Support & Movement 2: Clin Path S1 Flashcards
FIP findings/differentials
- 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
- NEOPLASIA
Can RULE OUT NEOPLASIA by doing a SERUM PROTEIN ELECTROPHORESIS (SPE)
–> Look for monoclonal gammopathy
differentials for hypercalcemia (7)
- vitamin D toxicity
- addison’s disease (low Na and high K, LOW cortisol)
- renal disease
- osteolysis
- neoplasia
- granulomatous
- idiopathic
differentials for hypoglycemia (4)
- ARTIFACT
- SIRS/SEPSIS (systemic inflammatory response syndrome)
- from OVERWHELMING inflammatory changes - COUNTER-REGULATORY HORMONES (hormones that make glucose go down)
- glucagon
- epinephrine
- growth hormone
- glucocorticoid - LIVER FAILURE
- look for ABC GLUCOSE
- decreases in albumin, BUN, creatinine, glucose
how does HYPERcalcemia cause PU/PD?
increased Ca causes the body to RESPOND LESS TO ADH, and as a result POLYURIA –> POLYDIPSIA
describe the countercurrent exchange mechanism in the kidney (location, overall process)
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
in glomerular filtration, what STAYS INSIDE OF VESSELS?
WBCs, RBCs, LARGE PROTEINS (albumin)
basics of proximal convoluted tubule, loop of henle, distal convoluted tubule, and collecting duct
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
what 2 things determine rate of glomerular filtration (GFR)?
- PRE-RENAL factors
- blood pressure
- cardiac output
- volume of blood
**IF any of these are decreased, then decreased GFR - NUMBER of nephrons
- 1 glomerulus/nephron
what products do we expect to build up if glomerulus not filtering blood efficiently? (4)
NITROGENOUS WASTE PRODUCTS
(1) Urea
(2) Creatinine
(3) Phosphorus
(4) Hydrogen ions
what determines the tubular flow rate?
GFR/glomerular filtration rate, which is determined by…
Blood volume, blood pressure, CO, and number of nephrons
what does LOW urea indicate?
the kidneys are DYSFUNCTIONAL
the collecting tubule CANNOT reabsorb urea efficiently, so it’s excreted as waste
what does HIGH urea indicate?
DEHYDRATION
the collecting tubule will REABSORB MORE WATER AND UREA in response to ADH
where are juxtaglomerular cells? what do they do?
cells in the DCT that help sense BP and activate RAAS to regulate it
proportion of INTRACELLULAR to EXTRACELLULAR fluid?
2/3 to 1/3
what 4 components make up EXTRACELLULAR fluid?
(1) BLOOD (plasma)
(2) INTERcellular fluid (interstitium
(3) RUMEN (large animal)
(4) TRANSCELLULAR fluid (third space)
- pleural cavity
- abdominal cavity
- pericardial cavity
what does decreased USG indicate?
that the KIDNEY TUBULES ARE DAMAGED, renal injury!
carotid sinus baroreceptors and osmoreceptors in the hypothalamus
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
5 differentials of HYPERnatremia
(1) DEHYDRATION
(2) LOSS OF FREE WATER
(3) LOSS OF FREE WATER»_space; LOSS OF SODIUM
(4) SODIUM TOXICITY (SALT POISONING)
(5) EXCESS ALDOSTERONE (RARE)
4 causes of dehydration? what CBC findings indicate dehydration?
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
hypernatremia –> loss of free water, which hormone/disease does this involve? 2 differentials?
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
hypernatremia –> loss of free water»_space; loss of free sodium 2 differentials?
(1) osmotic diarrhea
(2) osmotic diuresis
why is it important to treat hypernatremia SLOWLY?
if giving too many fluids too soon, can rush into cells and cause them to SWELL/LYSE/DIE
3 differentials for NON-RENAL DISEASE causes of DECREASED USG
(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
function of PTH/parathyroid hormone? what controls it?
to INCREASE Ca and DECREASE P
acts based on IONIZED Ca levels!
NET effects of PTH, Calcitonin and Vitamin D IN BLOOD?
PTH = INCREASES Ca and DECREASES P
Vitamin D = INCREASES Ca/P
Calcitonin = DECREASES Ca/P
what are the 3 components of TOTAL calcium?
(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
6 things that determine levels of calcium in the body?
(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!
what 7 things influence phosphorus levels?
(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
how much Mg is bound to albumin?
about half
Magnesium and its relation to GI absorption, PTH, GFR, cell death
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
Milk fever & Grass tetany and Mg
(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
Hypercalcemia (HUGE acronym) with basics of each term
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)
what 4 products are usually excreted out from kidney?
(1) phosphate
(2) potassium
(3) BUN
(4) Creatinine
if ALBUMIN drops, would we expect Ca to change?
YES, half of total calcium bound to albumin
