Clin Path: Digestive Related Focus Flashcards
describe important proteins for GI
- albumin!
- globulins:
to calculate = total protein - albumin - acute-phase proteins
- coagulation proteins/factors: homeostasis!
-important digestive-related components of homeostasis
–many coagulation proteins/factors are made by the liver!
–several require vitamin K
–key role of calcium too
describe albumins
- synthesized in the liver
- 50% of total protein in plasma
-responsible for 80% of the colloid osmotic pressure - carrier protein for calcium, Mg, bilirubin, fatty acids, drugs, etc.
- 40% of calcium in ECF is bound to albumin
-total Ca = free (ionized) + bound/complexed Ca
describe globulina
- all proteins in serum other than albumin
- 3 fractions:
- alpha and beta: most synth in liver, includes lipoproteins, acute phase proteins, and some immunoglobulins
-gamma: immunoglobulins: made by B lymphocytes and plasma cells
describe acute phase proteins
- innate immune response
- change serum concentration by >25% in response to inflammatory cytokines
- positive APPs: increase production
-sensitive indicator of inflammatory disease
-include fibrinogen, C reactive protein, serum amyloid A and others
-increase in 1-2 days - negative APPs: decrease production/release
-include albumin and transferring
-decrease in hours-days
describe hyperproteinemia
- hemoconcentration: increase in albumins AND globulins or
- increase in globulin synthesis alone: due to inflammation or lymphoid neoplasia
describe hypoproteinemia
- increased protein loss
- decreased protein synthesis
- increased protein catabolism
- failure of passive transfer
- hemodilution: iatrogenic fluid overload, edematous disease (CHF, cirrhosis)
describe increased loss hypoproteinemia ddx
can be
- non-selective:
-losing albumin and globulins (panhypoproteinemia)
-blood loss/hemorrhage: also see red cells go down
-protein losing enteropathy: generalized mucosal disease, lymphatic disease (also losing lipids), or GI blood loss (parasites, neoplasia)
- selective:
-decreased albumin
-protein-losing nephropathy: glomerular damage; proteinuria +/- azotemia, isosthenuria
–nephrotic syndrome: hypoAlb, hyperchol, +/- edema/effusions
-protein-losing dermopathy/PLD: severe bite wounds, burns, skin infections, etc.
describe decreased production/increased catabolism hypoproteinemia ddx
- hepatic insufficiency/failure (decreased albumin)
-cirrhosis, necrosis, inflammation, PSS, neoplasia - malabsorption or maldigestion:
-intestinal mucosal +/- lymphatic disease, EPI - inflammation (decreased albumin)
-negative acute phase response - lymphoid hypoplasia/aplasia (decreased globulins)
-immunodeficiency (congenital, acquired) - cachexia (severe): chronic diseases, neoplasia, malnutrition, starvation
describe how protein and microvascular fluids are related
- water is 60% of body weight!
- 2/3 intracellular (ICF)
- 1/3 extracellular (ECF): 80% interstitium, 20% plasma/blood - moves through endothelial pores
-pores large enough for small nutrients (ions, glucose, AAs), waste but too small for cells and large proteins like albumin
-passively respond to concentration and pressure gradient - in health, the composition of plasma and interstitial fluid is similar (minus large plasma proteins)
-starling’s forces determine water distribution
describe abnormal fluid distribution
- imbalance between intravascular and interstitial compartments
- mechanism:
-increased microvascular permeability
-increased intravascular hydrostatic pressure
-decreased intravascular colloidal osmotic/oncotic pressure
-decreased lymphatic drainage - manifestations:
-interstitial edema
-cavitary effusion
-intracellular edema
-hypervolemia
describe the 2 main types of effusions
characterized by cellularity and protein concentration
-cytology +/- biochemical testing can facilitate underlying processes
- transudate:
-increased plasma hydrostatic pressure (portal hypertension) OR
-decreased plasma oncotic pressure (decreased albumin), which increases leakage of fluid from capillaries
-lowly cellular, poorly proteinaceous fluid - exudate:
-increased vascular permeability (inflammatory mediators) resulting in leakage of fluid from capillaries and recruitment/chemotaxis of inflammatory cells
-highly cellular, highly proteinaceous fluid
describe general guidelines for effusions!
transudate:
-TP <2.5
-NC: <1000
-cell types: mononuclear
-low cellularity
modified transudate:
-TP: 2.5-5.0
-NC: 1000-8000
-mononuclear, cell type caries with cause
nonseptic exudate:
-TP > 3.0
-NC: >3000
-neutrophils, nondegenerate
septic exudate:
-TP: >3.0
-NC: >3000
-neutrophils, degenerate, and bacteria
chylous:
-TP and NC variabke
-mostly lymphs
-grossly milky white, high triglycerides, low cholesterol
hemorrhagic:
-TP: >3/0
-NC: variable
-cells similar to blood
-erythrophagia+/- hemosiderin in macrophages
neoplastic:
-TP >2.5
-cells variable, neoplastic
-criteria of malignancy
describe abnormal electrolyte concentrations in blood
can result from one or more of:
- changes in free water
- decreased or increased intake
- shifts to and from ICF
-ICF: K+ rich
-ECF: Na+, Cl- rich - increased retention via kidney
- increased loss via kidney, GI tract, skin, or airways
these changes can create acid base abnormalities
describe sodium and water
- blood volume and plasma osmolality regulation affect serum sodium
- water and sodium love each other and love to follow each other
- serum sodium is indicative of amount of sodium relative to water in ECF
-can be used to infer total body sodium if consider hydration status and ECF volume
describe chloride and how it relates to other electrolytes
- sodium and chloride tend to move in parallel
-Na-Cl difference:
–30-40 = proportionate: similar ddx to aberrations
– >40 disproportionate (less Cl): due to loss or sequestration; vomiting of gastric contents, upper GI obstruction, GDV, displaced abomasum, abomasal atony - chloride has inverse relationship with bicarbonate
describe the metabolic and respiratory components of acid-base
- metabolic:
-primarily regulated by kidney
-status measuredby bicarbonate (HCO3-)
-increased bicarb = alkalosis, most commonly causes by sequestration or loss of HCl
-decreased bicarb = acidosis: either loss of bicarb fluids (diarrhea, secretional), or buffering of organic acids (lactate, ketones, titrational/high anion gap) - respiratory:
-regulated by ventilation (lungs)
-status measured by pCO2
-increased = acidosis
-decreased = alkalosis
describe minerals and GI
- calcium and phosphate absorbed in GI
-mediated by vitamin D (except in horses)
-conversion to active form via liver and kidney - calcium = ileum
-absorption also influenced by acidity (acidifying substances promote absorption), calcium-chelating dietary components, intestinal epithelium health
-absorption inhibited by corticosteroids
-excretion: kidneys excrete MOST, some by feces
- phosphate = jejunum, colon/cecum (horses)
-absorption enhanced by low dietary calcium, increased dietary acidity, growth hormone
-absorption decreased by high Ca:P diet, antacids
-excretion: kidneys more than feces; ruminants saliva much more than feces
describe hypercalcemia and hypocalcemia
hypercalcemia:
1. increased protein bound (rare)
2. increased bone mobilization
3. increased intestinal absorption
4. decreased urinary excretion
5. increased PTH, increased vitamin D
6. young animals (<3-6 months) can have increased Ca!
hypocalcemia:
1. decreased protein bound!!
2. inadequate bone mineralization
3. inadequate intestinal absorption
4. excess urinary excretion
5. decreased PTH, decreased vitamin D
describe common causes of hypocalcemia by species
dogs and cats:
-hypoalbuminemia
-GI disease
-renal disease
-pancreatitis
-sepsis/critically ill
-eclampsia
horses: colic af, cantharidin toxicity
ruminants: milk fever, endotoxemia, GI disease
describe hyper and hypophosphatemia
causes of hyper P:
1. decreased urinary excretion
2. increased intestinal absorption
3. increased bone mineralization
4. shifting from ICF to ECF
5. DECREASED PTH, increased vitamin D
6. young animals can have increased P
hypo P
1. excess urinary excretion
2. inadequate intestinal absorption
3. inadequate bone mineralization
4. shifting from ECF to ICF
5. INCREASED PTH, decreased vitamin D
describe hyper and hypomagnesemia
hyper Mg
1. decreased renal excretion
2. increased GI absorption
3. hemolysis (except cattle)
4. parturient paresis (cows)
hypo Mg
1. decreased protein-bound Mg
2. decreased GI absorption
3. increased excretion: saliva (ruminants), sweat (horses), diarrhea, urinary
4. grass tetany
describe BUN and creatinine
- should be interpreted together and in relation to GFR!
if mismatched:
- increased BUN and N- but decreased creatinine:
-decreased GFR: early pre-renal, renal azotemia
-normal GFR: upper Gi bleed, high protein diet, protein catabolism
-non-renal causes of decreased creatinine: decreased muscle mass, sepsis - decreased BUN and N-, increased creatinine:
-decreased GFR: hepatic failure, low protein diet, metabolism of UN by GI flora (horses, cattle)
-normal GFR: normal in muscled animals (greyhound, draft horse)
