOkalemia
24
Q

function of PTH/parathyroid hormone? what controls it?

A

to INCREASE Ca and DECREASE P

acts based on IONIZED Ca levels!

25
Q

NET effects of PTH, Calcitonin and Vitamin D IN BLOOD?

A

PTH = INCREASES Ca and DECREASES P

Vitamin D = INCREASES Ca/P

Calcitonin = DECREASES Ca/P

26
Q

what are the 3 components of TOTAL calcium?

A

(1) IONIZED calcium = ~50%
–> calcium that is FREE to perform REGULATION

(2) BOUND calcium = ~45%
–> calcium that is BOUND to ALBUMIN

(3) Calcium bound to OTHER THINGS = 5-10%
–> usually lactate or other substances that change daily

27
Q

6 things that determine levels of calcium in the body?

A

(1) AGE
–> younger animals tend to be more hypercalcemic

(2) ALBUMIN levels
–> determines the AMOUNT OF BOUND calcium, NOT ionized

(3) GI absorption
–> GI disease can negatively impact reabsorption by vitamin D/PTH

(4) RENAL function
–> helps to ACTIVATE VITAMIN D, so without it, vitamin D CANNOT increase Ca

(5) BONE resorption
–> controlled by vitamin D, calcitonin, and PTH

(6) Calcium and phosphorus interactions
–> if products are >70, then MINERALIZATION (bad)
–> Mineralization usually occurs in LUNGS/KIDNEY, BAD!

28
Q

what 7 things influence phosphorus levels?

A

(1) PTH
–> INCREASES Ca/Mg, DECREASES P

(2) Vitamin D
–> INCREASES Ca/Mg/P

(3) AGE/BONE GROWTH
–> animals <1.5 years = INCREASED P from bone growth

(4) **GLOMERULAR FILTRATION RATE
–> in normal animal, GFR keeps P LOW, but INCREASES IN GLOMERULAR DISEASE

(5) GI absorption
–> Vitamin D usually RESORBS Ca/P from intestines, INTERRUPTED IN DISEASE

(6) Bone
–> how much P is DEPOSITED vs. RESORBED from bone
–> in LACTATING COWS, likely to RESORB BONE to FREE Ca (and consequently P)

(7) INTRACELLULAR –> EXTRACELLULAR
–> if muscle is DISEASED/DYING, releases ATP so MORE P

29
Q

how much Mg is bound to albumin?

A

about half

30
Q

Magnesium and its relation to GI absorption, PTH, GFR, cell death

A

GI absorption
–> is ABSORBED with CALCIUM from GI
–> in GI disease, Mg DECREASES

PTH
–> INCREASES Mg/Ca, DECREASES P

GFR
–> Usually filters out Mg
–> if glomerular disease, then INCREASED Mg

Cell death
–> INCREASES Mg

31
Q

Milk fever & Grass tetany and Mg

A

(1) Milk fever
–> Hypocalcemic, so stimulates PTH and INCREASES Mg/Ca

(2) Grass tetany
–> Grass has LOW Mg, so tries to stimulate PTH, but ends up with LOW Ca and LOW Mg

32
Q

Hypercalcemia (HUGE acronym) with basics of each term

A

HARD-ON G

H = HYPOPARATHYROIDISM
- DOGS
- from parathyroid adenocarcinoma or carcinoma
- expect HYPOPHOSPHATEMIA and DECREASED USG (nephrogenic diabetes mellitus)
- diagnosis via measuring PTH and Ca PROPORTIONALLY moving

A = ADDISON’S DISEASE (HYPOadrenocorticism)
- LACK OF CORTISOL = BUILDUP OF Ca
- expect LACK of stress leukogram, LOW glucose, DECREASED Na/Cl, INCREASED K

R = RENAL DISEASE
- UNCOMMON, renal disease usually causes HYPOcalcemia, but MORE COMMON IN HORSES (usually excrete Ca in urine)
- CAN cause HYPERCALCEMIA + HYPERPHOSPHATEMIA

D = VITAMIN D INTOXICATION
- Rodenticides containing warfarin (clotting), cholecalciferol
- expect HYPERCALCEMIA and HYPERPHOSPHATEMIA, and >70 product so MINERALIZATION in LUNG, KIDNEY, and GI
- pulmonary distress, acute renal failure, GI disease/bleeding

O = OSTEOLYTIC
- from OSTEOSARCOMA or MULTIPLE MYELOMA
- expect MONOCLONAL GAMMOPATHY, LAMENESS, HIGH GLOBULINS

N = NEOPLASIA
- Osteolytic (osteosarcoma, multiple myeloma)
- PTHrP = parathyroid-related peptide caused by one of 3 neoplasias…
1. lymphoma
2. multiple myeloma
3. anal sac adenocarcinoma

G = GRANULOMATOUS
- from epithelia macrophages in response to FUNGAL or BACTERIAL infections
- produces a “vitamin D-like substance”
- expect INCREASED Ca/P, INFLAMMATION in LEUKOGRAM, ENLARGED LNs, PULMONARY DISEASE (fungi go to lungs)

33
Q

what 4 products are usually excreted out from kidney?

A

(1) phosphate

(2) potassium

(3) BUN

(4) Creatinine

34
Q

if ALBUMIN drops, would we expect Ca to change?

A

YES, half of total calcium bound to albumin

35
Q
A

Year 1/2 (139 decks)

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