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Flashcards in Ruminants Deck (23)
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1

Acute lactate acidosis: local Consequences

a, decreased rumino-reticular (forestomach) motility b, increased ruminal osmotic pressure (osmolality)
physiological: 200-250 mOsm
pathological: > 400 mOsm
c, mucosal injury (ruminitis)
d, decreased activity (even death) of microorganisms,
especially protozoa. Overgrowth of Clostridia/coliforms, later funghi

2

Acute lactate acidosis: general Consequences

a, dehydration (hypovolaemic shock): PCV↑
b, metabolic acidosis (lactate acidosis, lactacidaemia)
c, increased production and absorption of endotoxins (death of Gram negative bacteria)
d, increased biogen amine (histamine etc.) production:
1. in the ruminoreticulum  ↓bacterial effect 2. in the wall of reticulorumen  inflammatory
effect
e, ethanol, methanol production  : depression of CNS

3

Clinical symptoms of SARA(sub-acute(chronic) rumen acidosis)

•Low or fluctuating dry matter intake
•Decreased milk production
•Poor milk quality (low milk fat)
•Episodes of lameness (laminitis, sole abcesess, ulcers) •Episodes of diarrhea
•Unexplained high culling rate due to vague health problems

None of these are specific symptoms for sara!

4

EFFECT OF MODERATE NH3 EXCESS (before toxicosis) in RU: local and general

Local consequences
-disorders in ruminoreticular motility
- pH increases
- Decreased microbial activity (especially protozoa)
- Ruminal mucosa damage
Alkalosis: pH alkalitic, ammonic smell

General consequences
➡️protein deficiency
➡️threatening NH3-toxicosis
- Increased urea synthesis and excretion

5

NH3 POISONING (TOXICOSIS) Causes:

- sudden high protein or NPN (non - protein nitrogen, ie. urea) ingestion (without adaptation)
Ruminal NH3 concentration > 60-100 mmol/l
(300-500% fold increase, as normal value < 20-30 mmol/L)

6

NH3 POISONING (TOXICOSIS) consequences: local and general

Local
- motility decreases
- gas production increases  tympany
- absorption of inorganic compounds (ie. Ca2+) decreases
General
-first: compensated metabolic alkalosis
- second: incompensated respiratory acidosis
- tetany (decreased Ca2+, increased Na+, increased K+)
- hypersalivation, CNS symptoms, incoordination
- increased lipid mobilization (increased FFA in the blood) - ketone production

7

RUMINAL PUTREFACTION causes

-death of useful bacteria following acute acidosis, survival
and owergrowth of putrefactive bacteria (E. coli, Pasteurella)
– starvation
– protein (NPN-) overload (absolute)
– energy- (CHO-) deficiency (relatíve protein-overload)
– consumption of putrefactive food
– non accomodated rumen for the type of protein given

8

RUMINAL PUTREFACTION Consequences:

– alkalosis (local and general)
– decreased production (meat, milk)
– mucosal damage, potential bacterial invasion
– dyspepsia(indigestion)
Putrefaction: ruminal content is dark brown, stenchy,
ammonic or fecal smell, watery consitency

9

Simple Indigestion (Mild dietary indigestion)

Almost any dietary factor that can alter the intraruminal environment can cause simple indigestion.
Causes:
– Hand-fed dairy and beef cattle - variability in the quality and
quantity
– Sudden change in the pH
decreased: rapid fermentation,
increased: forestomach hypomotility and putrefaction
– Sudden excess to highly palatable feeds (corn or grass silage), relatively indigestible (poor-quality roughage, poor- quality straw, grain, spoiled or frozen feeds), introducing urea to a ration, turning cattle onto a lush cereal grain pasture

10

Simple Indigestion (mild dietary indigestion) consequences

-Anorexia, drop in milk production
– Rumen is full, firm, and doughy
– Primary contractions: decreased or absent, secondary contractions: decreased in strength
– Normal temp., heart rate, breathing rate, normal feces, but reduced in quantity
– Recovery usually is spontaneous within 24–48 hr

11

Lipid supplementation in ru

1. Fat of animal origin ( tallow) up to 2% of DM is accepted (fat of fish origin - mammalian source is not allowed
anymore (BSE) 2. Lipid of plant origin (oils and seeds)

12

Consequences of lipid overload in ru

- protein, carbohydrate maldigestion
- ruminal C3 and C4 increases, C2decreases - abnormal motility
- milk protein decreases
Protected or "bypass" fat
types: fat treated with formaldehyde, microcrystalline, soya flour, Ca- soaps
Important: rate of protection shows negative correlation with the
utilization
PUFA-rich fat  mammary gland TG uptake : LMF syndrome
58

13

INHIBITING FACTORS OF FORESTOMACH MOTILITY

1. Neurogen effects
a) central (sympathetic) effects decrease while parasympathetic effects increase the motility
b) peripherial (reflex)

2. Changes in the content of reticulorumen
a, physical/mechanical factors (fiber, sand, gas, temperature, strech – sympathetic effectes)
b, chemical factors
- pH<5.5 or pH>7.8 decreases motility
- toxic metabolites (ie. Amines, histamin derivates)
3. Other factors
a, blood constituents (NH3, VFA, glucose etc.) b, omasal obstruction
c, inflammatory processes (reticulo-peritonitis) d, decrease of the abomasal and duodenal pH

14

DISORDERS OF ERUCTATION causes

a, Generally: impaired forestomach motility (local inflammation, adhesion, stress)
b, Oesophageal spasm, obstruction, compression
c, Injury of the eructation reflex arc

15

DISORDERS OF RUMINATION

(regurgitation, remastication, reinsalivation, redeglutition)
Causes:
a, central (excitement, stress, fever, intoxication)
b, peripherial
- changes in the ruminal content - impaired forestomach motility
- organic causes (local inflammation, adhesion, stress)

16

RETICULAR (OESOPHAGEAL) GROOVE REFLEX Influenced by

• reflex arch injuries,
• sympathetic effects,
• nutritive factors (temperature, quantity, quality)
• endocrine system (ADH/vasopressin),
• water balance (thirst),
• other chemical compounds having local effect (copper sulphate, sodium bicarbonate)
• suckling, milk protein content

17

Forestomach, or abomasal obstrukctive syndrome (vagal indigestion, Hoflund syndrome)

Left upper, and right lower dilation of the abdominal cavity
Cause: chronic reticuloperitonitis
The question is whether the forms are independent processes or stages of the same problem .
): Investigations over disturbances in the functions of the by damage of the Nervus vagus causes

18

The three forms of vagal indigestion

Hypermotoric rumen (Truncus vagalis dorsalis injury) increased peristalsis
salivation
left sided foamy bloat
decreased ruminal emptying, inappetance reticulo-omasal functional stenosis bradycardia
Atonic rumen (Truncus vagalis dorsalis vs. ventralis injury) decreased peristalsis
decreased ruminal emptying, inappetance left sided gasous bloat
reticulo-omasal functional stenosis
Pylorus-stenosis (Truncus vagalis ventralis injury) decreased abomasal emptying
abomasal (righ-lower sided) dilation
reflux (Cl- > 30 mmol/l)
metabolic alkalosis

19

MALDIGESTION DUE TO ALTERED SECRETION OF GASTRIC JUICE

Hyposecretion is more important in animals than hypersecretion:
– hypochlorhydria, acholhydria, – Hypopepsia*,
– achylia gastrica

Consequences of hyposecretion:
*pepsinogen (precursor) Active: on low pH, Inactivated.: neutr. pH
decreased bactericid effect in the stomach
⬇️
pathogenic bacterial population in the small intestine can develop (dysbacteriosis, SIBO = small intestinal bacterial overgrowth)
⬇️
bacterial maldigestion, endotoxaemia
⬇️
diarrhoea
Enzymatic function of stomach is not essential regarding the digestion.

20

MALDIGESTION DUE TO ALTERED PRODUCTION OF INTESTINAL JUICE (MUCUS*, SUCCUS ENTERICUS)

1️⃣Hypo- or hypersecretion occurs
(site: mainly the Liberkühn crypt secretory cells)
Consequence of hyposecretion: maldigestion hypersecretion: K+, HCO3-, protein and water loss
2️⃣ Enzymopathy, enzyme-deficiency
congenital form: decreased activity of disaccharidases (lactase, maltase), dipeptidases - lactose intolerance
⬇️
dyspepsia/maldigestion osmotic diarrhoea
acquired form: generalised carbohydrate malabsortion- villus atrophy

21

3. MALDIGESTION DUE TO ALTERED PRODUCTION OR CONDUCTION OF PANCREATIC JUICE

Hypofunction: EPI
Consequence
- pancreatogen maldigestion (dyspepsia)
- osmotic diarrhoea
- steatorrhoea (physiol.: fat is absorbed by 95%!!)
- amylorrhea
- protein loosing enteropathy (creatorrhea)
- vitamin B12-deficiency
- Small Intestinall Bacterial Overgrowth (SIBO) - decrease absorption (incretin effect)

Hyperfunction: can cause pancreatitis

22

4. MALDIGESTION DUE TO IMPAIRED BILE PRODUCTION

Hypofunction is important (hyperfunction is a theoretical problem and normal after a meal in monogastric species)
Consequence of decreased bile production:
a, impaired fat digestion ➡️ steatorrhea (hepatogenic dyspepsia)
b, impaired endotoxin-fragmentation
⬇️ (ALP destroys endotoxins in the blood circulation)
physico-chemical defence of the body decreases
⬇️
endotoxin production increases
⬇️
shock

23

MALDIGESTION DUE TO BACTERIAL DYSFUNCTIONS affects what

Decreased and increased bacterial digestion is equally important.
Intestinal defence against harmful bacterial effects:
1. Persitalis (self cleansing mechanism)
2. Gastric acidity caused bactericide effects
3. Bile and pancreatic juice caused antibacterial effetcs
4. Intestinal mucous barrier
5. Gastrointestinal immune system
6. Bacterial competition
7. Ileocolic valve