endocrinology

10 some unit

with the Na/K/ATP pump by inhibiting Na+
release Ach
contraction of muscle

bloat, the rumen can't contract

Ca is needed for NT releaes low Ca2+ can result in a coma
Ca2+ is needed for release of glucose

Mg2+

1,25 di-OH D3

Stimulus for release: high ECF [Ca++
Promotes deposition of Ca into bone
Promotes loss of Ca into urine
Net effect: to reduce [Ca++]]

dairy cattle
beef cattle and sheep- prepartum

within 48 hours of calving

Caused by onset of heavy milk production that depletes serum Ca++so rapidly that hormonal controls can’t keep up

flaccid paralysis

Tends to occur in older cows ( >3 yrs) –as animals age, the bone and gut are less responsive to PTH and Vitamin D

channel breeds

Onset of lactation pulls approximately ten times the ECF calcium content into the milk within several hours

bone resorption(takes 48hr)
intestinal absorption (takes 24hr)

Milk fever results from a failure of the hormone systems to keep up with calcium loss into colostrumand milk

Once clinical signs start, the cow’s condition will rapidly become worse
Untreated cases of milk fever result in death!

standing, irritable, tremors.

Hypersensitive
Excitable, nervous, weak
Cows will shift weight from side to side
Ataxia
Tachycardia; mild HYPERthermia
Feces often firm (long transit time)
Stage 1 rapidly progresses to stage 2 (1 hour)

stick their tongue out

recumbent and depressed
poor cardiac function

Sternalrecumbency
•Head tucked to side
•S-shaped curvature of neck 9their mm are very weak)
•Recumbencyis due to flaccid paralysis
•Muscle fasciculations

Tachycardia, but usually < 90 bpm
•Decreased intensity of heart sounds
Poor perfusion:
Subnormal rectal temperature (<100ºF)
Cold extremities: ears and distal feet
Mild bloat
Constipation; inability to urinate
Pupils:
Pupillarylight reflex may be depressed

Lateral recumbency
Progressive loss of consciousness
Severe bloat
Heart sounds may be inaudible
Tachycardia, usually > 100 bpm
Coma
death

Death soon follows -respiratory / cardiac arrest
or aspiration of rumen contents

•Bloat
•Aspiration pneumonia
•Muscular injury
•Compression
•Rupture
•Skeletal injuries
•Peripheral nerve injuries

Hypocalcemia= <7.5 mg/dl
•Reference range: 9.7-12.4 mg/dl

5.5-7.5 mg/dl

3.5-6.5 mg/dl

<2.0 mg/dl

Collect blood before treatment, that way you will have a baseline
if the cow does not respond to treatment

Calcium borogluconate 23% solution IV / SC
Oral calcium chloride / propionate gels

1 g. Ca2+/ 45 Kg body wt. (100lbs)
most 500 mL prep contain 8-12 g of calcium

so 1 bottle for 800-1200 lbs

Calcium is directly cardiotoxic!!
Administer slowly (10-20 minutes)
Auscult heart: arrhythmia/bradycardia

25-100 g. of calcium

its an irritant. if you give this too fast or if they aspirate then it will cause erosions in trachea, bronchi and could liquefy the lungs

no, this is an emergency- start treating!

Oral calcium gels
Subcutaneous calcium gluconate

Intravenous calcium salts

Eructation
Urination
Defecation
Increased intensity of heart; decreased heart rate
Muscle fasciculations
Improved responsiveness
Standing before you leave farm
*Shiver, Sh*t, Shuffle to their feet!*

Good footing
Of paramount importance!!!!
Keep cows sternal
Don’t force them to get up too soon
Roll from side to side if recovery is prolonged
Provide fresh water

25-30% relapse within 24-48 hours
Relapses more common in older cows

deficient in Mg2+, K+, and or PO4

Subcutaneous Calcium
Given at initial IV treatment
Do NOT use products containing dextrose

Feed a diet low in calcium during the last 3-4 weeks prior to calving

you want the calcium from the bones to be put into the blood stream to make it available during parturition

anionic salts 2-3 wks prior to calving. To make the blood more acidic

Calcium stores in the body are mobilized under acidic conditions!

Alkaline pH promotes hypocalcemia
Conformational structure of Parathyroid Hormone receptor is changed:
lock-and-key interaction between PTH and receptor is disrupted

parathyroid hormone

acidification through diet
↑ urinary excretion of Ca2+
↑ resorption of Ca2+ from bone

osteoclasts exchange Ca2+ for H+
↑ vit D formation

Estimates whether a diet has the potential to be acidogenic or alkalogenic
Goal is to create diet which is more negatively charged (higher in anions)

High incidence of milk fever, approaching upper limit of the kidneys to regulate pH

High incidence of hypocalcemia, milk fever a potential problem

Borderline range, hypocalcemia still a potential problem

optimum level for jerseys

Excessive acidification, approaching lower limit of the kidneys to regulate pH

PTH

it is doomed

Energy exchange through ATP
•Skeletal growth/maintenance
•Reproductive function
•RBC integrity

Vitamin D3

P042-loss

Severe, acute hypophosphatemia

hemolyzing cow- I dont get it

rickets

poor growth/ infertility

spontaneous fractures, rickets, pica

RBCs depleted of ATP, lyse. Rare.

normal 4-8 mg/ dl
young ruminants 5-8.5 mg/dl
idk if we need to know this

<1 mg/dl

2-3.5 mg/dl

< 2mg/dl

stop giving the calcium

shut it down

potassium

maintenance of resting membrane potential

diet

renal
salivary
GI
milk

moderate to severe ketosis
cows that had delivered a calf less than 30 days before dz
all cows had been treated with isoflupredone acetate (predef)

Muscle fasciculations
Skeletal muscle weakness
Profound muscle flaccidity
Recumbency
Neck muscles affected
Head resting against flank
Cardiac arrhythmias
Atrial fibrillation
Ventricular tachycardia

Hypokalemia
Potassium < 2.5 mEq/L
Hypophosphatemia
Mild elevations in creatine phosphokinase activity

imbalance of external potassium regulation
imbalance of intracellular potassium homeostasis

anorexia (DA, Mastitis, ketosis)

kaliuresis
minerealcorticoid effect
predef> dexamethasone

Alkalosis results in cellular uptake of potassium in exchange for hydrogen ions

insulin and gluocose
insulin drives gluocose into the cell

cellular uptake of glucose is accompanied by intracellular movement of potassium

IV and oral K+
IV is not effective alone
IV K+ (5% KCl soln)
isotonic KCl: 11.5 grams KCl/L sterile water

0.5 mEq/kg/hour

capsules, mix it in water, stomach tube, morton lite salt, rumen transfaunation KCl, rumen microbes

change her diet every few weeks- stat with hay, some concentrate, then more concentrate

absorbed in the portal circulatoin and sent to the liver

propionate

brain, RBC, kidney, mammary gland (needs to convert gluc to lactose), placenta/fetus

mitochondria

very little

60-85% of BG goes to the mammary gland for milk production

in the 3rd trimester the fetus grows a lot and if there are multiple babies this can cause complications

When energy demand exceeds supply,
[insulin] decreases,
[glucagon] increases,
and the animal mobilizes its energy stores

Glycogen
In liver and muscle. Polymer of glucose.
Muscle amino acids
Can be converted to glucose.
Lactate
Can be converted to glucose.

Fat
In the body, 3 fatty acids are linked to one glycerol to form triglyceride (fat).
Abundant hydrocarbons for oxidation as fuel!

Promote lipolysisthrough stimulation
of Hormone Sensitive Lipase:
glucagon
cortisol
catecholamines

Non-esterifiedFatty Acids (NEFA)

The control center for regulation of energy metabolism

FA-> liver cells->ß-oxidation -> acetyl-CoA (2 carbons)-> krebs
will also need dietary proproionate to make glucose

there is insufficient proprionate
they can't eat enough to meed their energy demands
everything is mobilized
tons of Acetyl-CoA-> ketone formation

Insufficientpropionatesupply from rumen,
glycogenstores eventually depleted,
and only a finite amount of muscleamino acidsandlactatecan be mobilized….

mobilize lg amounts of body fat

Short carbon-chain organic acids
Also called “ketoacids, ketone bodies

acetoacetate, (OH)butyrate, acetone)

The result of incompleteoxidation of fatty acids
Why incomplete?
There is insufficient oxaloacetate(not enough carbohydrates) to allow acetyl CoAto enter the TCA cycle