Otras preguntas Flashcards
What are antigenic epitopes (antigenic determinants)?
An antigen is composed of many molecular units to which an antibody binds. A single antigen may be composed of many antigenic epitopes.
Cross-reactive epitopes
Antigenic epitopes can be shared among different bacteria and host cell
Composition of G+ bacteria wall
Peptidoglycans
Composition of G- bacteria wall
Thin lippolysacharides (endotoxin)
Antigenic structures of bacteria
G+: peptidoglycans wall cell G-: Lippoporisacarides wall cell Capsule: polysaccharides Pili Flagella: Flagellin Nucleic acids
Antigenic structures of virus
envelop or capsule
What is antigenicity /immunogenicity?
degree of immune response induced by an antigen
Characteristics that contribute to potent antigenicity
Forein versus self antigens
Size
Biochemical structure and complexity (Proteins>lipids/carbohydrates)
Stability and degradability
What is the first line of defence?
External body surface
The second line of defence?
Macrophage-monocyte lines
Phagocytic cells of the myeloid
Time of life of Neutrophils
12 h in circulation but longer in tissue
Phases destruction of antigens by neutrophils
Phagocytosis
Respiratory Burts
Neutrophils can present antigens to lymphocytes?
NO
NETosis
neutrophil cell death
Neutrophils are activated by
LPS
TNF-alpha
IL-8
What are NETs
neutrophil cellular traps
Release during NETosis
Lyme disease (borreliosis)
B. burgdorferi
The tick in Lyme disease (borreliosis)
Ixodes scapularis
In Lyme disease the transmission in the ticks
is transstadial but not transovarial
Lyme Borrelia spp
Spiral-shaped, motile, G- spirochetes
Lyme disease (borreliosis) cause
Arthritis
Nephritis
Diagnostic test for Lyme disease
PCR
SNAP-4DxPlus test
C6Quant test Idexx
SNAP-4DxPlus test
Heartworm antigen
Antibodies: Ehrlichia canis
E. Chaffensis
E. ewiingii
Anaplasma phagocytophilum
A. platysC6Quant test Idexx
Gives a quantitative result
Mycobacterium
Intracellular, aerobic, acid-fast, non-spore-forming, environmental resistant bacilli.
Nocardiosis
Gram-positive, variably acid-fast, catalase-positive, non-motile aerobic bacteria that form filaments that may break into bacillus and coccal forms.
Treatment of Nocardiosis
Sulphonamide antibiotics
Tetanus
Clostridium; G+, anaerobic; spore-forming bacteria
Agent of Tetanus
Clostridium tetani
motile, Gram-positive, non-encapsulated, anaerobic, spore-forming, rod-shaped bacterium.
Fase of the organism sensitive to chemical and physical treatments
Spores are resistant
The vegetative form is sensible.
Presence of Clostridium tetani means infection?
No because not not all the strains possess the plasmid
Exotoxins of Clostridium tetani
Tetanolysin
Tetanospasmin
Action of tetanolysin
Clostridium tetani exotoxin that damage the surrounding tissue and obtein conditions for bacterial multiplication.
Action of tetanospasmin
Clostridium tetani exotoxin that prevent the neurotransmitter release by cleaving and inactivating synaptobrevin, a mb or “docking” protein necessary for the export of intracellular vesicles containing the neurotransmitter.
What is Synaptobrevin
It is a member of the SNARE protein family, a highly conserved group of proteins essential for docking and fusion of neurotransmitter vesicles with the presynaptic menbrane.
What neurons are more affected by tetanospasmin
inhibitory interneurons that release GABA
Clasification of tetanus severity
I: only facial signs.
II: Generalized rigidity or dysphagia, with or without class I signs.
III: Class I or Class II with seizures.
IV: Dogs have class I, II or III with abnormal heart rate, respiratory rate or blood pressure measurements.
Diagnosis of Tetanus
Clinical signs.
Serum antibodies to tetanospasmin.
Treatment strategies in Tetanus
- Toxins present in the body outside the CNS should be neutralized.
- Organisms present in the body should be destroyed to prevent further toxin release.
- The effects of the toxin already in the CHS should be minimized.
INTENSIVE CARE
- The effects of the toxin already in the CHS should be minimized.
Tetanus antitoxin
Anti-tetanus equine serum.
human tetanus immune globulin (more chance of reaction).
Antibiotic in case of tetanus
Metronidazole is superior to penicillin
Why benzodiazepines in tetanus
Because it augments GABA agonism at the GABAa receptor.
Agent of botulism
Clostridium botulinum
Clostridium botulinum
Gram +; anaerobic; spore-forming; rod bacteria
The target of the botulism toxins
SNARE protein that light in prevents the presynaptic release of acetylcholine at the neuromuscular junction, resulting in flaccid (lower motoneuron) paralysis and evident of autonomic nervous system dysfunction.
Clinical presentation of botulism
afebrile, acute-onset, progressive, flaccid paresis, with additional involvement of the autonomic nervous system.
(Mydriasis with depressed pupillary light reflexes).
Diagnosis botulism
demostration of botulinum toxin early in the course of the disease, either in blood or intestinal contents.
Treatment botulism
Supportative
Bartonella agent
Gran negative
urine specific gravity often in dog with hypercalcemia and hyperthyroid
< 1020
Treatment canine thyroid carcinoma
Doxorubicin, cisplatin and mitoxantrone
Most frequently B-cells tumor
insulinomas
carcinomas
Frequently metastasis in cases of insulinomas
Regional linfonodes and liver
level of glucose that stop the release of insulin
<80 mg/dl
Causes of decreased glucose production
Hypoadrenocorticism Hypopituitarism GH deficiency Liver insufficiency Glucogen storage disease
Treatment acute insulinoma
Bolus 50% dextrose (0.5g/kg IV diluited at ratio 1:3 in 0.9% sodium chloride). The bolus should be followed with an IV continuous rate infusion CRI of 2.5% to 5% dextrose.
The lowest amount of glucose deemed necessary must be administered with cation because glucose stimulate insulin secretion.
Medical treat insulinoma
Streptozocin (nitrosiurea antibiotic)
Prednisone
Diazoxide (benzothiadiazine)
Octreotide (long-acting synthetic somatotatin analogue.
Action of the prednisone in the treatment of the insulinoma
increased blood glucose concentration by increasing gluconeogenesis and glucose 6-phosphatase activity while decreasing blood glucose uptake into tissues and stimulating glucose secretion.
Actions of antiepileptic drugs as phenyton
enhance the inactivation of sodium channels ( in the neuron potential action), making it less likely that an action potential will be propagated.
Action of toxins as pyrethrins in the CNS
Pyrethrins block sodium channel inactivation, increasing action potential generation an causing tremors and seizures
Two factors that influence the speed at which the action potential travels down an axon
- Axonal diameter: Increasing the diameter of the axon increases the number of available for currents to flow.
- Myelin: Permits the ions to flow between the unmyelinated areas (nodes of Ranvier) in a saltatory fashion.
How botulism toxin works
Botulism toxin binds to one of the vesicle docking proteins, preventing the release of acetylcholine at the neuromuscular junction.
Kinds of neurotransmitter receptors
- Ionotropic receptors regulate ion channels.
- Metabotropic receptors: act through second messengers.
Three families of inotropic receptors
- Nicotinic acetylcoline (ACh).
- Gamma-amino butyric acid (GABA) and glycine.
- ATP or purine P2X receptor
What happened in myasthenia gravis
Autoantibodies directed against the alpha1 subunit partially block the ACh receptor in the neuromuscular junction. This make more difficult for ACh to open the channel and produces the fatigue that is the hallmark of the disease.
How Acetylcholinesterase work
this in the synaptic cleft breaks down ACh to choline and acetic acid, which are taken up into the presynaptic terminal and used to resynthesize ACH.
How GABA works
GABA is the major inhibitory neurotransmitter. The GABA-A receptor and the closely related glycine receptor have a similar structure to the ACh receptor, but the ion channel in only permeable to the anion Cl. When channel opens, Cl can diffuse into the cell, creating a inhibitory postsynaptic potential (IPSP) that hyperpolarizes the cell.
How antiepileptic drugs work? Diltiazem and phenobarbital.
they bind to extracellular sites on the GABA-A receptor. They do not open the ion channel, but they alter the kinetics of the channel, increasing the time the pore is open when GABA binds to its receptor.
The major excitatory neurotransmitter in the CNS?
Glutamate
Subtypes of ionotropic glutamate receptors
AMPA (releasing Mg)
NMDA (increased conductance of Na and intracelurarCa) EPSP
Excitotoxicity
An excessive NMDA receptor activation can cause the accumulation of intracellular Ca that trigger cell death.
Metabotropic receptors (act through second messenger systems such as G-proteins and produce more prolonged influences on function.
Muscarinic acetylcholine receptors metabotropic glutamate receptors GABA-B Serotonin receptors norepinephrine epinephrin histamine dopamine neuropeptides endocabinoides
Mecanism of D2 dopamine receptor
decrease AMPc levels and increased aeurosal
Mecanism adenosine receptor
increased cAMP levels and decreased aeurosal.
Caffeine
Adenosine receptor block leaving dopaminergig activity unopposed and thus increased arousal.
How serotoning work
The activity of serotoning on its post-synaptic receptor is determined by reuptake of serotoning into the presynaptic terminal by the serotoning transporter.
Myotatic reflex
When a muscle is streched, receptors in the muscle spindle are stimulated. The action potentials generated by the stimulus travel to the spinal cord where they synapse directly on the motor neuron that innervates that muscle, producing contraction
Defecation
There are two main anal sphincters; an internal and external sphincter. The internal anal sphincter is controlled by parasympathetic fibres which relax involuntarily. The external anal sphincter is skeletal muscle that is controlled by somatic nerve supply from the Inferior anal branch of the Pudendal nerve (S2,3,4), which allows conscious control of defecation.
When the rectum is distended the rectosphincteric reflex is initiated and relaxes the internal sphincter. If defecation is not desired, voluntary contraction of the external sphincter can delay it. If defecation is appropriate, then a series of reflexes take place that lead to:
Relaxation of the external sphincter
Contraction of abdominal wall muscles
Relaxation of pelvic wall muscles
Peristaltic waves then facilitate the movement of faeces through the anal canal.
Parashympatetic
a) Cholinergic
b) Adrenergic
a) cholinergic (acetilcholine)
_ Sympathetic- adrenergic-Norepinephrine/epinephrine_
What neurolocalisation would a Schiff-Sherrington posture suggest?
C1-C5
T3-L3
C6-T2
L4-S3
T3-L3
What cells are involved in the Schiff-Sherrington posture?
Purkinje cells
Border cells
Renshaw cells
Schwan cells
Target cells
Border cells
When a patient presents unconscious but can still be roused by painful stimuli he should be described as:
Confused
Obtunded
Stuporous
Comatose
Alert
Stuporous
Which nerve is the most important for the patellar reflex in the pelvic limb?
Tibial
Perineal
Pudendal
Sciatic
Femoral
Femoral
Which nerve is the most important for the withdrawal reflex in the pelvic limb?
Sciatic
Femoral
Perineal
Pudendal
Tibial
Sciatic
The cutaneous trunci reflex can be very useful in helping localisation of thoracolumbar spinal cord and possibly brachial plexus lesions. The sensory stimulus starts after pinching of the skin, it uses a sensory nerve to travel to the spinal cord where it will ascend until synapse with the lateral thoracic nerve (which results in contraction of the cutaneous trunci muscles bilaterally). At which segment of the spinal cord does the connection with the lateral thoracic nerve occurs?
T1-T2
C7-C8
C8-T1
T2-T3
T3-L3
C8-T1
Non-ambulatory paraparesis means that there is:
Reduced movement in the pelvic limbs and the patient is unable to walk
Reduced movement in the pelvic limbs but the patient can still walk unassisted
Loss of pain perception of the pelvic limbs
Loss of coordination of the pelvic limbs
Loss of ability to move the pelvic limbs
Reduced movement in the pelvic limbs but the patient can still walk if weight is supported
A patient with non-ambulatory paraparesis is graded as having a spinal injury:
Grade 5
Grade 1
Grade 2
Grade 4
Grade 3
Grade 3
Why might the spinal reflexes in the pelvic limbs be reduced in a patient with an upper motor neuron lesion?
Spinal shock
Schiff-Sherrington posture
Loss of pain perception
Decerebrate rigidity
Decerebellate rigidity
Spinal shock
The palpebral reflex uses as afferent and efferent the following cranial nerves:
Trigeminal and vestibulocochlear nerves
Ophthalmic and trigeminal nerves
Trigeminal and facial nerves
Oculomotor and vestibulocochlear nerves
Optic and facial nerves
Optic and facial nerves
What is strabismus?
Mydriasis due to lesion affecting parasympathetic supply to eye
Involuntary, unpredictable, conjugate fast eye movements in different directions
Miosis due to lesion affecting sympathetic supply to eye
Rhythmical, involuntary movements of the eyeball
Abnormal position of the eyeball that the animal cannot overcome
Abnormal position of the eyeball that the animal cannot overcome
What is jerk nystagmus?
Nystagmus with equal oscillations
Congenital nystagmus that happens with visual disorders
Normal nystagmus that occurs in response to moving of the head
Nystagmus with slow and fast phase
Nystagmus that occurs at varying speeds to different directions
Nystagmus with slow and fast phase
In Horner’s syndrome, what is NOT a clinical feature?
Mydriasis Ptosis Enopthalmos Conjuntival hyperemia 3 eyeliner protusion
Mydriasis
Horner’s syndrome is associated with a lesion affecting the sympathetic supply to the eye; this pathway is long and lesions in many different areas of the body could result in this presentation. Which of these locations though if affected should NOT result in Horner’s syndrome? Brainstein C7-C8 nerve roots Cervical spinal cord Retrobulbar region Tympanic bulla
C7-C8 nerve roots
Compulsive circling suggests a lesion in the …?
Ipsilateral peripheral vestibular system
Contralateral brainstem
Contralateral forebrain
Contralateral peripheral vestibular system
Ipsilateral forebrain
Ipsilateral forebrain
Proprioceptive deficits are caused by a lesion in the
Contralateral forebrain
Ipsilateral spinal cord
Ipsilateral cerebellum
Ipsilateral brainstem
All of the above are possible causes for proprioceptive deficits
All of the above are possible causes for proprioceptive deficits: Contralateral forebrain Ipsilateral brainstem Ipsilateral cerebellum Ipsilateral spinal cord
The postural test that involves picking up the patient and bringing the limbs to the edge of a table to see how quickly the paw is repositioned is called:
Paw position
Wheelbarrow
Placing test
Hopping test
Extensor postural thrust
Placing test
A normal (positive) response to testing pain perception (pinching a toe) in a limb is:
The animal shows a behavioural response by looking uncomfortable, vocalising or trying to bite
The animal urinates
The animal withdraws (flexes) the limb
The animal extends the limb
All of the above are correct
The animal shows a behavioural response by looking uncomfortable, vocalising or trying to bite
What cranial nerve is affected?
Loss of smell
I Olphatory
What cranial nerve is affected?
Partial or complete blindness ( Dilated unresponsible pupils)
II Optico
What cranial nerve is affected?
Ventrolateral strabismus, inhabiliy to rotate eye dorsaly, ventrally and medially, dilated irresponsible pupil, ptosis upper lid
III Oculomotor
What cranial nerve is affected?
dorsolateral strabism
IV Troclear
What cranial nerve is affected?
MM atrophy and jaw weakness (if bilateral dropped jaw) neurotrophic keratitis
V Trigeminus
What cranial nerve is affected?
Medial strabism, inability to move lat eyeball and to retract.
VI Abducent
What cranial nerve is affected?
Dropped, inability to move ear and lip
VII Facial
What cranial nerve is affected?
Deafness, vestibular signs
VIII Vestibulococlear
What cranial nerve is affected?
Dysphagia absence gag
IX Glosopharingeo
What cranial nerve is affected?
Dysphagia, inspiratory dyspnea, dysphonia, regurgitation, absence gag.
X Vago
What cranial nerve is affected?
Trapezius atrophy
XI Accesory
What cranial nerve is affected?
Tonge desviation
XII Hipoglosso
What we are evaluating with the palpebral reflex?
V ; VII ; Bainstem
What we are evaluating with the corneal reflex?
V; VII; VI; Brainstem
What we are evaluating with the physiological nystagmus?
VIII; III; IV; VI; brainstem
What we are evaluating with the Menace response?
II; VII; forebrain; cerebellum; brainstem
What we are evaluating with the Nasal mucose stim?
V; forebrain; c brainstem
What we are evaluating with the PLR?
II; III; brainstem
What we are evaluating with the gag?
IX; X; brainstem
Allele
one of number of different forms of the same gene
Heterozygous
Having two different copies (alleles) of a gene for a specific trait or disease. One of the two is usually the wild type.
Homozygous
Having two identical copies of a gen for a specific trait or disease
Phenotype
The observable characteristic of an animal that result from the interaction of the animal´s genetic makeup and the environment.
Polygenic
A sisease or trait caused by the interaction of two or more genes.
Transcription
First step in gene expression when the DNA gets transcribed to RNA.
Translation
Second step in gene expression in which RNA becomes to form amino acids.
Gen
Region of the ADN that code for the production of polypeptides.
Exons
coding region of the ADN
Introns
Untranslated regions of the ADN
Enhancers and silencers
Regions in the ADN that serve to regulate the transcription process.
Promoter region
Area of regulation in the ADN that help to initiate the transcription process.
Start codon
first aa that is translated by the ribosome. In eukaryotes this almost always produces the aminoacid methionine.
Stop codon
Is the codon that signals the end of translation and is typically one of the following codons:
TAG
TAA
TGA
Dog genome
38 autosomal chromosome pairs and 1 pair of sex chromosome
Cat genome
18 autosomal chromosome pairs and 1 pair of sex chromosome
Autosomal recessive pedigree
Two aparent silent carriers of the disease are bred the disease is produced at approximately 25% prevalence.
Autosomal dominant pedigree
Affected individuals only need one copy of the abnormal gene to show the disease. It does not skip generations. If two animals that are heterozygous for the trait are bred, both affected and unaffected individuals can be produced.
X linked recessive trait
An affected male passes the X chromosome to the daughters who can carriers of the trait. When bred, the X chromosome with the abnormal gene can be passed to some of the male offspring who will show the trait.
Karyotyping
evaluation of the number and apparence of chromosomes
Missense mutation
a single nucleotide change that results in the formation of a different amino. acid is typically observed.
Nonsense mutation
A single nucleotide change that results in the development of a stop codon, prematurely.
Penetrance
Proportion of individuals with a disease gene variant that will develop the disease.
Incomplete penetrance
Some individuals with the disease gene variant (mutant) will not develop the disease.
Phenotype
The observable characteristics of an animal that result from the interaction of the animal´s genetic makeup and the environment.
Polymorphism
Naturally occurring single base pair variants in the DNA sequence that have no adverse effects in the animal and are generally observed in at least 5% of the population.
Wild Type
The most common copy (allele) of the gene, typically that found in the normal individuals.
Thiopurine Methyltransferase (TPMT)
Is important for metabolizing a number of cancer and and immunosuppressive agents including azathioprine and 6-mercaptopurine.
Blepharitis
inflammation of the eyelids
Myxedema coma
Rare, life-threatening manifestation of hypothyroidism. Clinical signs include mentation changes due to brain edema, hypothermia without shivering, non`pitting skin edema, and bradycardia.
Thiamine deficiency
lessions in the hippocampal formation.
Thiamine is essential for decaroxylation of pyruvic acid and other alpha-keto acids.
Hypocalcemia alterations
CAuse increases in mb excitability in both muscle and CNS. This leads to generalized stiffness, lameness, muscle twitching, nervousness, behaviour changes, tetany, and seizures
Calculation free water deficit
Free water deficit= 0.6x body weight (kg)x[(plasmaNa/148)-1]
Antibodies in rheumatoid arthritis
IgA; IgG and IgM
Type of hypersensitivity reaction in nonerosive polyarthritis
Type III hypersensitivity reaction
When an animal is considered overweight?
> 10% his ideal weight
When an animal is considered obese?
> 20% of his ideal weight
Characteristics transudate
clear, colourless. <2.5 g/dl total protein ; 1000-1500 cells/mcl (nucleated cell count); occasional mesotelia cells
Characteristics modified transudate
slightly cloudy; straw-colored; 2.5-5 g/dl total protein; >1000<500 cells/mcl. Mesothelial cells, non-degenerate neutrophils, macrophages, lymphocytes.
Exudate
Turbid to opaque; tan, may be blood-tinged; >2.5 g/dl total protein; >5000 cells/mcl nucleated cell.
Non sepctic: mesothelial cells, non degenerate neutrophils, macrophages, lymphocytes, occasionally neoplastic cells.
sepctic: Ddegenerate neutrophils, intracellular bacteria.
Eosiniphilic effusions
transudates or exudates with > 10% eosinophils
Starling´s equation
La suma de las fuerzas hidrostática y coloidosmótica a través de la membrana glomerular, que da lugar a la presión de filtración neta.
Q= K(Pmv-Ppmv)- (pmv-ppmv)
(pag 82)
Level of albumina as cause of peripheral edema
< 2 g/dl
Proportionate dwarfism is consecuence of
GH deficiency
Desproporcionate dwarfism
Juvenile Hypothyroidism
Feeding center
lateral hypothalamic nuclei
Satiety center
ventromedial hypothalamic uclei
what tissue release leptin?
adipose. Contribute to a sense of satiety.
Localization of the cough receptors
larynx
trachea
bronchi
Does irritation of the smaller bronchi, bronchioles and alveoli elicit cough?
No
when is considered the cough chronic
> 8 weeks
What is the guaifenesin
Expectorant
Mucolitycs
acetylcysteine, guaifenesin, ambroxol, bromhexine
cough suppresants
buthorphanol, codeine, hydrocordone, dextromethorphan
Bronchodilators
inhaled slabutamol/albutamol/albuterol, theophyline, aminiphylline and terbutaline
Dipherential diagnosis for hypercalcemia
respuesta
Paracrine
The messenger diffuses through the interstitial fluids, usually to influence adjacent cells.
Autocrine
the messenger acts in the cell of its origen
Neurotransmitter
which affect communication between neurons, or betwen neuron and target cells
transmitter found in endocrine and neural tissues
Epinephrine
Dopamine
Histamine
Somatostatin
Protein Hormons
GH
Insulin
Corticotropin (ACTH)
Peptides Hormos
Oxitocin
Vasopresin
Amines Hormones
Dopamine
Melatonine
Epinephrine
Steroid Hormons
Cortisol Progesterone Vit D glucocorticoides mineralocorticoids estrogenos androgenos
Hormones in the energy metabolism
Insuline Glucagon Cortisol Epinephrine Thyroid Hormone GH
Hormones in the mineral metabolism
Parathyroid H Calcitonin Aldosterone Angiotensin Renin
Hormones correlated with the growth
GH Thyroid Insulin Estrogen Androgen Growth factors
Hormones correlated with the reproduction
Estrogen Androgen Progesterone Luteinizing H Follicle-stimulating Prolactine Oxitocin
Differences between protein hormones and steroids
Protein hormones are synthesized as prohormones and then cleaved in the rough endoplasmic reticulum to form prohormones, and in the Golgi apparatus to form the active hormone, which is stored in granules before being released by exocytosis.
Steroids are synthesized from cholesterol which is synthesized by the liver; steroids are not stored but are released as they are synthesized
Protein hormones are hydrophilic
Steroids hormones are lipophylic
Dihydrotestosterone (metabolite) is more potent than testosterone
True
Localization of the hypothalamus
Third ventricle in the diencephalon
Precursors of Oxytocin and Vasopressin
Prepropressophysin- (neurophysin II)-Vasopressin
Preprooxyphysin- (neurophysin I)- Oxytocin
Main action of oxitocin
Contraction of the smoth muscle in the mamarian glan and the uterus.
What produce the Hypotalamus?
GHRH Dopamina CRH TRH GNRH
What produce the adenohypophysis
Glycoproteins: FSH; LH; TSH
Somatotropins: GH; PRL
Proopiomelanocortin: ACTH
How somatostatin work?
Inhibition GH
How Dopamine work?
Inhibition GH and prolactine
How TRH work?
Stimulation TSH
How GHRH work?
Stimulation LH +FH
How GH work?
Stimulation production IGF-1
Lipolisis
Inhibition insulin
How ACTH work?
estimula la generación de glucocorticoides y androgenos por la corteza suprarrenal.
Mantiene el tamaño de las zonas fasciculadas y reticulada de la corteza.
Células d ela glándula parathyroides
Follicular cells (T3-T4 production) Parafolicular cells (calcitonine)
Function of tiroglobulina
Transport of T3-t4 into folicular cell
Euthyroid sick syndrome
Increased TT4 decrease T3
Trigger of Dyspnea
Hypoxemia o Hypercarbia (PaO2<60 mmHg; PaCO2>50 mmHg)
Causes of hypoxemia
- -Decreased fraction of inspired O2
- Hypoventilation
- Diffusion impairment
- Right to left cardiovascular shunt
- Ventilation-perfusion (VQ) inequality
- Abnormal hemoglobin
If there is an increase of effort in the inspiration the obstruction
is in the upper airway
If there is an increase of effort in the expiration the obstruction
in in the lower airway
Paradoxical breathing pattern appeared when
greatly increased work of breathing and respiratory muscle fatigue.
mild hemorrhege is possible with a platelet count ..
<25.000 platelets/mcL
moderate hemorrhege is possible with a platelet count ..
<10.000 platelets/mcL
severe hemorrhege is possible with a platelet count ..
<5.000 platelets/mcL
Spasticity
increase in muscle tone due to hyperexcitable muscle stretch (myotatic) reflexes.
Myotonia
prolonged contraction or delayed relaxation of a muscle after voluntary or stimulated contraction.
A drug that can be helpful in presence of myotonia
Procainamida
How the strychnine cause tetania
It blocks the neurotransmitter glycine.
What happens in tetanus
Clostridium tetani under anaerobic conditions, produce the toxine tetanospasmin that interferes with release of inhibitory neurotransmitters glyvine and gamma-aminobutyric acid.
GABA is excitatory or sedative
excitatory
How works dexmedetomidine
is a central alpha-2-adrenoreceptor agonist with a site of action at the locus coeruleus, influencing Purkinje cell and GABAergic output
The hallmark of the cerebellar disease
Intention tremor
Shaker pup syndrome
Inherent develoopmental disorders of central myelination
What is ataxia
Ataxia is an inhability for the patient to coordinate the position of its head, trunk and limbs into space. Ataxia is a sensary, NOT MOTOR, dysfunction that can only be identified when the patient moves.
Sistemic condition that can cause ataxia
Hypocalcemia–Cerebral ataxia
Thiamine deficiency—Vestibulara ataxia
Tipes of ataxia
Propioceptive
Cerebellar
Vestibular
Head tilt
Vestibular ataxia. Usually the side of the head tilt indicates the side of the lesion.
Signs of vestibular ataxia
Head tilt Leaning Falling Rolling Occasionally circling, strabismus, and nystagmus.
The propioceptive positioning deficits are ipsilateral to the head tilt.
True, excep in cases of paradoxical vestibular syndrome, where proprioceptive deficits are contralateral to the head tilt.
Nystagmus in peripheral vestibular disease
Is always in the same direction, either horizontal or rotatory, BUT NOT VERTICAL
A characteristic alteration in cerebellar ataxia
Dysmetria
Paresis
Partial loss of motor function, which is usually manifested as weakness.
Paralysis (plegia)
Complete loss of motor function
Localization of the lesion in presence of paresis whithout ataxia
The lesion is located outside of the central nervous system and therefore not affecting the spinal cord.
The hallmarks of UMN signs
Paralysis or paresis with increased extensor tone (spasticity or hypertonus), normal to increased spinal refex (hyperreflexia), and slowly progressive muscle atrophy from disuse.
The hallmarks of LMN signs
paresis or paralysis with absent to decreased extensor tone (flaccidity or hypotonus), decreased or absent spinal reflex and rapid and severe muscle atrophy.
Localization of lesion in presence of Schiff-Sherrintong phenomenon
T2-L7
Clinical division of the spinal cord
C1-C5 cervical
C6-T2 cervicothoracic
T3-L3 Thoracolumbar
L4-S3 Lumbosacral
Localization of the lesion if involve all four limbs
C1-C5 or C6-T2
Localization of the lesion if involve all four limbs with increased tone and reflex in the pelvic limbs, normal to increased tone and reflex (UMN signs) in the thoracic limbs
C1-C5
Localization of the lesion if involve all four limbs with decreased tone and reflex in the thoracic limbs, (LMN signs) in the thoracic limbs
C6-T2
Lession localization in presence of paraplegia or paraparesis
Caudal T2
Cutaneus trunci reflex help to reconize a lesion in the segment
T3-L3
Lession localization in presence of paraplegia or paraparesis with normal to increased reflexes and muscle tone points
T3-L3
Localization with lesions in the nerve roots for pelvic limbs, peripheral region, sphinters and tail /refecting involvement of sciatic, pudendal, pelvic and caudal nerves).
L4-S3
Patient flexes the limb but does not have conscious perception of the painful stimulus
severe spinal cord lesion and carried a guarded prognosis.
Lesion localization in presence of stupor or coma
Brainstem or rerebral cortex
Structures in the caudal transtentorial herniation
Portions of the temporal lobe shift ventral to the tentorium cerebelli and cause midbrain compression.
Structures in the foramen magnum herniation
It is the most commun form. The caudal cerebellar vermis moves through the foramen magnum, causing compression of the displaced cerebellum and the medulla oblongata.
Lessions in the brainstem at the level of the pons can cause unilateral or bilateral pupillary…
constriction (miosis)
Lessions in the brainstem at the level of the midbrain can cause unilateral or bilateral pupillary…
Dilation (Mydriasis)
Nerves involves in the oculocephalic and doll´s eye reflexes
VIII; the brainstein (vestibular nuclei, medial longitudinal fasciculus), the cerebelum (flocculonodular lobe) and III; IV and VI
Cheyne-Stokes respiration
Hyperpnea alterning with apnea and can be an indication of a bilateral cerebral hemisphere or diencephalic lesion.
Kussmaul respiration
deeper than normal breaths occurring in an other wise normal pattern. (diabetic ketoacidosis)
Drugs that can be used in cases of Ptyalism
Atropine
glycopyrrolate
Phenobarbital (idiopathic ptyalism)
scopolamine
Nerves and center involving in the gagging
Trigeminal, glossopharyngeal and vagus
Center in the medula oblonga
The haustral contraction
Are coordinated contractions of the circular and longitudinal smooth muscle of the colon that result in accumulation of colonic contents in unstimilated segments. This mixing of colonic contents increases exposure of contents to colonic mucosa for maximum water and electrolyte absorption.
Inhibition of GHRH
Somatostatina and GH
Production of GHRH
Hypotalamo
GHRH stimula the pruduction of
GH
GH stimul the production of
IGF-1 (liver)
Inhibitory effect IGF-1
GH and GHRH
Effects GH
Rapid catabolic actions (insulin antagonist): lipolysis, gluconeogenesis, restricted glucose transport across cell membranes and hyperglycemia).
Slow anabolic actions: (insulin like growth factors IGFs)long term growth promoting actions.
Major determinant of the body size.
Diagnosis of acromegaly in cat. Level of IGF-1
> 1000 ng/ml
Tissue thatsintetize GH
hypophysis (pulsatil) and mamaria gland (constant production)
Progesterone receptor blockers
Aglepristone
What cobinations of hormones alterations are frequently in the dwarfism
GH. TSH and prolactine deficiences
Impared relax of gonadotropins
Normal adenocorticotropes hormones (ACTH)
Mutation in the pituitary dwarfism
LHX3
Diagnosis of GH deficiency
Stimulation with GHRH or alphaadrenergic drugs (clonide or xylacine)
A plasma concentration >5mcg/L 20 min after IV administration of 2mcg/kg ghrelin, exclude pituitary dwarfism.
What is the stimulos for secretion of vasopresin
Increase plasma osmolality
Angiotensina II
Action vasopresin
in the luminal collecting duct cell. Binding V2 receptors: - Expresion of Aquaporing 2 that enhances permeability and water reabsorption. - Release Von Willebrand factor. - Release tissue plasminogen activator. - Release atrial natriuretic peptide.
Binding V1 receptors:
- Vascular smooth muscle contraction
- glycogenolisis
- platelec activation
Within the anterior pituitary gland:
- Synergic effect with CRH to stimulate ACTH release.
Other effects:
Stimulates synthesis of NO
Increases concentrations of coagulation factor VIII
Neurotransmitter and chemical mediator within the brain
Treatment nephrogenic diabetes insipidus
Thiazide diuretic (decrease Na reabsortion from distal tubules. Potassium-sparing diuretics.
False increased of TCa
Hemolisis and lipemia
How hypoproteinemia affected Ca analysed
Lowers measured TCa concentrations but does not affect iCa
How Ph affected Ca concentrations
Low PH iCa increase
Increased PH decreased iCa
Circulating Ca concentrations are under control of four main factors:
PTH
Calitonin
Vit D
Parathyroid hormone-related protein (PTHrP)
How affect Vit D to the PTH
increased Vit D decreased velocity PTH gen trasncription
PTHrP
Parathyroid hormone-related protein is integralto calcium homeostasis in the fetus.
Where is produce calcitonnin
C-cells by thyroid glands
place in the kidney of Ca absortion (PTH)
distal convoluted tubules and thick ascending loops of Henle
Hallmark of hyperparathyroidism
increased iCa and TCa while PTH are within or above normal range.
PTH inhibits renal phosphate resorption, and serum concentrations are low-normal or below reference range.
Furosemida can be used in PHTP when the animla is corrected hidratated
Furosemide can further enhance renal Ca excretion
Thyroglobulin
A large glycoprotein containing iodotyrosines, components of thyroids hormone.
Thyroid peroxidase
Enzyme that is involve in most of the steps of thyroid hormone synthesis.
Proteins bound the thyroid hormones in circulation
Thyrosine binding globulin 60%
Transthyretin 17%
Albumin 12%
Cause of secondary hypothyroidism
glucocorticoid excess
Diagnosis of lymphocitic thyroiditis
Presence of TgAAs (Thyroglobulin autoantibodies)
Autoimmune polyendocrine syndrome type 1
Rare autosomal recesive disorder:
mucocutaneus candidiasis
Autoimmune thyrid disease
Addison´s disease.
Autoimmune polyendocrine disease type II
development of two or more of the following: Addison´s disease Grave´s disease Autoimmune thyroiditis Type1 DM primary hypogonadism Myasthenia gravis Celiac disease
Euthyroid sick syndrome
changes in thyroid hormones concentration secondary to acute and chronic illnesses.
Drug that can induce hypothyroidism and even myxedema coma because of their ability to reversibly inhibit TPO
Sulfonamides
The single most acurate test for diagnosing hypothyroidism
FT4
apathetic hyperthyroidism
Hyperthyroid cat lethargic, obtunded and with poor appetite.
Poliurya in hyperthyroidism is caused by
down-regulation of aquaporin water
Effects of thyroid hormone on the renal tubular function
enhanced reabsoprtion of chloride ion in proximal tubules and in the loop of Hendle
Increased Na/K ATPasa activity and Na/H exchange
tubular reabsorcion of Ca
increased secretion of creatinine
increase glomerular filtration.
Cell that produce insuline
B-cells
Drugs reported hypoglicemia
insulin oral hypoglycemics salicylates acetaminophen B-blockers B2-agonists ethanol ACEi Lidocaine others..
Use of prednisone in insuline secreting tumors
Increases blood glucose concentration by increasing gluconeogenesis and glucose 6-phosphate activity while decreasing blood glucose uptake into tissues and stimulating glucagon secretion.
What is Diazoxide
Benzothidiazine used in the treatment of insuline secreting tumors. Inhibit closure of pancreatic B-cell ATP-dependent K channels, preventing depolarization and inhibiting opening of voltage-dependent Ca channels. Decreased Ca influx result in decreased exocytosis of insulin-containing secretory vesicles.
What is Diabetes type 1A?
Insulinitis. Presence of serum antiantibodies of pancreatic components.
Goals treatment DM
Glucose levels 180-250 mg/dl arround the time of insuline injection.
Fructosamine levels 360-450 mcmol/L
Levels of glicemia around the day between 90-250mg/dl
Glucose nadir
Time of peak insuline effect (should be 90-150 mg/dl
Catarat in DM is secondary to
intra-cellular accumulation of sorbitol and galactitol, produced following the metabolism of glucose and galactose by enzymes within the lentes
Amylin
ia a hoemone whimodulates insuline actions
Dose to start treatment with insulin
0.25 U/KG
Diet for diabetics dogs
if ideal body weight give a consistent calorie-dense and lower fiber diet .
Calories should be provided mainly by complex carbohydrates and proteins. The amount of fat in the diet should be minimized to avoid increasing circulating cholesterol, triglycerides, free glycerol and free fatty acids.. Dietary fat may directly contribute to insulin resistance, promote hepatic glucose production and In healthy dogs, suppress B cell function
Factors reported with DM remision in cats
Low carbohydrate diet Long acting insulin (glargine) Higher age lower maximum dose of insulin Recent corticosteroid administration early institution of tight gycemic control
Diet for diabetics cats
Low carbohydrate-low fiber diet
Oral hypoglycemics
Sulfonylureas Meglitinides Biguanides Thiazolidinedione Alpha-glucosidase inhibitors
Increatins
Are gastrointestinal hormones rapidly released in response to food intake that stimulate synthesis and release of insulin while suppressing glucagon secretion.
Glucocorticoides in insuline resistance
Glucocorticoides induce DM by imparing insulin sensitivity, decreasing glucose uptake in peripepheral tissues, increasing hepatic gluconeogenesis, and may inhibitinsulin secretion from pancreatic beta-cell.
Stimul for ACTH (hypophysis)
CRH (Corticotropin releasing hormone (hypotalamus)
Inhibition CRH
Glucocorticoids and somatostatin
Stimulation CRH
IL-1 IL-6 THF alfa Leptin Dopamine Arginine vasopresin Angiotensine II
Precursor molecule of ACTH
pro-opiomelanocortin
Layers of the adrenal cortices
Outder-Glomerulossa
Middle-Fasciculata
Inner-reticularis
Enzyme need to syntesis of adrenal steroids
cytochrome P45
Enzyme need for the syntesis of cortisol and androgenos
17-alpha hydroxylase
Pituitary tumors
Ademonmas
CArcinomas
Cushing´s pseudomyotonia
Rarely dogs with HAC develop a myopathy characterized by persistent, active muscle contraction after cesation of voluntary effort. It usually affects the pelvic limbs causing a stiff gait.
Stress leukogram
lymphopenia
eosinopenia
neutrophilia
monocytosis
How Trilostano woks
Competitive inhibitionr of the enzyme 3-beta-hydroxysterroid dehydrogenase which catalyzes adrenocortical conversion of pregnenolone to progesterone.
Block systesis cortisol and reduction aldosterone
Ketoconazole in cats
Ketoconazole is an inhibitor of steroidogenesis in humans and dogs, but is ineffective in cats.
Place of action of aldosterone in the kidney
Distal nephrone to promote Na reabsorption and K and H excretion.
Hemogas in aldosterone-secreting adrenal tumors
metabolic alkalosis due aldosterone-mediatd hydrogen ion excretion
Aldosteronoma suspicion
hypokalemia and hypertension
Atypical primary hypoadrenocorticism
Failure of the adrenal cortex in which cortisol secretion is absent but sodio and potassium concentrations are still normal.
In dog, atipica HA is transsient
Glucocorticoides are important to mantein the mucosal gastric barrier.
True
Hemogas in addison
hyponatremia, hyperkalemia, pypercalcemia, hypocloremia, mild acidosis (becoause aldosterone facilitates urine hydrogen excretion)
Na:K<24
Glucocorticoids facilitate calciuresis.
Treatment addison
Fludrocortisone acetate (contiains glucocorticoids and mineralocorticoids) DOCP
Production of Secretin
S cell in duodenum
Stimulation secretion secretin
Presence of H+ in duodenum (containing in gastric secretions)
Action secretin
Stimulation of bicarbonate-containing fluid and bile, rrespectively, from pancreatic ductal cells and biliary epithelium.
Inhibition of gastric secretion, gastric acid production and GI motility
Place of production of glucagon
Alpha cell in pancreatic islotes
Glucagon actions
Stimulus hepatic gluconeogenesis and glycogenolisis
The most potent insulin secretogogue
integrin GLP-1
Secretion of Gastrin
Synthesized and secreted by neuroendocrine G cells located in the antrum and duodenum
Stimuli for gastrin secretion
ingeste proteins and gastric distension
Inhibition gastrin
Low intraluminal Ph <3
Gastrin actions
plus Histamine and acetylcoline(parasympatic stimulus) regulate H secretion from gastric parietal cells
trophic effects on gastric epiteliumand stimulates mucosal blood flow, pepsinogen release, and antral motility.
Also influences in pancreatic enzyme production.
Secretion of CCK
Synthesized by I cell in the duodenum and jejunum
stimulation of CCK secretion
H+ ,fatty acid and aa in duodenum
CCK effects
Stimulation gallblader contraction and pancreatic enzyme secretion.
Coordinateoverall digestive function including stimulation of pancreatic fluid secretion, inhibition of gastric emptying, sphincter of Oddi relaxation and stimulation of pancreas growth.
Production od somatostatine
Synthesized in the hypothalamus
pancreatic islet delta cells
GI D cells in response to nutrients
Somatostatine actions
Inhibition gastric acid, pepsinogen, gallbladder contraction, insulin secretion, pancreatic exocrine function, GI motility and nutrient absorption
INHIBITION GH
Secretion motilin
GI cells. Endocrine actions occure during fasting.
Functions motilin
During fasting. Coordinating migrating motility complexes.
Coordinate biliary-pancreatic-gastric secretions.
Stimuly motilin
H+ in stomach and lipid enter in small intestine.
Ghrelin production
stomach
Ghrelin functions
Stimulate appetite, adipocyte groowth and pituitary grwth hormone synthesis and secretion.
Ghrelin provides a link between dietary nutrients, caloric energy and the pituitary-GH axis.
Zollinger-Ellison Syndrome
In case of gastrinoma, the gastrin overproduction can cause gastric antral hypertrophy, hyperacidity and ulceration.
Cells origen of pheochromocytoma
cromaffin cells of the adrenal medula
What is syntetiside in the adrenal medula
Catecholamine (epinephrine and norepinephrine)
Cathecolamine metabilites in urine
metanephrine and normetanephrine
Neuroendocrines markers for pheocromocitoma
Stained, chromogranin A
Odynophagia
Painful swallowing
Vomiting centre localization
Medulla oblongata in the brainstem
Receptors of apomorphine
Dopaminergicos (D1 and D2). Stimuli emesis, but less effective in cats suggesting lack in D2.
Most sensitive and specific test for EPI
TLI
These haustral contractions
Are coordinated contractions of the circular and longitudinal smooth muscle of the colon that result in the accumulation of colonic contents in unstimulated segments (occur continuously)
Prolongued exposure to estrogen can cause
persisten sanguineous discharge. Failure to ovulation that can be demonstrated with low levels of plasma progesterone concentrations.
Polydipsia
water intake > 90-100 ml/kg/day
Polyuria
> 50 ml/kg/day
Marked hypostenuria
SG <1006 due to diabetes insipidus
SG in normal animals
dog 1006-1050
cats 1005-1090
Drugs that can cause polyuria/polidipsia
glucocorticoids
diuretic
phenpbarbital
plasma osmolality equation
2[(Na)+{(glucosa/18) +BUN/2.8)}
Causes of hyperbilirubinemia
Prehepatic hemolisis
liver failure
post hepatic obstruction or rupture of the biliary tract
Myoglobinuria
severe muscle damage increase CK
bilirubine concentration to have jaundice
> 2 mg/dl
S3
Protodiastole
Sobrecarga de volumen
S4
Presistole/ contracción atrial
Hipertrofia ventricular
3 AVB
Reynolds numbers
RN=radio x velocidad x densidad / viscosidad
Austin Flint murmur
occasionally massive aortic regurgitation causes premature closure of the mitral valve producing functional mitral stenosis and a diastolic murmur.
Pulse parvus et tardus
Dogs with severe aortic stenosis may have a weak hypokinetic pulse, and or may have a pulse pressure that has a later-than-normal
Pulsus paradoxus
Increased expiration decreased in inspiration
Pulsus alternans
severe left ventricle disfunction
Immune-mediate anaemia
Spherocytes, agglutination, ghost cell
Oxidant-induce anemia
Heinz bodies, eccentrocytes, pyknocytes
Iron deficiency
Hypochromic RBCs, and microcytic Hypochromic RBC indices. Presence of schistocytes, keratocytes an acanthocytes.
low Iron and percentual saturation transferrin
Intravascular hemolisis
Hemoglobinemia and hemoglobinuria
regenerative anaemia (reticulocites account)
> 95000/mcl dog
>60000/mcl cat
Days for the maturation and release for the bone marrow of the neutrophils
6-9
Stimulos production neutrophils
Production: ILs 1-2-3-6 and 11; granulocite colony stimulating factor, granulocyte-macrophage stimulating factor and stem cell factor.
Release: granulocite colony stimulating factor, granulocyte-macrophage stimulating factor; TNF and C5a mediate release from the bone marrow.
Stimulo to produce Eosinophils
Th2 produce Il3-Il5 and granulocyte-macrophage stimulating factor
NK are producer in the bone marrow in aproximately 7 days unther the stimulus of…
IL-2 IL-7 IL-15 and SCF
White cell that increased in case of increased epinephrine but not cortisol
Lymphocytes
Major regulator of megakaryocyte maduration
cytokine thrombopoietin (TPO)
Platelet count to can produce hemorrhage
<30000/mcl
Drugs than can cause thrombocitopenias
estrogen, chloranphenicol, mehimazole, penicillin, procainamide and sulfa antibiotics
Hereditary thrombocytopenias are secondary to
beta 1 tubulin gen mutation
What means an increase in the positive acute phase proteins
Inflammation
Positive acute phase proteins
C-reactive proteins
Serum amyloid A
Haptoglobin
Negative acute phase proteins are those with decreased serum or plasma concentrations in inflammatory states.
IL-1 and IL-6 cause in the hepatocytes to decrease production of these proteins while increasing production of acute phase proteins.
Albumine is the main negative acute phase protein.
Value of hypoglycemia
<60 mg/dl
10-20mg/dl for have clinical signs
Renal threshold for hyperglycemia
180-200 mg/dl
Azotemia
increase in concentration of nitroge-containing substances in the blood, primarily BUN and creatinie.
Uremic syndrome
significant accumulation of substances (uremic toxins) usually excreted in the urine under normal physiologic conditions in a healthy animal.
Chronic Kidney disease clasification
Stage 1 creatinine <1.4mg/dl dogs and <1.6 mg/dl cats
Stage 2 creatinine concentrations 1.4-2 mg/dl dogs and 1.6-2.8 mg-dl cats
Liver. Hepatocellular leakage enzymes
ALT
AST (mitocondria)
Both in cytosol
Liver, cholestatic enzymes
ALP
GGT (cholangiocitos)
hepatocito canalicular membrana
Hyperlipidemia and hyperproteinemia increase or decrease Na concentration?
Decrease
Alteration of CL concentration assays
Hyperproteinemia
lipemia
administration of bromide
Sindrome of inapropiate ADH secretion (SIADH)
Hyponatremia with hypotonic plasma Urine osmolality above that of plasma Increased renal Na excretion Absence of edema or volume depletion Normal renal and adreanl function
Hypocloremia without parallel hyponatremia
Gastrointestinal o renal losses and in mix acid-base disturbances.
When serum CL concentration decrease with GI or renal loss, bicarb reabsorption increases proportionally, resulting in metabolic alkalosis.
Conversely, in chronic respiratory acidosis the increases of bicarbonate reabsorption is assumed to be associated with increased urinary losses of CL and hypocloremia
What happen with Cl with the admisnitration of furosemide
Loss of it
Primary regulate hormone in the [k]
Aldosterone
Where is excrete the K in the nephrone
Distal tubule
Possible cause of hypokalemia
Diabetic ketoacidosis poliuria withouth presence of compensatory polidipsia catecholamine release alkalemia B2 adrenergic drug overdose rattlesnake envenomation hypothermia
Pseudohyperkalemia
Severe thrombocytosis
severe leukocytosis
hemolysis in neonates
animals with high intracellular K (Akitas, Shiba Inu)
Drugs that can cause hyperkalemia
ACEi Angiotensin receptor blocker K-sparing diuretics prostaglandin nhibitors trimethoprim Cyclosporine nonspecific b-blockers heparin
Possible causes of hyperkalemia
Drugs
Hypoadrenocorticism
urethral obstruction or bilateral uretral obstructions
metabolic acidosis (translocation from ICF to ECF)
Main causes of hypercalcemia
Malignan hypercalcemia
primary hyperthyroidism
chronic kidney disease
Malignan hypercalcemia
Linphoma
Apocrine gland adenocarcinoma of the anal sac
Hypercalcemia inhibe the action of ADH
True
Bilirrubin crystals
Can be normal in concentrated urine and found in large numbers with significant bilirrubinuria
Calcium oxalate crystals
Dihydrate crystals: can be in healthy dogs
Monohydrate crystals form with hypercalciuria or hyperoxaluria: Ethylene glycol intoxication).
Cholesterol Crystals
non specific occasionally observed in healthy dogs
Urate Crystals
hepatic failure, portosystemic shunts
Xantine crystals
secondary to Allopurinol treatment
Immunoglobulines in the detection of Leptospira whit the eLISA
Ig M and Ig G
Hemotropic mycoplasmas (hemoplasmas)
Small wall-less bacteria that parasitize erythrocytes, living on the surface of the erythrocyte membrane.
Status Candidatus
This status is used in bacteria nomenclature for newly described organisms for which sequence data are available, but which cannot be phenotypically characterized to meet the needs of the internal Code of Nomenclature of Bacteria.
Prevalence feline hemoplasma
male, nonpedigree cats with access to the outdoors. Older cats
Treatment M. haemofelis
$ weeks antibiotics Tetracyclines Fluoroquilnolones Doxycicline Moarbofloxacine Oxytetracicline
Virulence factor in Clostridium perfringens
CPE (enterotoxin) is a protein encode by the cpe gene, whose expression is coregulated with sporulation of the organism.
Treatment clostridium perfringens
Ampicillin
Metronidazole
Tylosin
Toxins in Clostridium difficile
A and B
Clostridium difficile culture
Negative culture has a good negative predictive value. Detection of common antigen /glutamate dehydrogenase) and enzyme produced constitutively by toxigenic and nontoxigenic strains, is a sensitive but nonspecific test commonly performed in human and veterinary laboratories.
Transmision Campylobacter spp.
Fecal-oral
Cause of diarrhea in case of Campylobacter toxin
CDT. This toxin has 3 proteins, CdtA, CdtB and CdtC. All of which are required for cellular damage.
Increase in case of Campillobacter due the enterotoxin
cAMP, prostaglandin E2 and leukotriene
Pathogenesis Salmonella (G-, motile, non-spoeforming facultative anaerobic bacilli)
Ingestion of the organisms in contaminated food or water, followed by invasion of M-cells in Peyer´s patches.
Salmonella express several fimbriae that contribute to their ability to adhere to intestinal epithelial cells.
Salmonella pathogenicity islands
SPI-1 and SPI-2
Granulomatous colitis in boxer
Escherichia coli
treatment enrofloxacine
Antimicrobials that penetrate intracellutarly
Chloranphenicol
Trimethoprim-sulfonamides
Diagnosis of Giardia
eLISA plus fecal flotation
Diet in large bowel diarrhea
High fiber diarrhea
Toxoplasmosis:
Only cats complete the coccidian life cycle and pass environmentally resistant oocysts in feces.
Sporozoites develop in oocysts after 1-5 days of exposure to oxygen and appropriate environmental temperature and humidity.
Oocysts are shed in feces from 3-21 days.
Sporualted oocysts can survive in the environment for months to years and are resistant to most desinfectants.
True
Detection of toxoplasmosis in cats
Ig M
T gondii infections in human
For ingestion of sporulated oocysts
The primary histhological abnormalities in Leishmaniasis
Diffuse granulomatous inflammation with macrophages containing numerous amatigotes
Type of hyperglobulinemia in dogs with leishmania
Polyclonal
Babesia is transmitted by
Dermacentor reticulatus
Pathogenesis Babesia spp
Intracelular replication in red blood cells (RBCs) that result in intravascular hemolytic anemia. Immune-mediated reactions against the parasite or altered self-antigens worsen the hemolytic anemia and commonly result in a positive Coomb´s test.
Treatment babesia (no in the cases of B. gibsoni)
Imidocarb
Pathogenesis FIV
Transient “primary stage”
Chronic “asymptomatic stage”
Terminal “second stage”
Clinical signs FIV
Immune dysfunctions Respiratory infections Chronic gingivostomatitis Risk of high-grade lymphomas, extranodal and B-cell tumors. Neuropathology
Risk factors for FELV infections
illnes, male, adulthood, outdoor acccess and large scale cat hoarding.
· major outcomes of Felv infection
Progressive infection (antigen-positive, provirus positive) Regressive infection (antigen negative, provirus negative) Abortive infection (antigen-negative, provirus negative, antibody-positive)
Felv antigen
IFA p27
Felv vacination in case of positive animals
No value but risk of injection-site sarcoma.
Advice inactivated vaccine versus MLV (increases risk of side effects)
Replication of the feline coronavirus virus
In macrophages.
Important the Spike gen (S)
What happens with the activation of p38 MAPK
It is the pathway that regulates production of tumor necrosis factor alpha and intelukine 1 beta
Cytologic evaluation of the effusion in cats with FIP
Pyogranulomatous inflammation with a predominance of macrophages and neutrophils.
Important test in FIP to differentiate from effusions of other origens
Rivalta´s test
Gold standard in the dignosis of FIP
Immunohistochemistry
Some dates about Canine and Feline Parvovirus
The viron is a simple, not-enveloped, single-strandedDNA virus.
The capside proteins are the key structures determining host specificity and antigenicity.
Virus makes use of the transferrin receptor to gain entry to cells and polymorphism in this receptor are responsible for shot specificity.
Maternal immunity in case of parvovirus
90% of maternally derived antibody from colostrum and it has a half-life of around 10 days.
Parvovirus tropism
cells of the thymus, bone marrow, spleen and cryp cells of the gut epithelium lead in crypt necrosis.
Severe neutropenia in parvovirosis
Due partially to the high demande in the gut
Diagnosis parvovirus
Fecal antigen ELISA
Vaccination in parvovirus
Live attenuated and inactivated vaccines.
The most common cause for vaccine failure remains vaccine neutralization by maternally derived antibodies.
Rabia virus
Envelop virus
Diagnosis of Rabie
dFA is the glod standart with confirmation:
Postmorting testing: full cross-section of fresh brainstem and cerebellum.
Diagnosis is based on special silver-based staining (Sell´s stain) to detect Negri bodies, when applied to formalin-fixed brain tissue.
Canine infectious Respiratory disease “Kennel cough” agents
Adenovirus
Herpesvirus
Parainfluenza
Bordetella bronchieceptica
In cases of Distemper where is possible to see the intranuclear and cytoplasmatic viral inclusions
monocytes
lymphocytes
neutrophils
erythrocytes
Diagnosis Distemper
RT-PCR (reverse-transcription-polymerase chain
IFA: Ig M and Ig G
Gold standard: serum neutralization assay
Feline Upper Respiratory Infections
Herpesvirus
Calicivirus
(Bordetella, Chlamydia Mycoplasma)
Occular conditions in Feline Herpesvirus
Eosinophilic Keratitis
Corneal sequestration
Uveitis
Treatment of cryptococcosis
Amphotericin B
Fluconazole (cats)
Itroconazole
Aspergillosis in dogs the primary disfunction to predispose is
In TLR (Toll-like receptors)
Polydipsia
> 100ml/kg/day
Rubber jaw
deformity of the maxilla and mandible in young animals due to fibrous osteodystrophy secondary CKD
Hyperkalemia more frequently in AKI od CKD
AKI and in particular with post-renal causes of azotemia
the lesion in the nephron when there is glucosuria
proximal nephron
Calcium oxalate monohydrate crystal
Ethylene glycol poisoning
Prerenal azotemia
USS > 1030 in dogs and 1035 in cat
Characteristics of a good GFR marker
Free filter at the glomerulus
not circulate bound to plasma proteins
not undergo reabsorption or be secreted by the tubules
must not themselves alter GRF or be toxic to the kidneys
GRF range
- 5-4.5 ml/min dog
2. 5-3.5 ml/min cat
Urine Dipstick
Higher sensitivity for albuminuria than other urinary proteins.
Lower limit of detection of 30 mg/dl.
False negative: Bence Jones proteinuria
dilute
acid urine
False positive: alkaline urine
highly concentrated urine
pyuria/hematuria
Microalbuminuria
It is defined as a concentration of albunine that is >1mg/dl but below that typically detectable by urine dipstick <30 mg/dl.
UPC
UPC >0.4 cat >0.5 dog = >30 mg/dl albumine
UPC > 2 = glomerular disease
Nephrotic syndrome
Hypercholesteronemia
Proteinuria
Cavitary effusion or peripheral edema
Isisthenuria
USG 1008-1015 (urine Osmolality 300 mOsm/kg)
Indicate that the urine has the same solute concentration as the glomerular filtrate and plasma.
Hypostenuria
USG< 1008 (Uosm<300 mOsm/kg) indicating active tubular dilution
Hypersthenuria
USG >1015 (Uosm>300 mOsm/kg)
Glucosa transport in the proximal tube
Through SGLT2 and lesser SGLT1.
Glucosuria en presence of normoglycemia
Alteration in renl tubular function
Markers of tubular injury
Tubular proteins: NGAL; K1M1
Imflamatory marker IL-8
Cast=cylindruria
can be present in normal dogs and cats but high number is indicative of tubular damage.
Hyaline cast
After fever or exercise, alkaline or dilute urine.
Epithelial cast
tubular cellular damage
Granular cast
Ischemic or nephrotoxic renal tubular insult
Way cast
complete cellular degradation.
Fatty cast
Disorder in lipid metabolism
AKI
increase >0.3 mg/dl or >25% increase from baseline creatinine
AKI grade I
blood creatinine<1.6 mg/dl
Nonazotemic
Pregressive nonazotemic increase in blood creatinine >0.3 mg/dl within 48h
Mesured oliguria (<1ml/kg/h) or anuria over 6h
AKI grade II
blood creatinine 1.7-2.5 mg/dl
Mild AKI
AKI III
blood creatinine 2.6-5 mg/dl
AKI IV
blood creatinine 5.1-10 mg/dl
AKI V
blood creatinine >10 mg/dl
The four phases of AKI
mirar esquema
Nephrotoxicity aminoglycosides
They easily ionize to cationic complexes that bind to anionic sites on epithelial cells of the proximal tubule are then internalized by pinocytosis, which leads to renal cortical concentrations 10 times that of the plasma and can cause renal tubular damage.
Fanconi -like syndrome
glucosuria
aminoaciduria
hyperphosphatemia
(can be casue for tetracicline)
Fractional Excretion of Sodium (FEna)
(FEna)= [(Urine nax plama creatinine)/(plasma na x urine creatine)]
Response to high concentrations of CL in the distal tube, detected by the macula densa
Afferent arteriole vasoconstriction
Manitol actions
An osmotic diuretic that causes extracellular volume expansion and inhibits renal Na reabsorption by inhibin renina.
Place of accion of furosemide
NA CL K pump in the luminal cell mb of the loop of Henle
Survivil time prognostic fartors in CKD
PO4
Proteinuria
Hypertension
Weight loss in cats is an reliable indication of deterioration
Clinnical manifestations of disturbed water and electrolites excretions
Edema, hypertension, hypoNa, hyperK, metabolic acidosis and hyperPO4
Uremic gastropatie
Ca and PO4 products (mucosal mineralization)
Increase gastrin and histamine levels
Organ systems most commonly affected by elevated blood pressure
eyes, kidneys, NS, cardiovascular system
Factors that promote renal secondary hyperparathyroidism
PO4 retention
increased FGF-23 that inhibit l-alpha-hydrolaxe activity thus leading to decrease calcitrol levels.
Mg in CKD
Hypermagnesemia is common because the kidneys are primarily responsible for Mg excretion.
SDMA increases for >3 m in dogs with serum creatinine
consistent with diagnosis of IRIS CKD stage I.
Nephritis syndrome
signs that develop secondary to renal inflammation, generally acute, that extends into the glomeruli: hematuria, edema, hypertension, azotemia, oliguria.
Urate calculi opacity
radiopaque
treatment urate calculy
allopurinol with purine restricted diet to prevent formation of xantine calculi
Dugs therapy to facilitate relaxation of the ureter for expulsion of uroliths
alpha-adrenergic antagonoists or selective beta-2/beta-3 agonists to relax the ureters and reduce uretral spasm
Most common composition of ureteroliths
Calcium oxalate
Prazosin
Alphaadrenergic antagonist
Most common neoplasm resulting in uretral obstruction in dogs
Transitional cell carcinoma located in the trigone of urinary bladder
Genes in bacteria important predictors of virulence (Lower urinary tract infections)
Hemolysin or the expression of urothelial adherence pili
Presence of 1 fimbriae in E.coli (low tract urinary infection)
It is associated with increase severyty infection
Agents more frequently associated with pyelonephrytis
Strreptococus and Enteroccocus
Encrusted cystitis
Corynebacterium urealyticum. It occurs when ureasepositive bacteria form mineralized plaques on the ulcerated and inflamated mucosa of the urinary tract.
Minimun diameter of urolitis in RX
2mm
Poor radiographic opacyty urolites
urate, cystine
More prevalenct calculy n dog male and femele
Male calcium oxalate
femele struvita
Radiopaque calculi
calcium oxalate
calcium phosphate
silicia
partial adiopaque calculi
struvite
radiolucent calculi
xantine
cystine
urate
Breed predisposition calculi
Calcium oxalate: szanuzer, yorkshire, chihuahua, shih tzu, bichon
Cystine: E. Bulldog
urate: dalmatian
Causes of calcium oxalate uroliti
hypercalciuria
Causes of struvite uroliti
urinary tract infections with bacteria that produce urease. Ureasa is responsible for converting urea to ammonia, with alkalinizes urine and favors struvite precipitations.
Causes of urate uroliti
portosistemic SHUNT
SLC2A9 mutation
Causes of cystine uroliti
failure of renal tubular reabsorption of cystine
compound uroliti
Inner layer of CaOx and outer layer of struvite
Causes of xantine uroliti
Allopurinol treatment
genetic deffect
Thiazide diuretics in case of CaOx uroliti
These drugs inhibit the sodium-chloride cotransporter in the distal tubule and by doing so stimulate calcium reabsorption and decrease urinary calcium excretion.
Prostatid cell growth in under the influence of
Dihydrotestosterona
ARDS
A systematically ill pet with respiratory distress, an inflammatory leukogram, and hypoalbuminemia
Etiopathology tracheal collapse
softening of cartilage rings seems to be due to a reduction of glycosaminoglycan and condrotin sulfate.
eosinophilic bronchopneumonia in dogs
> 50 % eosinophilos
increase BALF levels of procollagen type III amino terminal propeptide a protein marker of collagen type III synthesis.
Kartagener´s syndrome
bronchiectasis
complete left -right transposition of viscera (situs inversus)
chronic rhinosinusitis
Why fecal flotation in pulmonary parasites can be negative
because larval migration occurs before the mature worms have reach the intestine.
When is indicated start O2 suplementation
SpO2 <94%
PaO2< 80mmHg
Immunoglobulina indicative of active infection in Toxoplasma gondii
IgM
Objective O2 suplementation
SpO2 >90%
PaO2>60 mmHg
PaCO2<60 mmHg
Mild ARDS
PaO2/FiO2 =200 to 300 mmHg with positive end expiratory pressure [PEEP] or continuous positive airway pressure [CPAP]>5 cm H2O
Moderate ARDS
PaO2/FiO2 =100 to 200 mmHg with positive end expiratory pressure [PEEP] or continuous positive airway pressure [CPAP]>5 cm H2O
Severe ARDS
PaO2/FiO2 <100 mmHg with positive end expiratory pressure [PEEP] or continuous positive airway pressure [CPAP]>5 cm H2O
ET1 actions
Vasoconstriction
Stimulates smooth m growth
increased collagen synthesis
vascular remodeling
Prostacyclin
Vasodilator
Inhibits platelets activation
Antiproliferative properties
Thromboxane A2
Vasoconstrictor
Platelet agonist
PDGF (platelet derivated growth factor
Proliferation and migration of pulmonary artery smoth muscle cells
Nitric oxide
vasodialtor
inhibitor platelet activation
NT-proBNP concentration in pleural effusion indicative of cardiogenic effusion
> 322.3 pmol/ml
Aminiglicosides in intracellular infections or action in brain and prostate
Aminoglicosides are low lipophilic and as result are ineffective for intracelular infections and infections in tissues such as the brain and prostate.
Caracteristics of the drugs for transdermal and transmucosal administration
very lipophilic and un-ionizated
The two primary metabolism pathway
Phase I (metabolic): Oxidation reduction, hydrolisis and hydratation. Phase II (conjugations): Glucoronidation, sulfation, acetylation, aminoacid conjugation reactions.
Enzyme family catalyzing glucuronide conjugation
Urinide diphosphate glucuronosyltransferase.
CAts are deficients in some of them result in decreased or alteration in some conjugations as in acetaminophen and morphina.
Dogs lack in enzime for conjugation
N-acetyitransferase
Half live of a drug
The amoun of time it taks to eliminate 50% of the drug.
After 3 half live the concentration go to decreased until tby the 88%
after 5 half-lives go to decreased until 97%
after 7 half -live go to decreased until the 99%
Steady state
When no further increases in drug concentration occur with continue dosing (97% of elimination= 5 half live)
Dose rate equation
Dose rate= plasma clerance x average plasma concentration
Volumen of distribution
It is a mesure of the dilution of a drug into the body after administration
Dose=volumen of distribution x plasma concentration
Depot effect
sequestration in the stratum corneum (drug administration)
Advice antibiotics for G-
Fluoroquinolone
Cephalorporin
aminoglicoside
Organisms with unpredictable susceptibility
Pseudomona aeruginosa
Methilcillin-resistant Staphylococcus
Enterococcus spp
Anaerobios have unpredictable reaction to
Trimetroprin-sulfonamides
Ormetoprim-sulfonamides
Fluoroquinolones
Resistence ofBacteroides fragiles (anaerobio)
Has a beta lactamase that inactiva cephalosporins and ampicillin-amoxi
Pseudomones are resistant
Macrolide antibiotics
Cellular debris and infected tissue can inhibit the action of
trimethoprim-sulfonamide
Drugs that decreased the action fro the concentration of Mg, Ca, Fe and Al
Fluoroquinolones
Aminoglycosides
Acid enviroment decreased the action of
Clindamicin
Erythromicin
Fluoroquinolones
aminoglicosides
Antifungal that inhibits systesis of steroid hormones (cortisol and testosterone) and inhibit CYP P-450
also inhibition p-gp
Ketoconazol
If ketoconazol is administrate with cyclosporine
cyclosposin concentration increase 2-3 folds in dogs
Secondary effecto of voriconazole in cats
Neurotoxicosis
Chronic supresion of HPAA
Depot
repositol
In cats prednisone or prednisolone
In cats prednisolone is preferred
How anti Cox-1 produce aqua tetention
ADH is inhibit by prostagalndines, antiCox1 inhibi prostagglnadines so increase retention H2O
Metamizole
Toxic in cats doesn´t work in Cox1 and Cox2
Antiinflamatory potency of:
Cortisol
Prednisolone prednisolone
Dexametasone
Cortisol. 1
Prednisolone prednisolone 3.5-5
Dexametasone 25-30
Mineralocorticoid potency of:
Cortisol
Prednisolone prednisolone
Dexametasone
Cortisol 1
Prednisolone prednisolone 0.3-0.8
Dexametasone 0
Duration of action of:
Cortisol
Prednisolone prednisolone
Dexametasone
Cortisol <12h
Prednisolone prednisolone 12-36 h
Dexametasone < 48 h
Immunosupresive derived from the soil fungus Tolypocladium inflatum
Cyclosporine
Action of cyclosporine
inhibition calcineurin in the T´lynphocites
Inhibition IL-2 and prolipheration T-lymphocytes
Excretion cyclosporin metabolites
Biliary excretion
Secondary effects cyclosporine
lethargy gingival hyperplasia hirsutism coat shedding cutaneous papillomatosis footpad hyperkeratosis hepatotoxicosis/nephrotoxicosis
phase of action of the cell cicle for the Azatioprine
S-phase
phase of action of the cell cicle for the Mycophenolate mofetil
S-phase
Mechanism of acction of chlorambucil
Cell-cycle-nonspecific alkylating agent that is cytotoxic
Alkylating agents
Chlorambucil
Cyclophosphamide
Opioid receptor
mu receptor (G-protein couple) Kappa receptor
Full mu receptor agonist
Fentanyl remifentanil hydromorphone oxymorphone morphine methadone
Partial mu receptor agonist
buprenorphine
Kappa receptor agonist
butorphanol
secondary effects opioids
Vomiting, nausea, ileus, constipation, urinary retention, bradycardia, respiratory depression, sedation and dysphoria.
Cats opioids are associated with hypertermia
True or false: Cyclosporine can cause further insuline resistance in diabetic or overweight cats
true
What gulucocroticoid is advice to use in case water retention is detrimental
Dexametasone becasue has not mineralocorticoid actions.
Negative predictive factors in immunomediated anemia
bilirrubin >5 mg/dl, autoaglutination, hypoalbuminemia and intravascular hemolisis
More hepatotoxic immunosupressive drugs
Chlorambucil and azathioprina
Scot Syndrome
defect of procoagulant activity on theplatelet surface, it manifests as a coagulopathy because the platelet surface cannot support plasma coagulation protein activity
Feline factor XII deficiency (Hageman)
It is the most common defect of the intrinsic pathway factors. Cats with factor XII deficiency demonstrate prolonged PTT, but hemorrhage or other clinical signs do not result from this deficiency as in vivo clot formation is primarily dependent on factor VII and tissue factor activation.
Time of eritrocite formation
5-7 days
Spherocytes
suspicious of IMHAs
Heinz bodies anemia
Toxic (onion zinc..)
Evan-s syndrome
IMHA and immunomediated thrombocitopenia
palce of production of erythropoietin
Peritubular interstitial cells of the inner reanl cortex and outer medulla.
The primary physiologic stimulator in the develop of vasculature
hypoxia
Aneuploidia
Anormal numero de cromosomas
Cancer of epitelial cells
Carcinomas
cancer of connective tissue or muscle
sarcomas
blood forming cells tumors
leukemias
Chemoterapicos alkalinizzantes
yclophosphamide
Chlorambucil
Lomustine
Procarbazine
Chemotherapy antitumur antibiotics
Anthracyclines: Doxorrubicin, mitoxantrone
Chemoterapy mitotic inhibitors
Vinca alkaloids (inhibit assembly)
paclitaxel (inhibit disassembly)
Vincristine
Vinblastine
Platinum compounds (cross link in the DNA
Cisplatin
Tyrosine Kinase inhibitors
Toceranib (Palladia)
Masitinib (Masivet)
Highly myelosuppressive chemotherapy
Doxorrubicin Lomustine Cyclophosphamide Carboplatin Vinblastine Mitoxantone Vinorelbine
Moderately myelosuppressive chemotherapy
Vincristine Chlorambucil Melphalan Methottrexate cisplatin hydroxyurea 5-5-fluorouracil
Mildly myelosuppressive chemotherapy
Corticosteroids
L-asparginase
Vincristine (low dose)
immunosuppressive tumor microenviroment
Production of inhibitory cytokines by the tumor:
TGF beta
IL-10
recruitment of regulatory T cells Treg
BCG (bacillus of Calmette and Guérin) a biologic response modifier
nonspecific tumor immunotherapy
Cytokines with immunostimulatory properties
IL-2 IL-12 (can be effectively target to tummor tissue) IL-15 IFN-gamma TNF-alpha
True or false
Prostaglandines stimula the platelet agregation
Hypercholesteronemia increase platelet sensitivity
Hypoalbuminemia cause hypercholesteronemia
True
diferencia entre la Secreción bilis hepática y la vesícula biliar
En la vesícula biliar se reabsorbe na y cloro pero no el calcio y el potasio. Además se absorbe agua y bicarbonato.
Composición d ela bilis
Sales biliares bilirrubina colesterol ácidos grasos lecitina iones (Calcio y potasio) Agua
Estímulos secreción biliar
CCK (contrae la pared de la vesícula biliar y relaja el esfinter de oddi) estimulada por presencia de grasas en el estómago
Ach
Precursor de ácidos biliares
cholesterol
Acción de las sales biliares
Detergente
micelas
Secretina
Production in the S cell in duodenum and jejunum
Stimulation secretion of bicarbonates in the hepatic biliary conducts
Stimuli are the low ph
