Credit 3 Flashcards
Describe sinus tachycardia
(2 causes, ECG changes, characteristics) *
Characterized by increased heart-rate frequency.
Impulses are generated at the SA node, but at a faster than normal frequency.
It is associated with decreased vagal tone or an increased sympathetic
tone.
Pathologic responses that cause sinus tachycardia include: - fever - shock, - hypotension - anemia - congestive heart failure - hyperthyroidism and infections.
A large number of drugs can cause sinus tachycardia, either as a
desirable response or as a side-effect and include sympathomimetics,
parasympatholythics, and vasodilators.
Changes on the ECG include:
- the T-P interval shorters
- the P waves may be partially or completely fused with the preceding T waves.
For example:
Often associated with an increased temperature. The heart rate can then be 250 beats/min and at this speed the P waves are buried in the T waves of the preceding beats.
P waves are not distinguisable cause of the high temperature!
Cold water bath can help the patients temperature to decrease and P waves will be visible
Describe sinus bradycardia. Characteristics, cause and changes on ECG tracings *
Sinus bradycardia is a regular rhythm that originates from the sinus node but a rate is too slow.
Sinus bradycardia is observed in normal large-breed and well- conditioned dogs at rest and sleeping. Causes can also be result from: - increased in vagal tone - increases in cerebrospinal fluid pressure, gastrointestinal and respiratory disorders - hypothermia - hypothyroidism, - intoxicants - central nervous system lesion.
Changes on the ECG include T-P interval prolongation.
Example
In sleeping dog with sinus bradycardia wiyh 35 beats/min.
Everything is usually well visible of ECG but number of complexes / min are lower.
The heart rate frequency are too low but AV node generates impulses but at a lower frequency than normal
Describe sinus arrest
= Sinus rythm
Sinus node fails to fire impulse for the duration of 2 P-P intervals or longer, causing a pause and absence of P intervals
Causes: Sick sinus syndrome, drugs or electrolyte disturbances
Describe atrial flutter *
Characteristics:
- There are extremely rapid (more than 300 beats/min in dog) P or flutter waves, which give the baseline a sawtooth appearance.
- Physiologic block of some of the flutter waves in the AV node is common and results in a ventricular rate that is slower than the atrial rate.
- Conduction through the AV node to the ventricle may follow a
pattern expressed as 2:1 or 3:1 AV conduction, producing a regular ventricular rhythm, whereas at other times the conduction pattern
appears random, resulting in a very irregular ventricular rhythm that can mimic atrial fibrillation.
- QRS configuration are normal!
Atrial flutter is an uncommon rhythm disturbance in veterinary patients and is associated with:
- mitral stenosis
- myocarditis
- hyperthyroidism.
Describe Atrial fibrillation *
Due to a high number of disorganized atrial impulses bombarding the AV node
- Many of them approach the AV node in a refractory period and are NOT conducted to ventricles.
- The atrial depolarization rate are very rapid: From 400 - 600 beats/min
- The P waves are replaced by fibrillation waves, f waves which represents chaotic atrial activity.
QRS complexes are usually normal, the ventricular rate is rapid: 200 - 280 beats/min
Often associated with
- Cardiomyopathy
- Severe ischaemia
- Shock
- Electrolyte disturbances
Desribe the atrioventricular junctional rhythm *
- Escape rhythm (atrioventricular junctional rhythm).
- An escape rhythm can occur only when the normal cardiac pacemaker
(the SA node) stops or slows to a rate less than that of a subsidiary
automatic pacemaker. - The subsidiary pacemakers (AV nodal or junctional tissue and the Purkinje fibers in the ventricle) function as a rescue mechanism during
severe bradycardia. - Depolarizations that occur after a pause are called escape rhythms. An escape rhythm = A run of 3 or more complexes.
- Escape rhythms originate either from the AV junctional region (junctional) or from Purkinje fibers (ventricular).
- The heart rate of the junction is always lower. Usually less than 6 beats/min
An escape complex (beat) = A single spontaneous impulse from a lower pacemaker
There will be a negative P wave! Either before, after or masked by the QRS-complex
Describe premature ventricular depolarizations, characteristics ECG *
A type of ventricular arrythmia.
Result from the spontaneous depolarization of the distal to
the bifurcation of the bundle of His.
Since it starts the depolarization within the bundle branch the depolarization are not able to use the conduction system in the ventricles but instead must occur from myocardial -> myocardial cell which is a longer process.
Resulting in a
- QRS complex that is wider than normal.
- Large, bizzare T wave
= Premature QRS complex followed by the bizarre T wave with an opposite polarity
It can appear in two patterns
- Ventricular bigeminy = Each sinus beat is followed by a VPD for a period
- Ventricular trigeminy = Every 3rd depolarization is a VPD
1st degree AV block *
First-degree AV block is simply a delay in conduction across the AV
node.
The P-R interval is prolonged with the normal P wave and QRS
complexes, at a 1:1 ratio
Occur due to
- drug administration
- hyperkalaemia
- increased vagal tone
2nd degree AV block *
Second-degree AV block results when not all of the sinus impulses are
conducted to the ventricles.
This produces an abnormal heart rhythm and is also a cause of cardiac
arrhythmia.
It can range in severity from only an occasional P wave not followed by
a QRS complex on the ECG to most P waves being blocked.
However most often:
- P wave is present without QRS complex
- More P waves than QRS complexes
Second-degree AV block is classified as either type I or type II.
3rd degree AV block *
Can be a complete heart block.
- There is no conduction between the sinus node and the ventricles. All of the impulses generated by the sinus node are blocked at the AV node or bundle brances.
The sinus node depolarizes at its own inherent rate, depolarizing the atria and producing P waves, whereas the ventricles are depolarized by a subsidiary pacemaker (either the AV node or Purkinje fibers) that depolarizes at a slower rate, depolarizing the ventricles and producing QRS complexes.
Changes on the ECG:
There is no relationship between the P waves and QRS complexes, resulting in varying P-R interval from beat to beat.
Atrial rate is faster than the ventricular rate.
- The ventricles function as a rescue mechanism
- Atria contracts faster than ventricles cause they are controlled by different pacemakers
Define myopathy *
Non inflammatory degeneration of skeletal and cardiac muscle
• Characterized by
- Muscle weakness
- Myoglobinuria
- Increased activity of several enzymes like CPK, LD, AST
- Often myoglobinuria
In the affected muscle occurs
- Atrophy, Necrosis or degeneration
Degeneration = Loss of specialized function of muscle cells e.g. Ca salts, fat or fibrous tissue may be deposited in the affected muscle
Necrosis = Death of muscle cells in demarcated area.
Necrosis can also cause a different morphological forms
- Focal = Small areas of necrosis
- Coagulation = Caused by agents that rapidly abolish vital processes
- Zenker’s = Death of striated muscle cells -> Coagulation of the proteins contained in these cells.
Nutritional myopathy, in piglets *
Young rapidly growing pigs/animals fed high energy, low vitamin E and selenium diet or diet rich in unsaturated fatty acids.
Deficiency of vitamin E and selenium cause - lipoperoxidation of the tissue
- hepatic necrosis
- fibrin presence of the myocardium also known as Mulberry disease
Name the 7 types of myopathies. *
a) Nutritional myopathies
b) Non-nutritional myopathies
c) Exercise-related myopathies
d) Metabolic and hormonal myopathies
e) Ischemic myopathies
f) Inherited myopathies
g) Myopathies caused by plant
Mechanism of development of myopathies caused by selenium and vitamin E deficiency *
Nutritional myopathy and Nutritional muscular dystrophy; also called white muscle disease
Selenium is a component of the enzyme glutathione peroxidase acting in the breakdown of hydrogen peroxidase into catalase -> Responsible for protecting the body from oxidative damage
Deficiency can be from
- legume feed
- prolonged transport
• Vitamin E maintains the integrity of cellular membrane
• In conjugation both selenium and vitamin E protect the cell membrane and lipid
containing organelles such mitochondria and endoplasmic reticulum
• In lambs, calves and foals fed a diet with deficiency in vitamin E and selenium cause Lipo-peroxidation of the tissue ( skeletal and myocardial) leading to degeneration of muscle causing
- acute heart arrest
- necrosis of muscle cells
- retention of Calcium in muscle fibers also known as calcification
- release of enzymes such as LD, CPK, ALT
Clinical signs: inability to stand, stiffness, trembling and weakness
• In young, rapidly growing pigs fed a diet with deficiency in vitamin E and selenium cause Lipo-peroxidation of the tissue,
hepatic necrosis and fibrin presence of the myocardium also known as Mulberry disease in pigs
Mechanism of development of non-nutritional myopathy in piglets. *
Myodegeneration induced by iron of piglets.
- An acute poisoning and seen in piglets if deficient in Se or vit E and will be administered with exogenous Iron to prevent iron deficiency - for anemia for example.
Piglets born from sows deficient in vitamin E and Se, and by addition of Iron will damage muscle cell membrane leading to an leakage of K+ from muscle cells to plasma, causing Hyperkaliemia which has a toxic effect on cardiac activity since very young piglets are unable to excrete administered K+
Can lead to cardiac arrest and sudden death.
On ECG;
- Tall and peaked T waves
- Prolonged P wave and QRS duration
- Later decreased and disappeared P wave
Myoglobinuria in horse, characterize *
Exercise related myopathy. Also called
- Monday morning disease
- Exercise associated myositis
Occurs after light exercise in horses during under going training who have rested for one or more days but being maintained on full carbohydrate diet.
Clinical signs: • Stiff , stilted gait • Sweating • Tachypnoea • Muscles of gluteal or femoral groups are swollen and hard
May be caused by
- Sudden elevation or intensity of training
- Diet: High in carb.
- Factors altering the blood supply of working muscle
Causes
- Accumulation of glycogen in the muscle fibres during rest.
1/5 of the stored glycogen will be form CO2 and O2 for production of energy.
4/5 during exercise due to inadequate blood supply to muscles will oxygen will cause glycogen to be converted into lactic acid, causing pain and irritation
- Red or chocolate brown discoloration of urine
- CPK is increased roughly in proportion with how secere the disease is. Peaking 4-8h after exercise and back to normal after 4 - 6 days
- AST levels are peaking 24-48h but takes several weeks to return back to normal.
Myopathies caused by hormonal imbalances *
- Hyperkalaemic periodic paralysis
- Hypothyroidism
- Cushing’s syndrome
Hyperkalemic periodic paralysis - Occurs in horses between 1 and 5 years of age. Characterized by - Spontaneous muscle contractions/twitches of certain area - weakness - Paresis of pelvic limbs - increased level of potassium in blood. - Genetic basis of disease
Causes of disease are
- Membrane abnormality in skeletal muscle of the neck and trunk:
* Causing alteration of ionic permeability of muscle
* Hyperkaliemia: More
generalized fasiculations and recurrent episodes of muscular
fasciculation
Hypothyroidsm
In the skin are proteins complexed with polysccharides, sulphuric acid and hyaluronic acid.
Where these complexes SC
accumulate and causes myxoedema which are edematous deposition of
polysacharides and a water and sodium retention
Characterized by insufficient synthesis of thyroid hormones, T3 and T4 of thyroid gland.
Generally a decreased metabolic ragte and special changes in skin or subcutaneous tissue can be seen.
Cushing’s syndrome
- Chronic cortisol excess
- Glucocorticoids increase the hepatic glucose output and provide substrate for hepatic GNG.
Typical with muscle wasting and muscle weakness due to excess protein catabolism and decreased muscle protein synthesis
What is Splayleg syndrome? *
An inherited myopathy in newborn piglets and is characterized by temporary inability to stand with the hindlimb
• Affected hindlimb are splayed sideways or forwards and animals are resting in sternal recumbency (laying position) and have difficulty to access the nourishment
- Causes:
- Hereditary predisposition
- Maternal stress (glucocorticoid myopathy)
- Maternal nutrition
- Toxins
- Slippery floors
- Mechanism of development
Development of neuromuscular system in forelimbs is completed before the hindlimb
- This late development affects the muscles of the hindlimb
• Semitendinosis
• Longissimus dorsi
Are characterized by
- Decreased number of myofibrils and their
size (IMMATURITY OF MUSCLES)
- Increased permeability of muscle cells
Increased permeability will also increase the enzyme activity of CPK, LD and AST in the blood
• Immaturity can be overcome by rapid growth if piglets are fed artificially
Mechanism of development of enzootic calcinosis *
Chronic disease in cattle and sheep after eating chronically plants on pasture containing calcinogenic glycosides –> causing calcification of soft tissue
- especially BV and endocardium
• Results in Glycoside hydrolization by microbial enzymes in rumen to form vitamin D3 analog
• This will synthetize Ca2+ binding protein and mobilize calcium from bones –> Resulting in hyperkalcemia
• Hyperkaclemia causes calcification of soft tissue, blood vessles, endocardium
which will make animal reluctant to move and stiff.
Prognosis:
Not so good since resorption of Ca deposits is minimal after removing animal from the affected pasture
Analog vit D3 = 1,25 dihydrocalciferol: Active form of vit D
Primary hyperparathyroidism – characterize, describe mechanism. *
An excessive secretion of PTH which causes hypercalcemia, muscle weakness, demineralization and fracture of bone.
• Common in older dogs.
Mechanisms:
o In bone: increased bone resorption, cause loss of bone tissue - result in fibrous dystrophy in mandible and vertebrae.
o In kidneys: increased retention of salts, Ca2+ and increased excretion of P - result in precipitation of calcium phosphalate and oxalate in renal tissue and urinary tract.
o Increased bone resorption and increased retention of Ca2+ also cause hypercalcinaemia.
Secondary hyperparathyroidism – characterize, describe mechanism. *
2 types; Renal and nutritional.
Renal secondary hyperparathyroidism:
Excessive secretion of PTH is caused by extra parathyroid diseases
- A chronic renal failure results in:
- Decreased glomerular filtration rate
- Unable to excrete P
- Decreased synthesis of 1,25 DHCC which further decreases Ca2+ absorption and results in Hypocalcaemia
- Leads to increased levels of P in blood plasma which stimulate PTH release
–> PTH levels increases and cause demineralization of bones = rubber jaw
Nutritional secondary hyperparathyroidism:
- Young growing animals or adult dogs and cats fed on a low Ca diet / low P, normal Ca, and inadequate amounts of vitamin D3 –> hypocalcaemia.
- Horses and birds fed on high P diet –> suffer from hyperphosphatemia
Both of these stimulate PTH and result in increased bone resorption and bone demineralization.
Difference between osteoporosis and osteomalacia *
Osteoporosis Is characterized by excessive loss of the bone mass. May produce - weakness - stiffness gait - pain on bones and joints and fractures
Causes due to
• Insufficient stimulation of osteoblasts in prolonged immobilization, E2 deficiency
• Disorders of bone matrix formation in
- protein deficiency because of starvation and malnutrition, pregnancy
- glucocorticoids excess
- hypothyroidism
- Prolonged heparin therapy and
- Deficiency of calcium due to unbalanced diet
Osteomalatia
Is a metabolic disease of the bone of mature animals characterized by decrease of the mineral component of the bone.
• It is rickets of adult animals
Causes of osteomalatia:
- Lack of vitamin D due to insufficient solar irradiation
- Impaired absorption from diet
- Severe chronic diseases of liver
- Increased resorption of bone minerals
- Excessive demineralization
Similar etiology to Rickets:
- Decreased of Ca2+, P and vit D and imbalance btw the need and supply to animal
3 causes of rickets *
Causes:
• Insufficient solar irradiation
• Renal disorders
- Renal 1-a-hydroxylase deficiency (renal failure) –> in which vit D is not converted to its active form: 1,25 DHCC
- Vitamin D receptor defect (vit. D deficiency)
- Lack of Calcium
- Decrease reabsorption of phosphate by the kidneys.
• Increased ALP, lack of density of affected bones compared to normal
ones
Characterize Rickets *
Metabolic disease of bone in young growing animals
characterized by defective calcification of growing bone.
Causes:
• Insufficient solar radiation
• Renal disorders
- Renal 1-alpha-hydroxylase
deficiency
- Vitamin D receptor defect
- Decreased reabsorption
of P by the kidneys.
Calcium and Phosphorous are principal ions found in bones.
Main difference between Rickets and Osteomalacia is
In Rickets
- Bone deformity
- NO fracture
In Osteomalacia
- NO bone deformity
- Fracture
But both are very fragile
What is myxoioedema *
Accumulation of polysaccharides, sulphuric acid and hyaluronic acid.
These 3 complexes subcutaneously causes myxoedema which is edematous deposition of polysaccharides
• In hypothyroidism, sodium and retention can also cause it
Mechanism of development of acute ruminal acidosis *
= Acute lactate acidosis
- Excessive intake of highly fermentable carbohydrates causes a shift in the production of VFA -> result in decreased acetic acid production and increased propionate production -> cause a decrease in the pH in rumen -> cause a shift in the bacterial population by replacing the cellulotic, methanogenic gram negative bacteria with gram positive streptococcus bovis cause even more decreased pH replace streptococcus by lactobacillus which produce high amounts of lactic acid. When fibres are absent from diet -> decreased salivation (saliva acts as a buffer) -> cause acidosis in the rumen.
Mechanism of development of acute ruminal alkalosis *
Ruminal alkalosis are divided into acute and chronic lactate alkalosis in ruminants.
- Also urea poisoning
- When too much urea is provided with carbohydrate diet and cattle hasn’t acclimatized to it.
- Microbes in the rumen will break urea –> NH3 by Urease and causing pH do increase due to high amount of free NH3 in rumen.
High pH causing increased absorption of NH3 –> blood and further –> liver –> brain. - In liver NH3 –> urea.
Liver exceeds its capacity (wastes ATP) and HCO3- levels will rise = pH increase = Alkalosis
= Less energy for Krebs cycle and cell respiration.
Mechanism of development of chronic ruminal alkalosis *
- Overfeeding of proteins for a longer period -> cause an increased pH and ammonia -> alters the proportion of ruminal microorganisms -> increase the number of coli and proteus bacteria -> they produce toxic amines (methylamines) -> result in damage of liver cells and rumen epithelium.
Describe mechanism of development of central and peripheral inhibition of rumenoreticular motility induced by bacterial pyrogens at the febrile stage of infectious disease. *
- Febrile anorexia:
- First are exogenous pyrogens stimulating the depression of gastric centres, which cause inhibition of RR motility -> then later during the course of fever, endogenous pyrogens cause RR smooth muscle relaxation -> causing a reduction in tension receptor activity -> causes a reduction in the excitatory afferent inputs to the gastric centres -> which will depress the gastric centres -> result in inhibition of RR motility.
In chronic ruminal acidosis, name 7(6?) systemic consequences & explain mechanism of development of 2 of them *
1) Laminitis
- Lysis of altered rumen microflora -> cause release of histamine -> cause engorged veins and pulsating digital arteries -> result in distortion, sloughing and loosing of the hooves.
2) Ruminal parakeratosis
- Ruminal papillae get enlarged and dark in colour -> cause clumping of papillae and thickness of cornified portion of the ruminal epithelium -> causes parakeratosis
- > result in decreased ruminal absorption.
3) Ruminitis and liver abscess
4) Demineralization of the bone
5) Cerebrocortical necrosis
6) Low-milk-fat syndrome.
3 principle causes of ruminal tympany (bloat) & 1 mechanism of development *
- Dietary origin: legume pastures and grains cause rapid digestion -> contain pectic substances which are converted to pectin in the rumen -> Pectin will eventually cause gelification of rumen content -> which causes increased rumen fluid viscosity -> result in inhibition of eructation.
o Legumes also contain soluble leaf proteins, which are able to form liquid lamellae between the gas bubbles -> inhibit eructation. - Physical obstruction of the esophagus
- Failure of oesophageal groove function.
- Interference with normal tone and motility of musculature of the rumen.
Explain mechanism of development of low fat milk syndrome of dairy cows. *
Milk arise from short-chain and long-chain FA.
In mammary gland - Short chained:
- Acetate
- B-hydroxybutare
Long-chained:
- VLDL chylomicrons
- FFA after lipolysis from adipose tissue
After a shift in the VFA proportion that result in decreased acetate and increased propionate -> decreased acetate causes directly low-milk-fat- syndrome, but an increased propionate -> cause increased insulin secretion -> which cause decreased lipolysis of adipose tissue -> cause a decreased amount of free fatty acids in the blood -> result in low-milk-fat syndrome.
Name and explain 4(3) consequences of ruminal tympany *
- Ruminal pressure: decreased heart minute volume -> cause occlusion in the vena cava -> increases the peripheral resistance -> increase the blood pressure.
- Intra-abdominal pressure: pressure on diaphragm give dyspnoea and hypoxia.
- Intraruminal pressure: Cause retention of CO2 and formation of acidosis, that result in hyperkalemia.
Describe mechanism of development of feedlot (grain bloat) in ruminants.
- Dietary origin: legume pastures and grains cause rapid digestion -> contain pectic substances which are converted to pectin in the rumen -> Pectin will eventually cause gelification of rumen content -> which causes increased rumen fluid viscosity
- > result in inhibition of eructation.
- Legumes also contain soluble leaf proteins, which are able to form liquid lamellae between the gas bubbles -> inhibit eructation.
Consequences of Ca, P and Vitamin D deficiency
Due to imbalances of endocrinopathy of both PTH and Calcitonin and dietary deficiencies
Causing disorders of: • Growth and appetite • Reproduction • Milk production • Bone
