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Pancreas
Gland organ composed of endocrine and exocrine portions.
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Endorine pancreas
Islets of Langerhans, containing Beta cells (Insulin), Alpha Cells (glucagon), Delta cells (Somatostatin) and F cells (Pancreatic polypeptides).
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Islets of Langerhans
- Endocrine pancreas
- Beta cells (insulin)
- alpha cells (glucagon)
- delta cells (somatostatin)
- F cells (pancreatic polypeptides)
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Beta cells
- From endocrine pancreas, islets of langerhans.
- Create insulin, which pulls glucose into cells to facilitate metabolism.
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Alpha cells
- From endocrine pancreas, islets of langerhans.
- Create glucagon, which deals with glucose and metabolism (opposite of insulin)
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Delta cells
- From endocrine pancreas, islets of langerhans.
- creates somatostatin, which deals with lipid metabolism.
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F cells
- from endocrine pancreas, islets of langerhans.
- creates pancreatic polypeptides, which deal with protein metabolism.
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Exocrine pancreas
- Largest functional part of pancreas.
- Acinar cells: secrete digestive enzymes (trypsin, amylase, lipase) and release through ducts into insides of organs.
- Leaked into circulation from trauma to pancreas.
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Acinar cells
- secrete digestive enzymes (trypsin, amylase, lipase) through ducts into insides of other organs.
- Leak from damage to pancreas into systemic circulation.
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Pancreatitis
- inflammation of pancreas
- Acute or chronic, causes leakage of digestive enzymes.
- Chronic is more common, sometimes a flare-up presents as acute.
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Predisposing factors for pancreatitis
- obesity and high fat diet most common.
- Liver disease, infection, recent ab surgery, drugs (azathiopine, furosemide, potassium bromide), duodenal fluid reflux, pancreatic trauma or ischemia, hypercalcemia, infectious agents like FIP, Toxoplam gondii
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acute clinical signs of pancreatitis
- sudden onset
- fever
- anorexia
- V/D (hemorrhagic)
- weakness
- cranial abdominal pain
- shock
- sudden death
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Ways to diagnose pancreatitis
- radiograph (hazy ground glass)
- abdominal ultrasound
- bloodwork (anemia, leukocytosis, hyperamylasemia*, hyperlipasemia*, increased liver enzymes (ALP, ALT), hyperbilirubiemia, prerenal azotemia, hyperglycemia, hyperlipidemia
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bloodwork of pancreatitis
- anemia (chronic inflammation, nonregenerative)
- variable leukocytosis
- hyperamylasemia (leaking)**
- hyperlipidasemia (leaking)**
- hyperbilirubinemia and increased liver enzymes (ALP, ALT), often cholestasis. Toxins build up and damage liver.
- prerenal azotemia (dehydration)
- hyperglycemia (glucagon)
- hyperlipidemia
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Lab tests for pancreatitis
- TLI (trypsin-like immunoreactivity) (for EPI)
- PLI (pancreatic lipase immunoreactivity) (for pancreatitis)
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TLI
- serum trypsin-like immunoreactivity
- antibodies to detect trypsin and trypsinogen
- Specific for exocrine pancreatic function in dogs (low sensitivity). Not specific for pancreatitis.
- Useful in detecting Exocrine pancreatic insufficiency (EPI) (decreased)
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EPI
- exocrine pancreas insufficiency.
- severe maldigestion and malabsorption and atrophied acinar cells.
- Loss of 85%-90% of exocrine pancreatic mass
- decreased TLI good test for it
- can be congenital (dogs) or acquired (cats)
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PLI
- serum pancreatic lipase immunoreactivity (cPLI or fPLI)
- measures mass of pancreatic lipase in serum rather than enzymatic activity
- sensitive for canine and feline pancreatitis
- Also IDEXX SNAP test, using elisa technology (looks for lipase)
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ELISA
enzyme-linked immunosorbant assay
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Treatment for pancreatitis
- get eating right away, low fat diet. Feeding tube if anorexic.
- control pain
- correct fluid/electrolyte, etc disturbances
- If necessary, give plasma (if albumin too low. DIC)
- antiemetics (to avoid loss of fluid/nutrients/electrolytes)
- H2 blockers
- +/- antibiotics (peritonitis)
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Acute pancreatitis
- Occurs in d/c, most common form in dogs, rare in cats
- can be severe and result in death, or reversible.
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Chronic pancreatitis
- Occurs in d/c, rare in dogs, most common in cats (triaditis).
- Significant scarring and atrophy of pancreas.
- Waxing and waning signs, irreversible changes.
- Rarely fatal.
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Triaditis
Pancreatitis with hepatitis and IBD, common in cats, who get chronic pancreatitis with GI involvement.
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Clinical signs of chronic pancreatitis
- VDA
- weight loss
- weakness
- abdominal pain
- dehydration
- if Islet cell destruction, EPI and diabetes mellitus
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cat EPI
- not too common, generally chronic pancreatitis.
- Usually older, GI trouble entire life, IBD
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dog EPI
- acinar atrophy most commonly
- Chronic pancreatitis less common, pancreatic hypoplasia very rare (G. Shep, congenital)
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Maldigestion
- EPI
- Insufficient synthesis and secretion of digestive enzymes by exocrine portion of pancreas.
- Weight loss, ravenous appetite, voluminous loose greasy stool, poor hair coat
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Clinical signs of maldigestion
- weight loss with ravenous appetite
- voluminous pale loose greasy stools
- poor hair coat
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Steatorrhea
voluminous pale greasy loose stools
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Diagnosis and treatment of EPI
- decreased TLI (dogs < 2.5, cats < 8.0)
- treat with pancreatic enzymes for life
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Juvenile Pancreatic Atrophy
- Congential EPI caused by lack of pancreatic enzymes
- common in young adult G. Shep
- Recognize, diagnose and treat like EPI
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Malabsorption disease
- Failure of digestive tract to absorb, but nutrients get digested. Variety of small intestinal causes
- chronic parasitism (hookworms)
- chronic IBD
- intestinal lymphoma
- severe dietary sensitivities
- lymphangietasia (obstruction and dysfunction of intestinal lymphatic system)
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Clinical signs of malabsorption disease
- +/- chronic diarrhea
- vomiting
- dehydration
- anemia
- ascites or edema
- altered appetite (anorexia or polyphagia, more common)
- weight loss despite ravenous appetite (coprophagia or pica)
- steatorrhea (pale, greasy loose stools) (sometimes)
- thickened bowl loops
- enlarged mesenteric lymph nodes
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pica
will eat ANYTHING, doesn't have to be food
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tests to diagnose malabsorption disease
- fecal sedimentation and culture (parasites and pathogenic bacteria)
- history (dietary indiscretion or sensitivity)
- lab work (CBC, chemistry and UA for systemic diseases, TLI, PLI, Cobalamin, Folate)
- Imaging (radiograph, ultrasound)
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Cobalamin
- B12 vitamin.
- Mostly absorbed in ileum so B12 deficiency if not absorbing in ileum.
- rapidly dividing cells need B12. Can be used up by bacteria
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Folate
- Test for malabsorption. Increased in IBD, decreased in PROFUSE small intestinal disease.
- absorbed in jejunum (proximal)
- Body needs folate to make DNA. Overgrown bacteria can use it all up.
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Folate and Cobalamine in EPI
increased or normal folate, decreased cobalamine
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Folate and cobalamine in bacterial overgrowth
increased folate decreased cobalamine
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folate and cobalamine in proximal small intestinal disease
decreased folate and normal cobalamine
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folate and cobalamine in distal small intestinal disease
normal folate and decreased cobalamine
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folate and cobalamine in diffuse small intestinal disease
both decreased
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diagnosis of malabsorptive disease
- TLI (to differentiate from EPI)
- Theraputic trials (deworming, antiprotozoals, antibiotics, pancreatic enzymes, food trial)
- Intestinal biopsy (definitive diagnosis)
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Therapeutic food trial
- Way to help diagnose malabsorptive disease.
- Consists of a novel, single-source protein (scrip to prevent cross-contamination) and hydrolyzed protein diet (smaller sized molecules can't set off a reaction)
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Intestinal biopsy to diagnose malabsorptive disease
- open laparotomy: full-thickness sample but invasive surgery. Can get multiple samples
- laparoscopic: less invasive, still can get full-thickness biopsy
- Endoscopy: less invasive, can do both ends, but tunnel vision, can't see outside, can't get full thickness. Easier on animal, may not give diagnosis
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Fecal starch
- Undigested starch in feces detected by staining feces with Lugol solution
- Fecal starch + suggests EPI
- test is insensitive and nonspecific.
- Meant to test malabsorptive vs maldigestive
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fecal fat
- undigested and digested fat in feces (stain is sudan III or IV)
- + direct fecal fat very specific for EPI.
- Insensitive
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Muscle fiber test
- undigested striated muscle fibers, stain with Lugol.
- Not senstive
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microscopic stained fecal fat, starch and muscle
suggests maldigestion, but not terribly accurate.
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Tests for maldigestion vs malabsorption
- fecal fat/starch/muscle fiber
- fecal proteolytic activity
- TLI, PLI
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Fecal proteolytic activity
- measures protease activity in stool (trypsin, chymotrypsin, and carboxypeptidase)
- Historically was the test for EPI in small animals, but TLI is better and easier.
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Electrolytes
- chemical substances that separate in solution to form electrically charged ions.
- anions: Cl-, HCO3-, HPO42-
cations: Na+, K+, Ca2+ - Function in energy production, enzyme reactions, acid base balance, osmosis and diffusion, and muscle contractions
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Renin Angiotensin system
- response of body to falling BP.
- Kidney notices decrease in BP
- kidney releases Renin
- Renin activates circulating angiotensinogen, made in liver, into angiotensin I
- Angiotensin converting enzyme (found in epithelium, esp lungs) turns angiotensin I into angiotensin II.
- Angiotensin II causes increased thirst, vasoconstriction, and stimulates the adrenal to make aldosterone
- Aldosterone stimulates kidney to retain Na and therefore water.
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Angiotensin-converting enzyme (ACE)
- found in endothelium, especially in the lungs but all over the body.
- Converts angiotensin I to angiotensin II in renin-angoitensin response to falling BP
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Hyperadrenocorticism and electrolytes
- Hypernatremia
- increase in aldosterone causes Na retention.
- Cushings.
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Hypoadrenocorticism and electrolytes
- decrease in aldosterone causes Na eliminationa and K retention.
- Hyponatremia, Hyperkalemia.
- Addison's.
- Plasma Na:K < 27:1 (normal 27:1- ~40:1)
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HCO3-
generated in body (lungs, gastric mucosa, kidneys and erythrocytes), altered by other electrolytes and acid-base balance
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Ways electrolyte concentration can be changed
- increase or decrease intake
- shift to/from ICF (out of gen. circ.)
- increased renal retention
- increased loss via kidneys, alimentary tract, skin, or airways or (HCO3) indirectly
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Sodium
- Principle cation in ECF
- Co-factor in metabolic reactions
- Driver of fluid movement
- Controlled by blood volume regulation or plasma osmolarity regulation.
- Enters body from food/drink intake
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Blood volume regulation of Na
- decreased blood volume, renin system, aldosterone increases Na retention.
- increased blood volume, decreased Na absorption due to atrial natriuretic peptide (amino acid found in myocytes of atria, released when stretched).
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Atrial natriuretic peptide
- amino acid found in atria of heart, released when atria are stressed by too much blood volume. Causes decreased Na absorption in distal nephron.
- Seen in congestive heart failure.
- New blood test that can look for it, detect heart problems in asymptomatic cats.
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Plasma Osmolarity regulation of H2O
- Hyperosmolarity causes more drinking and release of ADH, causing water resorption from collecting duct.
- hypoosmolarity causes decreased thirst and no ADH, so no water retention.
- Osmolarity of plasma usu ~300
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Self regulation of plasma Na
- hypernatremia causes decreased aldosterone, and therefore less resorption
- hyponatremia causes increased aldosterone and sodium retention
- Affected by plasma K+ levels and effective blood volume
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Major Na/K regulator
aldosterone
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Simple: Na levels are controlled by
- dietary/fluid intake
- renal H2O/Na resorption and secretion
- aldosterone
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Causes of hyponatremia
- V/D
- CRF (kidneys not responding to aldosterone)
- Addisons (less Aldosterone)
- diuretics (medullary washout, no gradient at Henle)
- CHF (blood volume)
- Hepatic cirrhosis (no angiotensinogen leads to no aldosterone)
- Over-hydrating with half saline
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Clinical signs of hyponatremia
- lethargy
- muscle weakness
- confusion
- seizures
- dullness
- coma
- nausea, vomiting
- DECREASED blood pressure
- increased aldosterone
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Hypernatremia causes
- Dehydration: H2O deprivation, defective thirst response, insensible loss (fever, panting, hyperventilation), diabetes insipidus, renal osmotic diuresis, diarrhea/vomiting
- Increase in body Na: salt poisoning, hypertonic saline, hyperaldosteronism.
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diabetes insipidus
decreased aldosterone production or nonfunctioning receptors in kidney for aldosterone.
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Renal osmotic diuresis
Washout of osmotic gradient in loop of Henle, washed out by too many diuretics.
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Clinical signs of hypernatremia
- lethargy
- weakness
- MUSCLE FASCICULATIONS
- disorientation
- behavior changes
- ataxia
- seizures
- stupor
- coma
- fluid retention (third-spacing)
- INCREASE in blood pressure.
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Potassium
- Principal cation of ICF (not shown in BW usu).
- Functions in resting membrane potential, repolarization, cardia rhythms and rate, Na in renal, acid-base metabolism (exchange for H+ in/out of cell)
- Regulated by renal excretion and distribution between ICF and ECF (dietary, feces and sweat a little).
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Aldosterone and K+
- Hyperkalemia and angiotensin II stimulate aldosterone, trade Na for K, so K goes into urine.
- Hypokalemia lowers aldosterone secretion.
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Causes of hypokalemia
- shift from ECF to ICF
- decreased intake--anorexic
- increased loss: increased insulin activity, diuretics, VDA, sweating in horses, hyperaldosteronism
- alkalosis
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How alkalosis causes hypokalemia
increased pH causes ECF to want to lose H+, swaps with K+ so less K+ in ECF
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Clinical signs of hypokalemia
- Profound muscle weakness
- In cats: ventroflexion of neck, forelimb hypermetria (goose-step), broad based hind limb stance
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Causes of hyperkalemia
- tissue necrosis (released from dying cells)
- renal failure (not excreted)
- UT obstruction or ruptured bladder (not excreted)
- hypoaldosteronism (often hypoadrenocorticism)
- administration of K+
- acidosis (too much H in ECF, switch with K)
- insulin deficiency (diabetes mellitus)
- inherited periodic hyperkalemia (horses)
- Oleander toxicity
- Pseudohyperkalemia (sampling error)
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Clinical signs of hyperkalemia
Cardiac effects. Life-threatening bradycardia can lead to arrest. Addisons often presents with bradycardia.
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Treatment of hyperkalemia
- Attempt to determine cause (oleanders, addisons) and treat
- decrease K+ intake, increase uptake into cells, increase excretion.
- Calcium supplementation decreases signs of cardiac toxicity.
- fluid therapy with 0.9% saline (exchange)
- Give insulin with dextrose, send K into cell
- sodium bicarb supplementation, gets K into cell and treats acidosis
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Chloride
- follows Na passively.
- Principle anion in ECF
- Maintains neutrality/balance
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Hypochloremia
- Loss of HCl or KCl (V/D)
- Upper GI obstruction
- drugs that block Cl transport
- Hyperalbuminemia (albumin is an anion, so Cl balances)
- decreased Na, so:
- CRF (kidneys not responding to aldosterone)
- Addisons (less Aldosterone)
- diuretics (medullary washout, no gradient at Henle)
- CHF (blood volume)
- Hepatic cirrhosis (no angiotensinogen leads to no aldosterone)
- Over-hydrating with half saline
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Hyperchloremia
- Drugs that block Cl transport
- hypoalbuminemia (Cl balances)
- Same as Na:
- Dehydration: H2O deprivation, defective thirst response, insensible loss (fever, panting, hyperventilation), diabetes insipidus, renal osmotic diuresis, diarrhea/vomiting
- Increase in body Na: salt poisoning, hypertonic saline, hyperaldosteronism.
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Three forms of Calcium
- ionized (50%)
- protein bound-bound primarily to albumin to minimize changes in body (40%)
- chelated-complex with phosphate, citrate, bicarb, sulfate or acetate (10%)
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PTH on Calcium and Phosporus
- Net effect, increase blood calcium, lower blood phosphate
- Low concentration of calcium in blood
- release of PTH
- pull Ca and P out of bone, decrease loss of Ca in urine by switching for P, tell kidneys to release calcitriol to absorb more Ca and P from intestines.
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Calcitonin on Ca and P
- Net effect, decrease blood Ca, increase in blood P
- Rising Ca in blood stimulates thyroid to release calcitonin.
- stimulates deposition of Ca in bone
- inhibits renal resorption of Ca, so no switch for P
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Calcitonin
released by thyroid in response to rising blood Ca levels. Lowers levels by sending to bone and stopping kidney resorption.
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Calcitriol on Ca and P
- Net effect, increase blood Ca and P
- low Ca in blood, PTH tells kidney to release/activate calcitriol.
- More Ca and P absorbed in intestine.
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Functions of Ca
- skeletal structure and function
- muscle contraction
- blood coagulation (clotting cascade)
- nerve impulses
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Functions of Phosphorus
- Skeletal structure and function
- energy reactions (ADP, ATP)
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Hypercalcemia Causes
- GOSHDARNIT
- Granolomatous
- Osteolytic
- Spurious
- Hyperparathyroidism
- D hypervitaminosis
- Addisons
- Renal failure
- Neoplasia (LYMPHOMA)
- Idiopathic
- Temperature
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Hypercalcemia clinical signs
- PU/PD
- CARDIAC ARRHYTHMIAS
- lethargy
- anorexia
- vomiting
- constipation
- weakness
- renal failure (mineralizing)
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Hypocalcemia causes
- Hypoproteinemia (hypoalbuminemia)
- hypoparathyroidism
- Hypovitaminosis D (renal, causes less absorption in intestine)
- antifreeze (ethylene glycol toxicity) (excretion)
- blister beetle toxicosis (excretion)
- fracture healing
- acute pancreatitis (not sure why)
- Eclampsia (pregnancy, mom's Ca fatally low)
- Milk fever (dairy cows after birth can't keep up)
- Alkalosis (protein ionizes, binds with more Ca)
- Ca binds with diffuseable anion
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Calculate hypocalcemia correcting for albumin
3.5 - albumin + calcium
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Clinical signs of hypocalcemia
- nervousness
- behavioral changes
- focal muscle twitching
- tetany
- seizures
- cardiac arrhythmias
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hyperphosphatemia causes
- decreased GFR, leading to decreased secretion (prerenal, renal or postrenal)
- increased absorption in intestine with calcitriol or phosphate enema
- shift into ECF from ICF in myopathies (endurance races)
- hyperthyroid in cats
- hyperadrenocorticism in dogs
- Increased in young, growing animals (like ALP and lymphocytosis)
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Causes of hypophosphatemia
- primary hyperparathyroidism (increased excretion)
- pseudohyperparathyroidism (lymphoma or anal gland tumors cause PTHrp, like PTH)
- less absorption due to anorexia or less calcitriol
- hyperinsulinism (OD causes shift from ECF to ICF)
- eclampsia (pregnancy, not enough from bone)
- equine renal disease
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2 major pumps in acid-base balance
- Cl-/HCO3- (resorbed/excreted in direct opposition)
- Na+/H+ (energy from Na+ gradient moves H+ out of cell in exchange for K+)
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Method to fix Acidosis
- decreased pH = increased H+ in cell. Na/H+ pump pumps H+ out of renal cells into tubules to be excreted
- Cl-/HCO3- pump inhibited to increase HCO3 inside cell.
- Intracellular H+ decreases, HCO3 increases, Cl decreases, pH becomes higher/more alkalotic/normal.
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Method to fix alkalosis
- increased pH = decreased H+ in cell. Na/H pump inhibited, keeping H in cell.
- Cl/HCO3 pump sends HCO3 out of cell to be excreted.
- As H+ increases and HCO3 decreases, cell moves toward normal pH.
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Respiratory acidosis
- increase in partial pressure of CO2
- hypoventilating. Anesthesia.
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Respiratory alkylosis
- decrease in partial pressure of CO2
- hyperventilating
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Metabolic acidosis
- decrease in HCO3
- Can be caused by chronic renal failure
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Metabolic alkylosis
increase in HCO3
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Blood gas, order to read and what it means.
- pH, then bicarb, then PCO2.
- pH tells you alkalosis or acidosis. If matches bicarb (both increased = metabolic alkalosis, both decreased = metabolic acidosis), metabolic.
- Look at PCO2. If same, trying to compensate. If dif, adding to problem (mixed disturbance).
- If PCO2 opposite pH and HCO3 opposite pH, respiratory with metabolic compensation.
- If normal, no compensation.
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