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Otras preguntas Flashcards

1
Q

What are antigenic epitopes (antigenic determinants)?

A

An antigen is composed of many molecular units to which an antibody binds. A single antigen may be composed of many antigenic epitopes.

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2
Q

Cross-reactive epitopes

A

Antigenic epitopes can be shared among different bacteria and host cell

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3
Q

Composition of G+ bacteria wall

A

Peptidoglycans

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4
Q

Composition of G- bacteria wall

A

Thin lippolysacharides (endotoxin)

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5
Q

Antigenic structures of bacteria

A 
G+: peptidoglycans wall cell
G-: Lippoporisacarides wall cell
Capsule: polysaccharides
Pili
Flagella: Flagellin
Nucleic acids
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6
Q

Antigenic structures of virus

A

envelop or capsule

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7
Q

What is antigenicity /immunogenicity?

A

degree of immune response induced by an antigen

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8
Q

Characteristics that contribute to potent antigenicity

A

Forein versus self antigens
Size
Biochemical structure and complexity (Proteins>lipids/carbohydrates)
Stability and degradability

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9
Q

What is the first line of defence?

A

External body surface

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10
Q

The second line of defence?

A

Macrophage-monocyte lines

Phagocytic cells of the myeloid

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11
Q

Time of life of Neutrophils

A

12 h in circulation but longer in tissue

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12
Q

Phases destruction of antigens by neutrophils

A

Phagocytosis

Respiratory Burts

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13
Q

Neutrophils can present antigens to lymphocytes?

A

NO

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14
Q

NETosis

A

neutrophil cell death

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15
Q

Neutrophils are activated by

A

LPS
TNF-alpha
IL-8

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16
Q

What are NETs

A

neutrophil cellular traps

Release during NETosis

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17
Q

Lyme disease (borreliosis)

A

B. burgdorferi

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18
Q

The tick in Lyme disease (borreliosis)

A

Ixodes scapularis

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19
Q

In Lyme disease the transmission in the ticks

A

is transstadial but not transovarial

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20
Q

Lyme Borrelia spp

A

Spiral-shaped, motile, G- spirochetes

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21
Q

Lyme disease (borreliosis) cause

A

Arthritis

Nephritis

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22
Q

Diagnostic test for Lyme disease

A

PCR
SNAP-4DxPlus test
C6Quant test Idexx

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23
Q

SNAP-4DxPlus test

A 
Heartworm antigen
Antibodies: Ehrlichia canis
                    E. Chaffensis
                    E. ewiingii
                    Anaplasma phagocytophilum
                    A. platys
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24
Q

C6Quant test Idexx

A

Gives a quantitative result

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25
Q

Mycobacterium

A

Intracellular, aerobic, acid-fast, non-spore-forming, environmental resistant bacilli.

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26
Q

Nocardiosis

A

Gram-positive, variably acid-fast, catalase-positive, non-motile aerobic bacteria that form filaments that may break into bacillus and coccal forms.

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27
Q

Treatment of Nocardiosis

A

Sulphonamide antibiotics

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28
Q

Tetanus

A

Clostridium; G+, anaerobic; spore-forming bacteria

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29
Q

Agent of Tetanus

A

Clostridium tetani

motile, Gram-positive, non-encapsulated, anaerobic, spore-forming, rod-shaped bacterium.

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30
Q

Fase of the organism sensitive to chemical and physical treatments

A

Spores are resistant

The vegetative form is sensible.

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31
Q

Presence of Clostridium tetani means infection?

A

No because not not all the strains possess the plasmid

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32
Q

Exotoxins of Clostridium tetani

A

Tetanolysin

Tetanospasmin

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33
Q

Action of tetanolysin

A

Clostridium tetani exotoxin that damage the surrounding tissue and obtein conditions for bacterial multiplication.

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34
Q

Action of tetanospasmin

A

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.

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35
Q

What is Synaptobrevin

A

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.

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36
Q

What neurons are more affected by tetanospasmin

A

inhibitory interneurons that release GABA

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37
Q

Clasification of tetanus severity

A

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.

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38
Q

Diagnosis of Tetanus

A

Clinical signs.

Serum antibodies to tetanospasmin.

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39
Q

Treatment strategies in Tetanus

A
    • 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
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40
Q

Tetanus antitoxin

A

Anti-tetanus equine serum.

human tetanus immune globulin (more chance of reaction).

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41
Q

Antibiotic in case of tetanus

A

Metronidazole is superior to penicillin

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42
Q

Why benzodiazepines in tetanus

A

Because it augments GABA agonism at the GABAa receptor.

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43
Q

Agent of botulism

A

Clostridium botulinum

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44
Q

Clostridium botulinum

A

Gram +; anaerobic; spore-forming; rod bacteria

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45
Q

The target of the botulism toxins

A

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.

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46
Q

Clinical presentation of botulism

A

afebrile, acute-onset, progressive, flaccid paresis, with additional involvement of the autonomic nervous system.
(Mydriasis with depressed pupillary light reflexes).

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47
Q

Diagnosis botulism

A

demostration of botulinum toxin early in the course of the disease, either in blood or intestinal contents.

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48
Q

Treatment botulism

A

Supportative

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49
Q

Bartonella agent

A

Gran negative

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50
Q

urine specific gravity often in dog with hypercalcemia and hyperthyroid

A

< 1020

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51
Q

Treatment canine thyroid carcinoma

A

Doxorubicin, cisplatin and mitoxantrone

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52
Q

Most frequently B-cells tumor

A

insulinomas

carcinomas

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53
Q

Frequently metastasis in cases of insulinomas

A

Regional linfonodes and liver

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54
Q

level of glucose that stop the release of insulin

A

<80 mg/dl

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55
Q

Causes of decreased glucose production

A 
Hypoadrenocorticism
Hypopituitarism
GH deficiency
Liver insufficiency
Glucogen storage disease
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56
Q

Treatment acute insulinoma

A

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.

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57
Q

Medical treat insulinoma

A

Streptozocin (nitrosiurea antibiotic)
Prednisone
Diazoxide (benzothiadiazine)
Octreotide (long-acting synthetic somatotatin analogue.

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58
Q

Action of the prednisone in the treatment of the insulinoma

A

increased blood glucose concentration by increasing gluconeogenesis and glucose 6-phosphatase activity while decreasing blood glucose uptake into tissues and stimulating glucose secretion.

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59
Q

Actions of antiepileptic drugs as phenyton

A

enhance the inactivation of sodium channels ( in the neuron potential action), making it less likely that an action potential will be propagated.

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60
Q

Action of toxins as pyrethrins in the CNS

A

Pyrethrins block sodium channel inactivation, increasing action potential generation an causing tremors and seizures

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61
Q

Two factors that influence the speed at which the action potential travels down an axon

A
  • 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.
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62
Q

How botulism toxin works

A

Botulism toxin binds to one of the vesicle docking proteins, preventing the release of acetylcholine at the neuromuscular junction.

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63
Q

Kinds of neurotransmitter receptors

A
  • Ionotropic receptors regulate ion channels.

- Metabotropic receptors: act through second messengers.

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64
Q

Three families of inotropic receptors

A
  • Nicotinic acetylcoline (ACh).
  • Gamma-amino butyric acid (GABA) and glycine.
  • ATP or purine P2X receptor
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65
Q

What happened in myasthenia gravis

A

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.

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66
Q

How Acetylcholinesterase work

A

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.

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67
Q

How GABA works

A

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.

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68
Q

How antiepileptic drugs work? Diltiazem and phenobarbital.

A

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.

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69
Q

The major excitatory neurotransmitter in the CNS?

A

Glutamate

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70
Q

Subtypes of ionotropic glutamate receptors

A

AMPA (releasing Mg)

NMDA (increased conductance of Na and intracelurarCa) EPSP

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71
Q

Excitotoxicity

A

An excessive NMDA receptor activation can cause the accumulation of intracellular Ca that trigger cell death.

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72
Q

Metabotropic receptors (act through second messenger systems such as G-proteins and produce more prolonged influences on function.

A 
Muscarinic acetylcholine receptors
metabotropic glutamate receptors
GABA-B
Serotonin receptors
norepinephrine
epinephrin
histamine
dopamine
neuropeptides
endocabinoides
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73
Q

Mecanism of D2 dopamine receptor

A

decrease AMPc levels and increased aeurosal

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74
Q

Mecanism adenosine receptor

A

increased cAMP levels and decreased aeurosal.

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75
Q

Caffeine

A

Adenosine receptor block leaving dopaminergig activity unopposed and thus increased arousal.

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76
Q

How serotoning work

A

The activity of serotoning on its post-synaptic receptor is determined by reuptake of serotoning into the presynaptic terminal by the serotoning transporter.

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77
Q

Myotatic reflex

A

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

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78
Q

Defecation

A

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.

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79
Q

Parashympatetic

a) Cholinergic
b) Adrenergic

A

a) cholinergic (acetilcholine)

_ Sympathetic- adrenergic-Norepinephrine/epinephrine_

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80
Q

What neurolocalisation would a Schiff-Sherrington posture suggest?
C1-C5

T3-L3

C6-T2

L4-S3

A

T3-L3

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81
Q

What cells are involved in the Schiff-Sherrington posture?
Purkinje cells

Border cells

Renshaw cells

Schwan cells

Target cells

A

Border cells

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82
Q

When a patient presents unconscious but can still be roused by painful stimuli he should be described as:
Confused

Obtunded

Stuporous

Comatose

Alert

A

Stuporous

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83
Q

Which nerve is the most important for the patellar reflex in the pelvic limb?
Tibial

Perineal

Pudendal

Sciatic

Femoral

A

Femoral

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84
Q

Which nerve is the most important for the withdrawal reflex in the pelvic limb?

Sciatic

Femoral

Perineal

Pudendal

Tibial

A

Sciatic

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85
Q

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

A

C8-T1

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86
Q

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

A

Reduced movement in the pelvic limbs but the patient can still walk if weight is supported

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87
Q

A patient with non-ambulatory paraparesis is graded as having a spinal injury:
Grade 5

Grade 1

Grade 2

Grade 4

Grade 3

A

Grade 3

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88
Q

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

A

Spinal shock

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89
Q

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

A

Optic and facial nerves

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90
Q

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

A

Abnormal position of the eyeball that the animal cannot overcome

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91
Q

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

A

Nystagmus with slow and fast phase

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92
Q

In Horner’s syndrome, what is NOT a clinical feature?

Mydriasis
Ptosis
Enopthalmos
Conjuntival hyperemia
3 eyeliner protusion
A

Mydriasis

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93
Q 
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
A

C7-C8 nerve roots

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94
Q

Compulsive circling suggests a lesion in the …?
Ipsilateral peripheral vestibular system

Contralateral brainstem

Contralateral forebrain

Contralateral peripheral vestibular system

Ipsilateral forebrain

A

Ipsilateral forebrain

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95
Q

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

A 
All of the above are possible causes for proprioceptive deficits:
Contralateral forebrain
Ipsilateral brainstem
Ipsilateral cerebellum
Ipsilateral spinal cord
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96
Q

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

A

Placing test

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97
Q

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

A

The animal shows a behavioural response by looking uncomfortable, vocalising or trying to bite

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98
Q

What cranial nerve is affected?

Loss of smell

A

I Olphatory

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99
Q

What cranial nerve is affected?

Partial or complete blindness ( Dilated unresponsible pupils)

A

II Optico

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100
Q

What cranial nerve is affected?
Ventrolateral strabismus, inhabiliy to rotate eye dorsaly, ventrally and medially, dilated irresponsible pupil, ptosis upper lid

A

III Oculomotor

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101
Q

What cranial nerve is affected?

dorsolateral strabism

A

IV Troclear

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102
Q

What cranial nerve is affected?

MM atrophy and jaw weakness (if bilateral dropped jaw) neurotrophic keratitis

A

V Trigeminus

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103
Q

What cranial nerve is affected?

Medial strabism, inability to move lat eyeball and to retract.

A

VI Abducent

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104
Q

What cranial nerve is affected?

Dropped, inability to move ear and lip

A

VII Facial

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105
Q

What cranial nerve is affected?

Deafness, vestibular signs

A

VIII Vestibulococlear

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106
Q

What cranial nerve is affected?

Dysphagia absence gag

A

IX Glosopharingeo

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107
Q

What cranial nerve is affected?

Dysphagia, inspiratory dyspnea, dysphonia, regurgitation, absence gag.

A

X Vago

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108
Q

What cranial nerve is affected?

Trapezius atrophy

A

XI Accesory

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109
Q

What cranial nerve is affected?

Tonge desviation

A

XII Hipoglosso

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110
Q

What we are evaluating with the palpebral reflex?

A

V ; VII ; Bainstem

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111
Q

What we are evaluating with the corneal reflex?

A

V; VII; VI; Brainstem

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112
Q

What we are evaluating with the physiological nystagmus?

A

VIII; III; IV; VI; brainstem

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113
Q

What we are evaluating with the Menace response?

A

II; VII; forebrain; cerebellum; brainstem

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114
Q

What we are evaluating with the Nasal mucose stim?

A

V; forebrain; c brainstem

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115
Q

What we are evaluating with the PLR?

A

II; III; brainstem

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116
Q

What we are evaluating with the gag?

A

IX; X; brainstem

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117
Q

Allele

A

one of number of different forms of the same gene

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118
Q

Heterozygous

A

Having two different copies (alleles) of a gene for a specific trait or disease. One of the two is usually the wild type.

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119
Q

Homozygous

A

Having two identical copies of a gen for a specific trait or disease

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120
Q

Phenotype

A

The observable characteristic of an animal that result from the interaction of the animal´s genetic makeup and the environment.

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121
Q

Polygenic

A

A sisease or trait caused by the interaction of two or more genes.

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122
Q

Transcription

A

First step in gene expression when the DNA gets transcribed to RNA.

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123
Q

Translation

A

Second step in gene expression in which RNA becomes to form amino acids.

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124
Q

Gen

A

Region of the ADN that code for the production of polypeptides.

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125
Q

Exons

A

coding region of the ADN

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126
Q

Introns

A

Untranslated regions of the ADN

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127
Q

Enhancers and silencers

A

Regions in the ADN that serve to regulate the transcription process.

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128
Q

Promoter region

A

Area of regulation in the ADN that help to initiate the transcription process.

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129
Q

Start codon

A

first aa that is translated by the ribosome. In eukaryotes this almost always produces the aminoacid methionine.

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130
Q

Stop codon

A

Is the codon that signals the end of translation and is typically one of the following codons:
TAG
TAA
TGA

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131
Q

Dog genome

A

38 autosomal chromosome pairs and 1 pair of sex chromosome

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132
Q

Cat genome

A

18 autosomal chromosome pairs and 1 pair of sex chromosome

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133
Q

Autosomal recessive pedigree

A

Two aparent silent carriers of the disease are bred the disease is produced at approximately 25% prevalence.

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134
Q

Autosomal dominant pedigree

A

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.

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135
Q

X linked recessive trait

A

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.

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136
Q

Karyotyping

A

evaluation of the number and apparence of chromosomes

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137
Q

Missense mutation

A

a single nucleotide change that results in the formation of a different amino. acid is typically observed.

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138
Q

Nonsense mutation

A

A single nucleotide change that results in the development of a stop codon, prematurely.

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139
Q

Penetrance

A

Proportion of individuals with a disease gene variant that will develop the disease.

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140
Q

Incomplete penetrance

A

Some individuals with the disease gene variant (mutant) will not develop the disease.

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141
Q

Phenotype

A

The observable characteristics of an animal that result from the interaction of the animal´s genetic makeup and the environment.

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142
Q

Polymorphism

A

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.

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143
Q

Wild Type

A

The most common copy (allele) of the gene, typically that found in the normal individuals.

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144
Q

Thiopurine Methyltransferase (TPMT)

A

Is important for metabolizing a number of cancer and and immunosuppressive agents including azathioprine and 6-mercaptopurine.

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145
Q

Blepharitis

A

inflammation of the eyelids

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146
Q

Myxedema coma

A

Rare, life-threatening manifestation of hypothyroidism. Clinical signs include mentation changes due to brain edema, hypothermia without shivering, non`pitting skin edema, and bradycardia.

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147
Q

Thiamine deficiency

A

lessions in the hippocampal formation.

Thiamine is essential for decaroxylation of pyruvic acid and other alpha-keto acids.

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148
Q

Hypocalcemia alterations

A

CAuse increases in mb excitability in both muscle and CNS. This leads to generalized stiffness, lameness, muscle twitching, nervousness, behaviour changes, tetany, and seizures

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149
Q

Calculation free water deficit

A

Free water deficit= 0.6x body weight (kg)x[(plasmaNa/148)-1]

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150
Q

Antibodies in rheumatoid arthritis

A

IgA; IgG and IgM

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151
Q

Type of hypersensitivity reaction in nonerosive polyarthritis

A

Type III hypersensitivity reaction

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152
Q

When an animal is considered overweight?

A

> 10% his ideal weight

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153
Q

When an animal is considered obese?

A

> 20% of his ideal weight

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154
Q

Characteristics transudate

A

clear, colourless. <2.5 g/dl total protein ; 1000-1500 cells/mcl (nucleated cell count); occasional mesotelia cells

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155
Q

Characteristics modified transudate

A

slightly cloudy; straw-colored; 2.5-5 g/dl total protein; >1000<500 cells/mcl. Mesothelial cells, non-degenerate neutrophils, macrophages, lymphocytes.

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156
Q

Exudate

A

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.

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157
Q

Eosiniphilic effusions

A

transudates or exudates with > 10% eosinophils

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158
Q

Starling´s equation

A

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)

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159
Q

Level of albumina as cause of peripheral edema

A

< 2 g/dl

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160
Q

Proportionate dwarfism is consecuence of

A

GH deficiency

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161
Q

Desproporcionate dwarfism

A

Juvenile Hypothyroidism

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162
Q

Feeding center

A

lateral hypothalamic nuclei

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163
Q

Satiety center

A

ventromedial hypothalamic uclei

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164
Q

what tissue release leptin?

A

adipose. Contribute to a sense of satiety.

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165
Q

Localization of the cough receptors

A

larynx
trachea
bronchi

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166
Q

Does irritation of the smaller bronchi, bronchioles and alveoli elicit cough?

A

No

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167
Q

when is considered the cough chronic

A

> 8 weeks

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168
Q

What is the guaifenesin

A

Expectorant

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169
Q

Mucolitycs

A

acetylcysteine, guaifenesin, ambroxol, bromhexine

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170
Q

cough suppresants

A

buthorphanol, codeine, hydrocordone, dextromethorphan

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171
Q

Bronchodilators

A

inhaled slabutamol/albutamol/albuterol, theophyline, aminiphylline and terbutaline

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172
Q

Dipherential diagnosis for hypercalcemia

A

respuesta

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173
Q

Paracrine

A

The messenger diffuses through the interstitial fluids, usually to influence adjacent cells.

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174
Q

Autocrine

A

the messenger acts in the cell of its origen

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175
Q

Neurotransmitter

A

which affect communication between neurons, or betwen neuron and target cells

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176
Q

transmitter found in endocrine and neural tissues

A

Epinephrine
Dopamine
Histamine
Somatostatin

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177
Q

Protein Hormons

A

GH
Insulin
Corticotropin (ACTH)

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178
Q

Peptides Hormos

A

Oxitocin

Vasopresin

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179
Q

Amines Hormones

A

Dopamine
Melatonine
Epinephrine

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180
Q

Steroid Hormons

A 
Cortisol
Progesterone
Vit D
glucocorticoides
mineralocorticoids
estrogenos androgenos
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181
Q

Hormones in the energy metabolism

A 
Insuline
Glucagon
Cortisol
Epinephrine
Thyroid Hormone
GH
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182
Q

Hormones in the mineral metabolism

A 
Parathyroid H
Calcitonin
Aldosterone
Angiotensin
Renin
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183
Q

Hormones correlated with the growth

A 
GH
Thyroid
Insulin
Estrogen
Androgen
Growth factors
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184
Q

Hormones correlated with the reproduction

A 
Estrogen
Androgen
Progesterone
Luteinizing H
Follicle-stimulating
Prolactine
Oxitocin
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185
Q

Differences between protein hormones and steroids

A

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

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186
Q

Dihydrotestosterone (metabolite) is more potent than testosterone

A

True

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187
Q

Localization of the hypothalamus

A

Third ventricle in the diencephalon

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188
Q

Precursors of Oxytocin and Vasopressin

A

Prepropressophysin- (neurophysin II)-Vasopressin

Preprooxyphysin- (neurophysin I)- Oxytocin

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189
Q

Main action of oxitocin

A

Contraction of the smoth muscle in the mamarian glan and the uterus.

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190
Q

What produce the Hypotalamus?

A 
GHRH
Dopamina
CRH
TRH
GNRH
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191
Q

What produce the adenohypophysis

A

Glycoproteins: FSH; LH; TSH
Somatotropins: GH; PRL
Proopiomelanocortin: ACTH

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192
Q

How somatostatin work?

A

Inhibition GH

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193
Q

How Dopamine work?

A

Inhibition GH and prolactine

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194
Q

How TRH work?

A

Stimulation TSH

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195
Q

How GHRH work?

A

Stimulation LH +FH

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196
Q

How GH work?

A

Stimulation production IGF-1
Lipolisis
Inhibition insulin

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197
Q

How ACTH work?

A

estimula la generación de glucocorticoides y androgenos por la corteza suprarrenal.
Mantiene el tamaño de las zonas fasciculadas y reticulada de la corteza.

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198
Q

Células d ela glándula parathyroides

A 
Follicular cells (T3-T4 production)
Parafolicular cells (calcitonine)
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199
Q

Function of tiroglobulina

A

Transport of T3-t4 into folicular cell

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200
Q

Euthyroid sick syndrome

A

Increased TT4 decrease T3

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201
Q

Trigger of Dyspnea

A

Hypoxemia o Hypercarbia (PaO2<60 mmHg; PaCO2>50 mmHg)

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202
Q

Causes of hypoxemia

A
  1. -Decreased fraction of inspired O2
    • Hypoventilation
    • Diffusion impairment
    • Right to left cardiovascular shunt
    • Ventilation-perfusion (VQ) inequality
    • Abnormal hemoglobin
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203
Q

If there is an increase of effort in the inspiration the obstruction

A

is in the upper airway

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204
Q

If there is an increase of effort in the expiration the obstruction

A

in in the lower airway

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205
Q

Paradoxical breathing pattern appeared when

A

greatly increased work of breathing and respiratory muscle fatigue.

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206
Q

mild hemorrhege is possible with a platelet count ..

A

<25.000 platelets/mcL

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207
Q

moderate hemorrhege is possible with a platelet count ..

A

<10.000 platelets/mcL

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208
Q

severe hemorrhege is possible with a platelet count ..

A

<5.000 platelets/mcL

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209
Q

Spasticity

A

increase in muscle tone due to hyperexcitable muscle stretch (myotatic) reflexes.

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210
Q

Myotonia

A

prolonged contraction or delayed relaxation of a muscle after voluntary or stimulated contraction.

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211
Q

A drug that can be helpful in presence of myotonia

A

Procainamida

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212
Q

How the strychnine cause tetania

A

It blocks the neurotransmitter glycine.

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213
Q

What happens in tetanus

A

Clostridium tetani under anaerobic conditions, produce the toxine tetanospasmin that interferes with release of inhibitory neurotransmitters glyvine and gamma-aminobutyric acid.

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214
Q

GABA is excitatory or sedative

A

excitatory

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215
Q

How works dexmedetomidine

A

is a central alpha-2-adrenoreceptor agonist with a site of action at the locus coeruleus, influencing Purkinje cell and GABAergic output

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216
Q

The hallmark of the cerebellar disease

A

Intention tremor

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217
Q

Shaker pup syndrome

A

Inherent develoopmental disorders of central myelination

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218
Q

What is ataxia

A

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.

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219
Q

Sistemic condition that can cause ataxia

A

Hypocalcemia–Cerebral ataxia

Thiamine deficiency—Vestibulara ataxia

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220
Q

Tipes of ataxia

A

Propioceptive
Cerebellar
Vestibular

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221
Q

Head tilt

A

Vestibular ataxia. Usually the side of the head tilt indicates the side of the lesion.

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222
Q

Signs of vestibular ataxia

A 
Head tilt
Leaning
Falling
Rolling
Occasionally circling, strabismus, and nystagmus.
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223
Q

The propioceptive positioning deficits are ipsilateral to the head tilt.

A

True, excep in cases of paradoxical vestibular syndrome, where proprioceptive deficits are contralateral to the head tilt.

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224
Q

Nystagmus in peripheral vestibular disease

A

Is always in the same direction, either horizontal or rotatory, BUT NOT VERTICAL

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225
Q

A characteristic alteration in cerebellar ataxia

A

Dysmetria

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226
Q

Paresis

A

Partial loss of motor function, which is usually manifested as weakness.

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227
Q

Paralysis (plegia)

A

Complete loss of motor function

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228
Q

Localization of the lesion in presence of paresis whithout ataxia

A

The lesion is located outside of the central nervous system and therefore not affecting the spinal cord.

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229
Q

The hallmarks of UMN signs

A

Paralysis or paresis with increased extensor tone (spasticity or hypertonus), normal to increased spinal refex (hyperreflexia), and slowly progressive muscle atrophy from disuse.

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230
Q

The hallmarks of LMN signs

A

paresis or paralysis with absent to decreased extensor tone (flaccidity or hypotonus), decreased or absent spinal reflex and rapid and severe muscle atrophy.

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231
Q

Localization of lesion in presence of Schiff-Sherrintong phenomenon

A

T2-L7

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232
Q

Clinical division of the spinal cord

A

C1-C5 cervical
C6-T2 cervicothoracic
T3-L3 Thoracolumbar
L4-S3 Lumbosacral

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233
Q

Localization of the lesion if involve all four limbs

A

C1-C5 or C6-T2

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234
Q

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

A

C1-C5

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235
Q

Localization of the lesion if involve all four limbs with decreased tone and reflex in the thoracic limbs, (LMN signs) in the thoracic limbs

A

C6-T2

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236
Q

Lession localization in presence of paraplegia or paraparesis

A

Caudal T2

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237
Q

Cutaneus trunci reflex help to reconize a lesion in the segment

A

T3-L3

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238
Q

Lession localization in presence of paraplegia or paraparesis with normal to increased reflexes and muscle tone points

A

T3-L3

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239
Q

Localization with lesions in the nerve roots for pelvic limbs, peripheral region, sphinters and tail /refecting involvement of sciatic, pudendal, pelvic and caudal nerves).

A

L4-S3

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240
Q

Patient flexes the limb but does not have conscious perception of the painful stimulus

A

severe spinal cord lesion and carried a guarded prognosis.

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241
Q

Lesion localization in presence of stupor or coma

A

Brainstem or rerebral cortex

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242
Q

Structures in the caudal transtentorial herniation

A

Portions of the temporal lobe shift ventral to the tentorium cerebelli and cause midbrain compression.

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243
Q

Structures in the foramen magnum herniation

A

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.

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244
Q

Lessions in the brainstem at the level of the pons can cause unilateral or bilateral pupillary…

A

constriction (miosis)

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245
Q

Lessions in the brainstem at the level of the midbrain can cause unilateral or bilateral pupillary…

A

Dilation (Mydriasis)

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246
Q

Nerves involves in the oculocephalic and doll´s eye reflexes

A

VIII; the brainstein (vestibular nuclei, medial longitudinal fasciculus), the cerebelum (flocculonodular lobe) and III; IV and VI

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247
Q

Cheyne-Stokes respiration

A

Hyperpnea alterning with apnea and can be an indication of a bilateral cerebral hemisphere or diencephalic lesion.

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248
Q

Kussmaul respiration

A

deeper than normal breaths occurring in an other wise normal pattern. (diabetic ketoacidosis)

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249
Q

Drugs that can be used in cases of Ptyalism

A

Atropine
glycopyrrolate
Phenobarbital (idiopathic ptyalism)
scopolamine

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250
Q

Nerves and center involving in the gagging

A

Trigeminal, glossopharyngeal and vagus

Center in the medula oblonga

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251
Q

The haustral contraction

A

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.

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252
Q

Inhibition of GHRH

A

Somatostatina and GH

253
Q

Production of GHRH

A

Hypotalamo

254
Q

GHRH stimula the pruduction of

A

GH

255
Q

GH stimul the production of

A

IGF-1 (liver)

256
Q

Inhibitory effect IGF-1

A

GH and GHRH

257
Q

Effects GH

A

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.

258
Q

Diagnosis of acromegaly in cat. Level of IGF-1

A

> 1000 ng/ml

259
Q

Tissue thatsintetize GH

A

hypophysis (pulsatil) and mamaria gland (constant production)

260
Q

Progesterone receptor blockers

A

Aglepristone

261
Q

What cobinations of hormones alterations are frequently in the dwarfism

A

GH. TSH and prolactine deficiences
Impared relax of gonadotropins
Normal adenocorticotropes hormones (ACTH)

262
Q

Mutation in the pituitary dwarfism

A

LHX3

263
Q

Diagnosis of GH deficiency

A

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.

264
Q

What is the stimulos for secretion of vasopresin

A

Increase plasma osmolality

Angiotensina II

265
Q

Action vasopresin

A 
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

266
Q

Treatment nephrogenic diabetes insipidus

A 
Thiazide diuretic (decrease Na reabsortion from distal tubules.
Potassium-sparing diuretics.
267
Q

False increased of TCa

A

Hemolisis and lipemia

268
Q

How hypoproteinemia affected Ca analysed

A

Lowers measured TCa concentrations but does not affect iCa

269
Q

How Ph affected Ca concentrations

A

Low PH iCa increase

Increased PH decreased iCa

270
Q

Circulating Ca concentrations are under control of four main factors:

A

PTH
Calitonin
Vit D
Parathyroid hormone-related protein (PTHrP)

271
Q

How affect Vit D to the PTH

A

increased Vit D decreased velocity PTH gen trasncription

272
Q

PTHrP

A

Parathyroid hormone-related protein is integralto calcium homeostasis in the fetus.

273
Q

Where is produce calcitonnin

A

C-cells by thyroid glands

274
Q

place in the kidney of Ca absortion (PTH)

A

distal convoluted tubules and thick ascending loops of Henle

275
Q

Hallmark of hyperparathyroidism

A

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.

276
Q

Furosemida can be used in PHTP when the animla is corrected hidratated

A

Furosemide can further enhance renal Ca excretion

277
Q

Thyroglobulin

A

A large glycoprotein containing iodotyrosines, components of thyroids hormone.

278
Q

Thyroid peroxidase

A

Enzyme that is involve in most of the steps of thyroid hormone synthesis.

279
Q

Proteins bound the thyroid hormones in circulation

A

Thyrosine binding globulin 60%
Transthyretin 17%
Albumin 12%

280
Q

Cause of secondary hypothyroidism

A

glucocorticoid excess

281
Q

Diagnosis of lymphocitic thyroiditis

A

Presence of TgAAs (Thyroglobulin autoantibodies)

282
Q

Autoimmune polyendocrine syndrome type 1

A

Rare autosomal recesive disorder:
mucocutaneus candidiasis
Autoimmune thyrid disease
Addison´s disease.

283
Q

Autoimmune polyendocrine disease type II

A 
development of two or more of the following:
Addison´s disease
Grave´s disease
Autoimmune thyroiditis
Type1 DM
primary hypogonadism
Myasthenia gravis
Celiac disease
284
Q

Euthyroid sick syndrome

A

changes in thyroid hormones concentration secondary to acute and chronic illnesses.

285
Q

Drug that can induce hypothyroidism and even myxedema coma because of their ability to reversibly inhibit TPO

A

Sulfonamides

286
Q

The single most acurate test for diagnosing hypothyroidism

A

FT4

287
Q

apathetic hyperthyroidism

A

Hyperthyroid cat lethargic, obtunded and with poor appetite.

288
Q

Poliurya in hyperthyroidism is caused by

A

down-regulation of aquaporin water

289
Q

Effects of thyroid hormone on the renal tubular function

A

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.

290
Q

Cell that produce insuline

A

B-cells

291
Q

Drugs reported hypoglicemia

A 
insulin
oral hypoglycemics
salicylates
acetaminophen
B-blockers
B2-agonists
ethanol
ACEi
Lidocaine
others..
292
Q

Use of prednisone in insuline secreting tumors

A

Increases blood glucose concentration by increasing gluconeogenesis and glucose 6-phosphate activity while decreasing blood glucose uptake into tissues and stimulating glucagon secretion.

293
Q

What is Diazoxide

A

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.

294
Q

What is Diabetes type 1A?

A

Insulinitis. Presence of serum antiantibodies of pancreatic components.

295
Q

Goals treatment DM

A

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

296
Q

Glucose nadir

A

Time of peak insuline effect (should be 90-150 mg/dl

297
Q

Catarat in DM is secondary to

A

intra-cellular accumulation of sorbitol and galactitol, produced following the metabolism of glucose and galactose by enzymes within the lentes

298
Q

Amylin

A

ia a hoemone whimodulates insuline actions

299
Q

Dose to start treatment with insulin

A

0.25 U/KG

300
Q

Diet for diabetics dogs

A

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

301
Q

Factors reported with DM remision in cats

A 
Low carbohydrate diet
Long acting insulin (glargine)
Higher age
lower  maximum dose of insulin
Recent corticosteroid administration
early institution of tight gycemic control
302
Q

Diet for diabetics cats

A

Low carbohydrate-low fiber diet

303
Q

Oral hypoglycemics

A 
Sulfonylureas
Meglitinides
Biguanides
Thiazolidinedione
Alpha-glucosidase inhibitors
304
Q

Increatins

A

Are gastrointestinal hormones rapidly released in response to food intake that stimulate synthesis and release of insulin while suppressing glucagon secretion.

305
Q

Glucocorticoides in insuline resistance

A

Glucocorticoides induce DM by imparing insulin sensitivity, decreasing glucose uptake in peripepheral tissues, increasing hepatic gluconeogenesis, and may inhibitinsulin secretion from pancreatic beta-cell.

306
Q

Stimul for ACTH (hypophysis)

A

CRH (Corticotropin releasing hormone (hypotalamus)

307
Q

Inhibition CRH

A

Glucocorticoids and somatostatin

308
Q

Stimulation CRH

A 
IL-1
IL-6
THF alfa
Leptin
Dopamine
Arginine vasopresin
Angiotensine II
309
Q

Precursor molecule of ACTH

A

pro-opiomelanocortin

310
Q

Layers of the adrenal cortices

A

Outder-Glomerulossa
Middle-Fasciculata
Inner-reticularis

311
Q

Enzyme need to syntesis of adrenal steroids

A

cytochrome P45

312
Q

Enzyme need for the syntesis of cortisol and androgenos

A

17-alpha hydroxylase

313
Q

Pituitary tumors

A

Ademonmas

CArcinomas

314
Q

Cushing´s pseudomyotonia

A

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.

315
Q

Stress leukogram

A

lymphopenia
eosinopenia
neutrophilia
monocytosis

316
Q

How Trilostano woks

A

Competitive inhibitionr of the enzyme 3-beta-hydroxysterroid dehydrogenase which catalyzes adrenocortical conversion of pregnenolone to progesterone.
Block systesis cortisol and reduction aldosterone

317
Q

Ketoconazole in cats

A

Ketoconazole is an inhibitor of steroidogenesis in humans and dogs, but is ineffective in cats.

318
Q

Place of action of aldosterone in the kidney

A

Distal nephrone to promote Na reabsorption and K and H excretion.

319
Q

Hemogas in aldosterone-secreting adrenal tumors

A

metabolic alkalosis due aldosterone-mediatd hydrogen ion excretion

320
Q

Aldosteronoma suspicion

A

hypokalemia and hypertension

321
Q

Atypical primary hypoadrenocorticism

A

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

322
Q

Glucocorticoides are important to mantein the mucosal gastric barrier.

A

True

323
Q

Hemogas in addison

A

hyponatremia, hyperkalemia, pypercalcemia, hypocloremia, mild acidosis (becoause aldosterone facilitates urine hydrogen excretion)
Na:K<24
Glucocorticoids facilitate calciuresis.

324
Q

Treatment addison

A 
Fludrocortisone acetate (contiains glucocorticoids and mineralocorticoids)
DOCP
325
Q

Production of Secretin

A

S cell in duodenum

326
Q

Stimulation secretion secretin

A

Presence of H+ in duodenum (containing in gastric secretions)

327
Q

Action secretin

A

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

328
Q

Place of production of glucagon

A

Alpha cell in pancreatic islotes

329
Q

Glucagon actions

A

Stimulus hepatic gluconeogenesis and glycogenolisis

330
Q

The most potent insulin secretogogue

A

integrin GLP-1

331
Q

Secretion of Gastrin

A

Synthesized and secreted by neuroendocrine G cells located in the antrum and duodenum

332
Q

Stimuli for gastrin secretion

A

ingeste proteins and gastric distension

333
Q

Inhibition gastrin

A

Low intraluminal Ph <3

334
Q

Gastrin actions

A

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.

335
Q

Secretion of CCK

A

Synthesized by I cell in the duodenum and jejunum

336
Q

stimulation of CCK secretion

A

H+ ,fatty acid and aa in duodenum

337
Q

CCK effects

A

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.

338
Q

Production od somatostatine

A

Synthesized in the hypothalamus
pancreatic islet delta cells
GI D cells in response to nutrients

339
Q

Somatostatine actions

A

Inhibition gastric acid, pepsinogen, gallbladder contraction, insulin secretion, pancreatic exocrine function, GI motility and nutrient absorption
INHIBITION GH

340
Q

Secretion motilin

A

GI cells. Endocrine actions occure during fasting.

341
Q

Functions motilin

A

During fasting. Coordinating migrating motility complexes.

Coordinate biliary-pancreatic-gastric secretions.

342
Q

Stimuly motilin

A

H+ in stomach and lipid enter in small intestine.

343
Q

Ghrelin production

A

stomach

344
Q

Ghrelin functions

A

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.

345
Q

Zollinger-Ellison Syndrome

A

In case of gastrinoma, the gastrin overproduction can cause gastric antral hypertrophy, hyperacidity and ulceration.

346
Q

Cells origen of pheochromocytoma

A

cromaffin cells of the adrenal medula

347
Q

What is syntetiside in the adrenal medula

A

Catecholamine (epinephrine and norepinephrine)

348
Q

Cathecolamine metabilites in urine

A

metanephrine and normetanephrine

349
Q

Neuroendocrines markers for pheocromocitoma

A

Stained, chromogranin A

350
Q

Odynophagia

A

Painful swallowing

351
Q

Vomiting centre localization

A

Medulla oblongata in the brainstem

352
Q

Receptors of apomorphine

A

Dopaminergicos (D1 and D2). Stimuli emesis, but less effective in cats suggesting lack in D2.

353
Q

Most sensitive and specific test for EPI

A

TLI

354
Q

These haustral contractions

A

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)

355
Q

Prolongued exposure to estrogen can cause

A

persisten sanguineous discharge. Failure to ovulation that can be demonstrated with low levels of plasma progesterone concentrations.

356
Q

Polydipsia

A

water intake > 90-100 ml/kg/day

357
Q

Polyuria

A

> 50 ml/kg/day

358
Q

Marked hypostenuria

A

SG <1006 due to diabetes insipidus

359
Q

SG in normal animals

A

dog 1006-1050

cats 1005-1090

360
Q

Drugs that can cause polyuria/polidipsia

A

glucocorticoids
diuretic
phenpbarbital

361
Q

plasma osmolality equation

A

2[(Na)+{(glucosa/18) +BUN/2.8)}

362
Q

Causes of hyperbilirubinemia

A

Prehepatic hemolisis
liver failure
post hepatic obstruction or rupture of the biliary tract

363
Q

Myoglobinuria

A

severe muscle damage increase CK

364
Q

bilirubine concentration to have jaundice

A

> 2 mg/dl

365
Q

S3

A

Protodiastole

Sobrecarga de volumen

366
Q

S4

A

Presistole/ contracción atrial
Hipertrofia ventricular
3 AVB

367
Q

Reynolds numbers

A

RN=radio x velocidad x densidad / viscosidad

368
Q

Austin Flint murmur

A

occasionally massive aortic regurgitation causes premature closure of the mitral valve producing functional mitral stenosis and a diastolic murmur.

369
Q

Pulse parvus et tardus

A

Dogs with severe aortic stenosis may have a weak hypokinetic pulse, and or may have a pulse pressure that has a later-than-normal

370
Q

Pulsus paradoxus

A

Increased expiration decreased in inspiration

371
Q

Pulsus alternans

A

severe left ventricle disfunction

372
Q

Immune-mediate anaemia

A

Spherocytes, agglutination, ghost cell

373
Q

Oxidant-induce anemia

A

Heinz bodies, eccentrocytes, pyknocytes

374
Q

Iron deficiency

A

Hypochromic RBCs, and microcytic Hypochromic RBC indices. Presence of schistocytes, keratocytes an acanthocytes.
low Iron and percentual saturation transferrin

375
Q

Intravascular hemolisis

A

Hemoglobinemia and hemoglobinuria

376
Q

regenerative anaemia (reticulocites account)

A

> 95000/mcl dog

>60000/mcl cat

377
Q

Days for the maturation and release for the bone marrow of the neutrophils

A

6-9

378
Q

Stimulos production neutrophils

A

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.

379
Q

Stimulo to produce Eosinophils

A

Th2 produce Il3-Il5 and granulocyte-macrophage stimulating factor

380
Q

NK are producer in the bone marrow in aproximately 7 days unther the stimulus of…

A

IL-2 IL-7 IL-15 and SCF

381
Q

White cell that increased in case of increased epinephrine but not cortisol

A

Lymphocytes

382
Q

Major regulator of megakaryocyte maduration

A

cytokine thrombopoietin (TPO)

383
Q

Platelet count to can produce hemorrhage

A

<30000/mcl

384
Q

Drugs than can cause thrombocitopenias

A

estrogen, chloranphenicol, mehimazole, penicillin, procainamide and sulfa antibiotics

385
Q

Hereditary thrombocytopenias are secondary to

A

beta 1 tubulin gen mutation

386
Q

What means an increase in the positive acute phase proteins

A

Inflammation

387
Q

Positive acute phase proteins

A

C-reactive proteins
Serum amyloid A
Haptoglobin

388
Q

Negative acute phase proteins are those with decreased serum or plasma concentrations in inflammatory states.

A

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.

389
Q

Value of hypoglycemia

A

<60 mg/dl

10-20mg/dl for have clinical signs

390
Q

Renal threshold for hyperglycemia

A

180-200 mg/dl

391
Q

Azotemia

A

increase in concentration of nitroge-containing substances in the blood, primarily BUN and creatinie.

392
Q

Uremic syndrome

A

significant accumulation of substances (uremic toxins) usually excreted in the urine under normal physiologic conditions in a healthy animal.

393
Q

Chronic Kidney disease clasification

A

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

394
Q

Liver. Hepatocellular leakage enzymes

A

ALT
AST (mitocondria)
Both in cytosol

395
Q

Liver, cholestatic enzymes

A

ALP
GGT (cholangiocitos)
hepatocito canalicular membrana

396
Q

Hyperlipidemia and hyperproteinemia increase or decrease Na concentration?

A

Decrease

397
Q

Alteration of CL concentration assays

A

Hyperproteinemia
lipemia
administration of bromide

398
Q

Sindrome of inapropiate ADH secretion (SIADH)

A 
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
399
Q

Hypocloremia without parallel hyponatremia

A

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

400
Q

What happen with Cl with the admisnitration of furosemide

A

Loss of it

401
Q

Primary regulate hormone in the [k]

A

Aldosterone

402
Q

Where is excrete the K in the nephrone

A

Distal tubule

403
Q

Possible cause of hypokalemia

A 
Diabetic ketoacidosis
poliuria withouth presence of compensatory polidipsia
catecholamine release
alkalemia
B2 adrenergic drug overdose
rattlesnake envenomation
hypothermia
404
Q

Pseudohyperkalemia

A

Severe thrombocytosis
severe leukocytosis
hemolysis in neonates
animals with high intracellular K (Akitas, Shiba Inu)

405
Q

Drugs that can cause hyperkalemia

A 
ACEi
Angiotensin receptor blocker
K-sparing diuretics
prostaglandin nhibitors
trimethoprim
Cyclosporine
nonspecific b-blockers
heparin
406
Q

Possible causes of hyperkalemia

A

Drugs
Hypoadrenocorticism
urethral obstruction or bilateral uretral obstructions
metabolic acidosis (translocation from ICF to ECF)

407
Q

Main causes of hypercalcemia

A

Malignan hypercalcemia
primary hyperthyroidism
chronic kidney disease

408
Q

Malignan hypercalcemia

A

Linphoma

Apocrine gland adenocarcinoma of the anal sac

409
Q

Hypercalcemia inhibe the action of ADH

A

True

410
Q

Bilirrubin crystals

A

Can be normal in concentrated urine and found in large numbers with significant bilirrubinuria

411
Q

Calcium oxalate crystals

A

Dihydrate crystals: can be in healthy dogs

Monohydrate crystals form with hypercalciuria or hyperoxaluria: Ethylene glycol intoxication).

412
Q

Cholesterol Crystals

A

non specific occasionally observed in healthy dogs

413
Q

Urate Crystals

A

hepatic failure, portosystemic shunts

414
Q

Xantine crystals

A

secondary to Allopurinol treatment

415
Q

Immunoglobulines in the detection of Leptospira whit the eLISA

A

Ig M and Ig G

416
Q

Hemotropic mycoplasmas (hemoplasmas)

A

Small wall-less bacteria that parasitize erythrocytes, living on the surface of the erythrocyte membrane.

417
Q

Status Candidatus

A

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.

418
Q

Prevalence feline hemoplasma

A

male, nonpedigree cats with access to the outdoors. Older cats

419
Q

Treatment M. haemofelis

A 
$ weeks antibiotics
Tetracyclines
Fluoroquilnolones
Doxycicline
Moarbofloxacine
Oxytetracicline
420
Q

Virulence factor in Clostridium perfringens

A

CPE (enterotoxin) is a protein encode by the cpe gene, whose expression is coregulated with sporulation of the organism.

421
Q

Treatment clostridium perfringens

A

Ampicillin
Metronidazole
Tylosin

422
Q

Toxins in Clostridium difficile

A

A and B

423
Q

Clostridium difficile culture

A

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.

424
Q

Transmision Campylobacter spp.

A

Fecal-oral

425
Q

Cause of diarrhea in case of Campylobacter toxin

A

CDT. This toxin has 3 proteins, CdtA, CdtB and CdtC. All of which are required for cellular damage.

426
Q

Increase in case of Campillobacter due the enterotoxin

A

cAMP, prostaglandin E2 and leukotriene

427
Q

Pathogenesis Salmonella (G-, motile, non-spoeforming facultative anaerobic bacilli)

A

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.

428
Q

Salmonella pathogenicity islands

A

SPI-1 and SPI-2

429
Q

Granulomatous colitis in boxer

A

Escherichia coli

treatment enrofloxacine

430
Q

Antimicrobials that penetrate intracellutarly

A

Chloranphenicol

Trimethoprim-sulfonamides

431
Q

Diagnosis of Giardia

A

eLISA plus fecal flotation

432
Q

Diet in large bowel diarrhea

A

High fiber diarrhea

433
Q

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.

A

True

434
Q

Detection of toxoplasmosis in cats

A

Ig M

435
Q

T gondii infections in human

A

For ingestion of sporulated oocysts

436
Q

The primary histhological abnormalities in Leishmaniasis

A

Diffuse granulomatous inflammation with macrophages containing numerous amatigotes

437
Q

Type of hyperglobulinemia in dogs with leishmania

A

Polyclonal

438
Q

Babesia is transmitted by

A

Dermacentor reticulatus

439
Q

Pathogenesis Babesia spp

A

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.

440
Q

Treatment babesia (no in the cases of B. gibsoni)

A

Imidocarb

441
Q

Pathogenesis FIV

A

Transient “primary stage”
Chronic “asymptomatic stage”
Terminal “second stage”

442
Q

Clinical signs FIV

A 
Immune dysfunctions
Respiratory infections
Chronic gingivostomatitis
Risk of high-grade lymphomas, extranodal and B-cell tumors.
Neuropathology
443
Q

Risk factors for FELV infections

A

illnes, male, adulthood, outdoor acccess and large scale cat hoarding.

444
Q

· major outcomes of Felv infection

A 
Progressive infection (antigen-positive, provirus positive)
Regressive infection (antigen negative, provirus negative)
Abortive infection (antigen-negative, provirus negative, antibody-positive)
445
Q

Felv antigen

A

IFA p27

446
Q

Felv vacination in case of positive animals

A

No value but risk of injection-site sarcoma.

Advice inactivated vaccine versus MLV (increases risk of side effects)

447
Q

Replication of the feline coronavirus virus

A

In macrophages.

Important the Spike gen (S)

448
Q

What happens with the activation of p38 MAPK

A

It is the pathway that regulates production of tumor necrosis factor alpha and intelukine 1 beta

449
Q

Cytologic evaluation of the effusion in cats with FIP

A

Pyogranulomatous inflammation with a predominance of macrophages and neutrophils.

450
Q

Important test in FIP to differentiate from effusions of other origens

A

Rivalta´s test

451
Q

Gold standard in the dignosis of FIP

A

Immunohistochemistry

452
Q

Some dates about Canine and Feline Parvovirus

A

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.

453
Q

Maternal immunity in case of parvovirus

A

90% of maternally derived antibody from colostrum and it has a half-life of around 10 days.

454
Q

Parvovirus tropism

A

cells of the thymus, bone marrow, spleen and cryp cells of the gut epithelium lead in crypt necrosis.

455
Q

Severe neutropenia in parvovirosis

A

Due partially to the high demande in the gut

456
Q

Diagnosis parvovirus

A

Fecal antigen ELISA

457
Q

Vaccination in parvovirus

A

Live attenuated and inactivated vaccines.

The most common cause for vaccine failure remains vaccine neutralization by maternally derived antibodies.

458
Q

Rabia virus

A

Envelop virus

459
Q

Diagnosis of Rabie

A

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.

460
Q

Canine infectious Respiratory disease “Kennel cough” agents

A

Adenovirus
Herpesvirus
Parainfluenza
Bordetella bronchieceptica

461
Q

In cases of Distemper where is possible to see the intranuclear and cytoplasmatic viral inclusions

A

monocytes
lymphocytes
neutrophils
erythrocytes

462
Q

Diagnosis Distemper

A

RT-PCR (reverse-transcription-polymerase chain
IFA: Ig M and Ig G
Gold standard: serum neutralization assay

463
Q

Feline Upper Respiratory Infections

A

Herpesvirus
Calicivirus
(Bordetella, Chlamydia Mycoplasma)

464
Q

Occular conditions in Feline Herpesvirus

A

Eosinophilic Keratitis
Corneal sequestration
Uveitis

465
Q

Treatment of cryptococcosis

A

Amphotericin B
Fluconazole (cats)
Itroconazole

466
Q

Aspergillosis in dogs the primary disfunction to predispose is

A

In TLR (Toll-like receptors)

467
Q

Polydipsia

A

> 100ml/kg/day

468
Q

Rubber jaw

A

deformity of the maxilla and mandible in young animals due to fibrous osteodystrophy secondary CKD

469
Q

Hyperkalemia more frequently in AKI od CKD

A

AKI and in particular with post-renal causes of azotemia

470
Q

the lesion in the nephron when there is glucosuria

A

proximal nephron

471
Q

Calcium oxalate monohydrate crystal

A

Ethylene glycol poisoning

472
Q

Prerenal azotemia

A

USS > 1030 in dogs and 1035 in cat

473
Q

Characteristics of a good GFR marker

A

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

474
Q

GRF range

A
  1. 5-4.5 ml/min dog

2. 5-3.5 ml/min cat

475
Q

Urine Dipstick

A

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

476
Q

Microalbuminuria

A

It is defined as a concentration of albunine that is >1mg/dl but below that typically detectable by urine dipstick <30 mg/dl.

477
Q

UPC

A

UPC >0.4 cat >0.5 dog = >30 mg/dl albumine

UPC > 2 = glomerular disease

478
Q

Nephrotic syndrome

A

Hypercholesteronemia
Proteinuria
Cavitary effusion or peripheral edema

479
Q

Isisthenuria

A

USG 1008-1015 (urine Osmolality 300 mOsm/kg)

Indicate that the urine has the same solute concentration as the glomerular filtrate and plasma.

480
Q

Hypostenuria

A

USG< 1008 (Uosm<300 mOsm/kg) indicating active tubular dilution

481
Q

Hypersthenuria

A

USG >1015 (Uosm>300 mOsm/kg)

482
Q

Glucosa transport in the proximal tube

A

Through SGLT2 and lesser SGLT1.

483
Q

Glucosuria en presence of normoglycemia

A

Alteration in renl tubular function

484
Q

Markers of tubular injury

A

Tubular proteins: NGAL; K1M1

Imflamatory marker IL-8

485
Q

Cast=cylindruria

A

can be present in normal dogs and cats but high number is indicative of tubular damage.

486
Q

Hyaline cast

A

After fever or exercise, alkaline or dilute urine.

487
Q

Epithelial cast

A

tubular cellular damage

488
Q

Granular cast

A

Ischemic or nephrotoxic renal tubular insult

489
Q

Way cast

A

complete cellular degradation.

490
Q

Fatty cast

A

Disorder in lipid metabolism

491
Q

AKI

A

increase >0.3 mg/dl or >25% increase from baseline creatinine

492
Q

AKI grade I

A

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

493
Q

AKI grade II

A

blood creatinine 1.7-2.5 mg/dl

Mild AKI

494
Q

AKI III

A

blood creatinine 2.6-5 mg/dl

495
Q

AKI IV

A

blood creatinine 5.1-10 mg/dl

496
Q

AKI V

A

blood creatinine >10 mg/dl

497
Q

The four phases of AKI

A

mirar esquema

498
Q

Nephrotoxicity aminoglycosides

A

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.

499
Q

Fanconi -like syndrome

A

glucosuria
aminoaciduria
hyperphosphatemia
(can be casue for tetracicline)

500
Q

Fractional Excretion of Sodium (FEna)

A

(FEna)= [(Urine nax plama creatinine)/(plasma na x urine creatine)]

501
Q

Response to high concentrations of CL in the distal tube, detected by the macula densa

A

Afferent arteriole vasoconstriction

502
Q

Manitol actions

A

An osmotic diuretic that causes extracellular volume expansion and inhibits renal Na reabsorption by inhibin renina.

503
Q

Place of accion of furosemide

A

NA CL K pump in the luminal cell mb of the loop of Henle

504
Q

Survivil time prognostic fartors in CKD

A

PO4
Proteinuria
Hypertension
Weight loss in cats is an reliable indication of deterioration

505
Q

Clinnical manifestations of disturbed water and electrolites excretions

A

Edema, hypertension, hypoNa, hyperK, metabolic acidosis and hyperPO4

506
Q

Uremic gastropatie

A

Ca and PO4 products (mucosal mineralization)

Increase gastrin and histamine levels

507
Q

Organ systems most commonly affected by elevated blood pressure

A

eyes, kidneys, NS, cardiovascular system

508
Q

Factors that promote renal secondary hyperparathyroidism

A

PO4 retention

increased FGF-23 that inhibit l-alpha-hydrolaxe activity thus leading to decrease calcitrol levels.

509
Q

Mg in CKD

A

Hypermagnesemia is common because the kidneys are primarily responsible for Mg excretion.

510
Q

SDMA increases for >3 m in dogs with serum creatinine

A

consistent with diagnosis of IRIS CKD stage I.

511
Q

Nephritis syndrome

A

signs that develop secondary to renal inflammation, generally acute, that extends into the glomeruli: hematuria, edema, hypertension, azotemia, oliguria.

512
Q

Urate calculi opacity

A

radiopaque

513
Q

treatment urate calculy

A

allopurinol with purine restricted diet to prevent formation of xantine calculi

514
Q

Dugs therapy to facilitate relaxation of the ureter for expulsion of uroliths

A

alpha-adrenergic antagonoists or selective beta-2/beta-3 agonists to relax the ureters and reduce uretral spasm

515
Q

Most common composition of ureteroliths

A

Calcium oxalate

516
Q

Prazosin

A

Alphaadrenergic antagonist

517
Q

Most common neoplasm resulting in uretral obstruction in dogs

A

Transitional cell carcinoma located in the trigone of urinary bladder

518
Q

Genes in bacteria important predictors of virulence (Lower urinary tract infections)

A

Hemolysin or the expression of urothelial adherence pili

519
Q

Presence of 1 fimbriae in E.coli (low tract urinary infection)

A

It is associated with increase severyty infection

520
Q

Agents more frequently associated with pyelonephrytis

A

Strreptococus and Enteroccocus

521
Q

Encrusted cystitis

A

Corynebacterium urealyticum. It occurs when ureasepositive bacteria form mineralized plaques on the ulcerated and inflamated mucosa of the urinary tract.

522
Q

Minimun diameter of urolitis in RX

A

2mm

523
Q

Poor radiographic opacyty urolites

A

urate, cystine

524
Q

More prevalenct calculy n dog male and femele

A

Male calcium oxalate

femele struvita

525
Q

Radiopaque calculi

A

calcium oxalate
calcium phosphate
silicia

526
Q

partial adiopaque calculi

A

struvite

527
Q

radiolucent calculi

A

xantine
cystine
urate

528
Q

Breed predisposition calculi

A

Calcium oxalate: szanuzer, yorkshire, chihuahua, shih tzu, bichon
Cystine: E. Bulldog
urate: dalmatian

529
Q

Causes of calcium oxalate uroliti

A

hypercalciuria

530
Q

Causes of struvite uroliti

A

urinary tract infections with bacteria that produce urease. Ureasa is responsible for converting urea to ammonia, with alkalinizes urine and favors struvite precipitations.

531
Q

Causes of urate uroliti

A

portosistemic SHUNT

SLC2A9 mutation

532
Q

Causes of cystine uroliti

A

failure of renal tubular reabsorption of cystine

533
Q

compound uroliti

A

Inner layer of CaOx and outer layer of struvite

534
Q

Causes of xantine uroliti

A

Allopurinol treatment

genetic deffect

535
Q

Thiazide diuretics in case of CaOx uroliti

A

These drugs inhibit the sodium-chloride cotransporter in the distal tubule and by doing so stimulate calcium reabsorption and decrease urinary calcium excretion.

536
Q

Prostatid cell growth in under the influence of

A

Dihydrotestosterona

537
Q

ARDS

A

A systematically ill pet with respiratory distress, an inflammatory leukogram, and hypoalbuminemia

538
Q

Etiopathology tracheal collapse

A

softening of cartilage rings seems to be due to a reduction of glycosaminoglycan and condrotin sulfate.

539
Q

eosinophilic bronchopneumonia in dogs

A

> 50 % eosinophilos

increase BALF levels of procollagen type III amino terminal propeptide a protein marker of collagen type III synthesis.

540
Q

Kartagener´s syndrome

A

bronchiectasis
complete left -right transposition of viscera (situs inversus)
chronic rhinosinusitis

541
Q

Why fecal flotation in pulmonary parasites can be negative

A

because larval migration occurs before the mature worms have reach the intestine.

542
Q

When is indicated start O2 suplementation

A

SpO2 <94%

PaO2< 80mmHg

543
Q

Immunoglobulina indicative of active infection in Toxoplasma gondii

A

IgM

544
Q

Objective O2 suplementation

A

SpO2 >90%
PaO2>60 mmHg
PaCO2<60 mmHg

545
Q

Mild ARDS

A

PaO2/FiO2 =200 to 300 mmHg with positive end expiratory pressure [PEEP] or continuous positive airway pressure [CPAP]>5 cm H2O

546
Q

Moderate ARDS

A

PaO2/FiO2 =100 to 200 mmHg with positive end expiratory pressure [PEEP] or continuous positive airway pressure [CPAP]>5 cm H2O

547
Q

Severe ARDS

A

PaO2/FiO2 <100 mmHg with positive end expiratory pressure [PEEP] or continuous positive airway pressure [CPAP]>5 cm H2O

548
Q

ET1 actions

A

Vasoconstriction
Stimulates smooth m growth
increased collagen synthesis
vascular remodeling

549
Q

Prostacyclin

A

Vasodilator
Inhibits platelets activation
Antiproliferative properties

550
Q

Thromboxane A2

A

Vasoconstrictor

Platelet agonist

551
Q

PDGF (platelet derivated growth factor

A

Proliferation and migration of pulmonary artery smoth muscle cells

552
Q

Nitric oxide

A

vasodialtor

inhibitor platelet activation

553
Q

NT-proBNP concentration in pleural effusion indicative of cardiogenic effusion

A

> 322.3 pmol/ml

554
Q

Aminiglicosides in intracellular infections or action in brain and prostate

A

Aminoglicosides are low lipophilic and as result are ineffective for intracelular infections and infections in tissues such as the brain and prostate.

555
Q

Caracteristics of the drugs for transdermal and transmucosal administration

A

very lipophilic and un-ionizated

556
Q

The two primary metabolism pathway

A 
Phase I (metabolic): Oxidation reduction, hydrolisis and hydratation.
Phase II (conjugations): Glucoronidation, sulfation, acetylation, aminoacid conjugation reactions.
557
Q

Enzyme family catalyzing glucuronide conjugation

A

Urinide diphosphate glucuronosyltransferase.
CAts are deficients in some of them result in decreased or alteration in some conjugations as in acetaminophen and morphina.

558
Q

Dogs lack in enzime for conjugation

A

N-acetyitransferase

559
Q

Half live of a drug

A

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%

560
Q

Steady state

A

When no further increases in drug concentration occur with continue dosing (97% of elimination= 5 half live)

561
Q

Dose rate equation

A

Dose rate= plasma clerance x average plasma concentration

562
Q

Volumen of distribution

A

It is a mesure of the dilution of a drug into the body after administration
Dose=volumen of distribution x plasma concentration

563
Q

Depot effect

A

sequestration in the stratum corneum (drug administration)

564
Q

Advice antibiotics for G-

A

Fluoroquinolone
Cephalorporin
aminoglicoside

565
Q

Organisms with unpredictable susceptibility

A

Pseudomona aeruginosa
Methilcillin-resistant Staphylococcus
Enterococcus spp

566
Q

Anaerobios have unpredictable reaction to

A

Trimetroprin-sulfonamides
Ormetoprim-sulfonamides
Fluoroquinolones

567
Q

Resistence ofBacteroides fragiles (anaerobio)

A

Has a beta lactamase that inactiva cephalosporins and ampicillin-amoxi

568
Q

Pseudomones are resistant

A

Macrolide antibiotics

569
Q

Cellular debris and infected tissue can inhibit the action of

A

trimethoprim-sulfonamide

570
Q

Drugs that decreased the action fro the concentration of Mg, Ca, Fe and Al

A

Fluoroquinolones

Aminoglycosides

571
Q

Acid enviroment decreased the action of

A

Clindamicin
Erythromicin
Fluoroquinolones
aminoglicosides

572
Q

Antifungal that inhibits systesis of steroid hormones (cortisol and testosterone) and inhibit CYP P-450
also inhibition p-gp

A

Ketoconazol

573
Q

If ketoconazol is administrate with cyclosporine

A

cyclosposin concentration increase 2-3 folds in dogs

574
Q

Secondary effecto of voriconazole in cats

A

Neurotoxicosis

575
Q

Chronic supresion of HPAA

A

Depot

repositol

576
Q

In cats prednisone or prednisolone

A

In cats prednisolone is preferred

577
Q

How anti Cox-1 produce aqua tetention

A

ADH is inhibit by prostagalndines, antiCox1 inhibi prostagglnadines so increase retention H2O

578
Q

Metamizole

A

Toxic in cats doesn´t work in Cox1 and Cox2

579
Q

Antiinflamatory potency of:
Cortisol
Prednisolone prednisolone
Dexametasone

A

Cortisol. 1
Prednisolone prednisolone 3.5-5
Dexametasone 25-30

580
Q

Mineralocorticoid potency of:
Cortisol
Prednisolone prednisolone
Dexametasone

A

Cortisol 1
Prednisolone prednisolone 0.3-0.8
Dexametasone 0

581
Q

Duration of action of:
Cortisol
Prednisolone prednisolone
Dexametasone

A

Cortisol <12h
Prednisolone prednisolone 12-36 h
Dexametasone < 48 h

582
Q

Immunosupresive derived from the soil fungus Tolypocladium inflatum

A

Cyclosporine

583
Q

Action of cyclosporine

A

inhibition calcineurin in the T´lynphocites

Inhibition IL-2 and prolipheration T-lymphocytes

584
Q

Excretion cyclosporin metabolites

A

Biliary excretion

585
Q

Secondary effects cyclosporine

A 
lethargy
gingival hyperplasia
hirsutism
coat shedding
cutaneous papillomatosis
footpad hyperkeratosis
hepatotoxicosis/nephrotoxicosis
586
Q

phase of action of the cell cicle for the Azatioprine

A

S-phase

587
Q

phase of action of the cell cicle for the Mycophenolate mofetil

A

S-phase

588
Q

Mechanism of acction of chlorambucil

A

Cell-cycle-nonspecific alkylating agent that is cytotoxic

589
Q

Alkylating agents

A

Chlorambucil

Cyclophosphamide

590
Q

Opioid receptor

A 
mu receptor (G-protein couple)
Kappa receptor
591
Q

Full mu receptor agonist

A 
Fentanyl
remifentanil
hydromorphone
oxymorphone
morphine
methadone
592
Q

Partial mu receptor agonist

A

buprenorphine

593
Q

Kappa receptor agonist

A

butorphanol

594
Q

secondary effects opioids

A

Vomiting, nausea, ileus, constipation, urinary retention, bradycardia, respiratory depression, sedation and dysphoria.
Cats opioids are associated with hypertermia

595
Q

True or false: Cyclosporine can cause further insuline resistance in diabetic or overweight cats

A

true

596
Q

What gulucocroticoid is advice to use in case water retention is detrimental

A

Dexametasone becasue has not mineralocorticoid actions.

597
Q

Negative predictive factors in immunomediated anemia

A

bilirrubin >5 mg/dl, autoaglutination, hypoalbuminemia and intravascular hemolisis

598
Q

More hepatotoxic immunosupressive drugs

A

Chlorambucil and azathioprina

599
Q

Scot Syndrome

A

defect of procoagulant activity on theplatelet surface, it manifests as a coagulopathy because the platelet surface cannot support plasma coagulation protein activity

600
Q

Feline factor XII deficiency (Hageman)

A

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.

601
Q

Time of eritrocite formation

A

5-7 days

602
Q

Spherocytes

A

suspicious of IMHAs

603
Q

Heinz bodies anemia

A

Toxic (onion zinc..)

604
Q

Evan-s syndrome

A

IMHA and immunomediated thrombocitopenia

605
Q

palce of production of erythropoietin

A

Peritubular interstitial cells of the inner reanl cortex and outer medulla.

606
Q

The primary physiologic stimulator in the develop of vasculature

A

hypoxia

607
Q

Aneuploidia

A

Anormal numero de cromosomas

608
Q

Cancer of epitelial cells

A

Carcinomas

609
Q

cancer of connective tissue or muscle

A

sarcomas

610
Q

blood forming cells tumors

A

leukemias

611
Q

Chemoterapicos alkalinizzantes

A

yclophosphamide
Chlorambucil
Lomustine
Procarbazine

612
Q

Chemotherapy antitumur antibiotics

A

Anthracyclines: Doxorrubicin, mitoxantrone

613
Q

Chemoterapy mitotic inhibitors

A

Vinca alkaloids (inhibit assembly)
paclitaxel (inhibit disassembly)
Vincristine
Vinblastine

614
Q

Platinum compounds (cross link in the DNA

A

Cisplatin

615
Q

Tyrosine Kinase inhibitors

A

Toceranib (Palladia)

Masitinib (Masivet)

616
Q

Highly myelosuppressive chemotherapy

A 
Doxorrubicin
Lomustine
Cyclophosphamide
Carboplatin
Vinblastine
Mitoxantone
Vinorelbine
617
Q

Moderately myelosuppressive chemotherapy

A 
Vincristine
Chlorambucil
Melphalan
Methottrexate
cisplatin
hydroxyurea
5-5-fluorouracil
618
Q

Mildly myelosuppressive chemotherapy

A

Corticosteroids
L-asparginase
Vincristine (low dose)

619
Q

immunosuppressive tumor microenviroment

A

Production of inhibitory cytokines by the tumor:
TGF beta
IL-10
recruitment of regulatory T cells Treg

620
Q

BCG (bacillus of Calmette and Guérin) a biologic response modifier

A

nonspecific tumor immunotherapy

621
Q

Cytokines with immunostimulatory properties

A 
IL-2
IL-12 (can be effectively target to tummor tissue)
IL-15
IFN-gamma
TNF-alpha
622
Q

True or false
Prostaglandines stimula the platelet agregation
Hypercholesteronemia increase platelet sensitivity
Hypoalbuminemia cause hypercholesteronemia

A

True

623
Q

diferencia entre la Secreción bilis hepática y la vesícula biliar

A

En la vesícula biliar se reabsorbe na y cloro pero no el calcio y el potasio. Además se absorbe agua y bicarbonato.

624
Q

Composición d ela bilis

A 
Sales biliares
bilirrubina
colesterol
ácidos grasos
lecitina
iones (Calcio y potasio)
Agua
625
Q

Estímulos secreción biliar

A

CCK (contrae la pared de la vesícula biliar y relaja el esfinter de oddi) estimulada por presencia de grasas en el estómago
Ach

626
Q

Precursor de ácidos biliares

A

cholesterol

627
Q

Acción de las sales biliares

A

Detergente

micelas

628
Q

Secretina

A

Production in the S cell in duodenum and jejunum
Stimulation secretion of bicarbonates in the hepatic biliary conducts
Stimuli are the low ph

Done (2 decks)

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