Final- Signs And Symptoms

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coagulopathy

Back 1

Coagulopathy – any defect in blood coagulation

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petechia

Back 2

Petechia – small pinpoint hemorrhages in the skin or mucus membranes

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ecchymoses

Back 3

Ecchymoses – Larger hemorrhages in the skin or mucus membranes

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hemostasis

Back 4

Hemostasis – the process of blood coagulation. It is classified as primary and secondary.

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thrombocytopenia

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Thrombocytopenia – decreased platelet numbers

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thrombocytosis

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Thrombocytosis – increased platelet numbers

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thrompbocytopathia

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Thrombocytopathia – decreased platelet function

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clotting cascade

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Clotting Cascade – the process of clotting factor activation that results in formation of the fibrin clot

Front 9

primary hemostasis

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involves platelet plug assembly- plugs small defects in blood vessels and stimulates formation of the fibrin clot. The injured endothelium releases thromboplastin which activates platelets in the area of the injury. In addition, a circulating clotting factor called von Willebrand factor also promotes platelet activation. Platelets become more adhesive and adhere to the injured site and to other platelets forming an initial plug at the site of injury. In small injuries, this is sufficient to stop hemorrhages.

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secondary hemostasis

Back 10

Secondary hemostasis involves the formation of the fibrin clot through activation of clotting factors in the blood. It involves the intrinsic, extrinsic and common clotting pathways.

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intrinsic system of secondary hemostasis

Back 11

Activation of this system involves clotting factors in the blood. These factors are XII → XI → IX → VIII (the sequence of activation). Each of these factors has been given names. For instance factor VIII the classic anti-hemophilia A factor and IX is called Christmas factor or an anti-hemophilia B factor. Factor XII is the Hageman factor.

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extrinsic system of secondary hemostasis

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Activation of this system begins with tissue injury and the release of tissue thromboplastin (factor III). Factor III activates factor VII (proconvertin).

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common system of secondary hemostasis

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This system can be activated by either the intrinsic or extrinsic systems or both. It involves several clotting factors. These factors are X (Stuart factor), V, prothrombin (factor II) and fibrinogen (factor 1). The sequence of the common system is X → V → prothrombin → thrombin → fibrinogen → fibrin.

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fibrinolysis

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This is the normal process of fibrin clot dissolution. It involves factors that are normally present in the blood that are activated by the fibrin clot. Both fibrinolytic promoters and inhibiters are present in the blood.

Front 15

abnormalies of primary hemostasis cause

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petechial or ecchymotic hemorhhages- most apparent in skin/mucous membranes. Epistaxis, melena, hematemesis in severe cases.

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most common cause of primary hemostasis

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TCP

Front 17

causes of TCP

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diseases that cause decreased production (bone marrow dysfunction) and those that cause increased destruction, consumption, or sequestration (immune mediated diseases, vascular neoplasia, and vasculitis).

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thrombocytopathies may be ____ or ____

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hereditary or acquired

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abnormalities of secondary hemostasis result in

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subcut hematomas, bleeding into joints (hemarthroris) or into body cavities, and rebleeding following venipuncture or surgery

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most common hereditary coagulation deficiti

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von willebrand dz

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acquired deficienes of clotting factors

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vitamin K defic, circulating anticoagulants, liver dz, DIC

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diagnostic plan of hemostatic disorders

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PT, aPTTT, TCT, RVVT, and specific coag factors. ACT more readily available as is BMBT

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ACT tests

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intrinsic and common systems

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normal ACT in dog/cat

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120s/75s

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when should a BMBT be performed?

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when platelet numbers are normal, but platelet dysfunction is suspected

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define alopecia

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loss or lack of hair in any amount or distribution up to complete baldness

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when does alopecia most commonly occur?

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secondary to an acquired disorder

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basic mechanisms that produce alopecia include

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(1) abnormalities in follicular structure; (2) abnormalities in follicular function (alteration of hair growth cycle); (3) structural abnormalities of the hair shaft; and (4) traumatic removal of hair.

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primary alopecia is caused by

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inherited abnormalities of follicular structure that range from complete abscent of hair follicles to absecent of follicles that produce hair of a certain color

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secondary / acquired alopecias may be caused by

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diseases that disturb the follicular environment, prompting the disruption of hair growth and the dislodgement of hair from the follicles. Bacterial folliculitis, demodectic mange, severe necrotizing processes, and follicular hyperkeratosis are examples of acquired diseases that adversely affect follicular structure.

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phases of follicular activity

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anagen (growth phase), catagen (transitional phase) and telogen (resting phase).

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the normal follicular cycles in the dog and cat have _____ however,

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seasonal variations; hair growth is not synchronized by follows a mosaic pattern

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the majority of follicles are in

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anagen

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certain conditions/diseases cause alopecia by promoting the development of

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telogen follicles

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what can delay the initiation of anagen?

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estrogen, testosterone and aderenocortical hormones

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what can accelerate follicular activity

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thyroid hormones

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what can cause the simultaneous precipitation of many follicles into catagen and telogen?

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severe illness, fever, pregnancy, and lactation

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what is the resulting alopecia called after simultatneous precipitation?

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telogen effluvium

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endocrine disorders may also produce

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follicular hyperkeratosis that results in follicular plugging. Follicular plugging disturbs normal hair growth.

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what is the pimrary mechanism for the alopecia that results from dermatophyte infections?

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weaken the hair shaft so that normal tension on the hair causes it to break

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what affect does hypothyroidism have on the hair?

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weakened, brittle, hair shafts

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common mechanism for the alopecia associated with pruritic dermatoses

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traumatic removal of hair

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how can alopecia be classified?

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by onset (primary/secondary) or by distribution

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distribution patterns of alopecia

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diffuse, regional, multifocal or focal

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diffuse alopecia

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primarily trunkal and tend to spare the head and limbs. Endocrine disorders are most common cause of nonpruritic diffuse alopecia. Occasionally, allergic, bacterial, fungal, or immune-mediated diseases cause generalized alopecia. Telogen effluvium has been previously described as a cause of diffuse alopecia.

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regional alopecia

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occur in a variety of dermatoses that have a predisposition for certain areas of the body. These distribution patterns are useful in formulating a differential diagnosis. The conditions likely to involve the face, ears, feet, mucocutaneous junctions, and caudal body are given in the accompanying lists

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multifocal alopecia

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most common distribution pattern. It may begin with a focal pattern, but multiple lesions develop as the disease progresses.

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focal alopecia

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may initiate a multifocal distribution pattern and is caused by many of the diseases that produce multifocal alopecia. Diseases such as demodectic mange, acral pruritic nodule, dermatophytosis, and solitary neoplasms may remain as a focal pattern throughout the course of the disease. Certain forms of follicular dysplasia (pattern baldness) may affect focal areas such as the ear pinnea.

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diagnostic plan for alopecia

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direct exam of hair shaft/root (trichogram),

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club hairs

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have a tiny white ball at the root end, root sheats are absent. Indicates a telogen hair follicle

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anagen hairs plucked form the follicle have

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a larger expanded root surrounded by a root sheath.

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importance of the anagen-telogen ration

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When telogen hairs predominate, endocrine disorders, normal shedding, and telogen effluvium should be considered.

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the reversibility of alopecia depends on two factors

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(1) the presence of viable hair follicles and (2) the correction of the underlying pathology.

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when is alopecia permanent

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hen hair follicles are congenitally absent or reduced in number (hypotrichosis) or when lesions heal with scar tissue formation. Scar tissue is devoid of hair follicles since it is derived from connective tissue.

Front 55

know which diseases cause which types of alopecia

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see notes

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pruritis

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defined as an unpleasant sensation that provokes the desire to scratch

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how can pruritis be differentiated from other stimuli such as burning?

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it cant be

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five primary cutaneous sensations

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heat, cold, pain, touch, pruritis

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axons that carry pruritic sensation

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small, unmyelinated C fibers that ascend in the ventrolateral spinothalamic tracts via the thalamus to the cerebral cortex

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mediators of pruritis

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endogenous compounds

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major mediators of pruritis in dogs and cats

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proteolytic enzymes / proteases

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______ and ______ can potentiate pruritis by increasing the accessibility of proteases to the nerve endings

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chronic inflammation and secondary bacterial infections

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primary physiologic response for the control or temporary relief of pruritis

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scratching

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how can scratching potentiate pruritis?

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induced epidermal damage (excoriations) releases additional proteolytic enzymes

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diagnostic plan for pruritis

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nature of lesions, distribution patterns, degree of pruritis. Expanded date base- fungal/bacteria, immunologic procedures, histpath, provocative exposure

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factors that may initiate pruritis

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physical factors, vasodilation, anoxia, proteolytic enzymes, histamine, serotonin, vile acids, calcium salts and uremia, asteatosis (Dry skin)

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know diseases, degree of prurities they cause, lesions and distribution

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see notes

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blindness

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loss of vision

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how can you ID a blind animal?

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begin bumping into objects or have trouble visually located objects

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4 general categories for blindness

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1) opacification of the clear media of the eye (mature cataracts) 2) retinal dz - failure to scan the image - progressive retinal atrophy 3) failure to transmit the scanned image - optic nerve/chiasm/tract dz 4) failure to process/develop image - optic radiation, occipital cortical dz

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ipsilateral pathways for vision

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retain, optic nerve

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contralateral pathways

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optic tract, lateral geniculate nucleus, opetic radiation, occipital cortex

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cross over pathways

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optic chiasm

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how can blindness be localized to one of the four categories

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papillary light reflexes and ophthalmological examination

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opacification of the clear media of the eye on exam

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opacity evident with exam with bright light. PLR normal

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retinal disease on exam

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pupiles dilated in room light. Absent or slow plr. Abnormal retinal exam

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failure to transmit the scanned image on exam

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unilateral optic n- pupils normal in room light. No PLR with penlight on affected side. On opposite side, normal PLR in both eyes. Bilateral- pupils dilated in room light. Absent pLR in both eyes

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occipital cortex on exam

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normal pupil size and normal plr; may have other signs of forebrain dz

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anisocora

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unequal pupil size

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two categories of blindness

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ocular and neurologic

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ocular causes of blindness

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corneal ulcer, anterior uveitis - cause a constricted pupil in the affected eye

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effect of iris atrophy and glaucoma on the pupil

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dilated

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neurological causes of anisocoria

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lesions in parasymp or symp innervation to the pupil

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PLR testing

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of the affected eye, results in constriction of the opposite eye but no consttriction of the affecte eye. Testing the normal eye results in pupil constriction of the normal eye and non constriction of the affected eye

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strabismus

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ocular deviation tha the patient can not correct. Can be congenital or acquired

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pathophys of strabismus

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extraocular eye muscles are innervated cy CN III, IV and VI

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what muscles are innervated by oculomotor n?

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dorsal, ventral, medial rectus

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lesions affecting the oculomotor nervce cause a _____ Strabismus and

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ventro-lateral, and ability to move the eye medially when conjugate eye movemnts are tested. Pupil may be dilated

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what muscles are innervated by the abducens nerve?

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lateral rectus and retractor bulbi muscles

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lesions affecting the abducens nervce cause a _____ Strabismus and

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medial strabismus and inability to abduct the eye when testing conjugate eye movements. There may be inability to retract the eyeball when testing menace response or the corneal reflex. Normal pupil size

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trochlear nerve innervates

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dorsal oblique muscle

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signs of trochlear nerve damage?

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no obvious signs

Front 93

what can induce nystagmus in the normal animal?

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when the head is turned laterally side to side- physiologic nystagmus or conjugate eye movements

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conjugate eye movements involve:

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the vestibular system and its projections that influence activity of CN III, IV, and VI

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what controls voluntary ocular movements?

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the front labe

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what does the optomotor produce?

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smooth following movements of eye

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define nystagmus

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rhythmic involuntary movement of the eyes. Characterized by the direction of the fast or jerk phase as horizontal, vertical or rotary. Can be slow or fast, spontaneous or induced

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which form of nystagmus is most commonly observed as a sign of vestibular dz?

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jerk nystagmus- away from the side of the lesion

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when can pendular nystabmus be seen?

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certain forms of cerebellar dz, congenital microphthalmos and in siamese cats

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ataxia results from

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failure of muscular coordination resulting in uncoordinated movements of the limbs and abnormal posture. It is a lack of kinesthesia- poor sense of motion or body/limb position

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three neuro systems responsible for maintaining posture of the head, body and limbs and for creating coordinated movements

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general proprioception/sensory ataxia, cerebellum/cerebellar ataxia, and vestibular system/vestibular ataxia

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where are sensory rc located?

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in muscle and tendons of limb

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spinocerebellar tracts

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transmit proprioceptive info to the cerebellum.

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crerebellum is responsible for

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coordinating muscle movements and needs to instantly know where the limbs, trunk and head are relative to space

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characteristic clinical sign of spinocerebellar lesions?

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uncoordinated limb movement, crossing/swinging legs, swaying trunk, and a base wide stance

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dorsal columns

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project to the cerebral cortex via the spinal cord and brain stem. Pathways cross near midbrain and project to the contralateral parietal lobe for conscious perception of kinesthesia

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clinical signs of dz of the dorsal columns

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creatse signs of mild ataxia and occasional knuckling of the paws on the affected side.

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lesions affecting the parietal lobe

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may cause suble signs in the contralateral limbs (occasional knuckling and a tendency for the body to drift opposite the side of the lesion)

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the cerebellum tends to inhibit ____ muscles and stimulate ___ muscles

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flexor; extensor

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signs of cerebellar dz

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intention tremors, generalized tremors, head bobbing. Dysmetric gait (hyper and hypo metria). Trunkal ataxia. Nystagmus (mostly pendular). Base wide stance.

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true or false: the cerebellum initiates motor activity and paresis is a sign

Back 111

FALSE

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vestibular system functions

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normal orientation relative to gavitational field; normal orientation of head and body during linear or rotary acceleration and tilting of the body; maintains position of eyes, trunk and limbs relative to position of the head.

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projections of the vestibular system

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vesibulospinal tracts; brainstem projections; projections to the cerebellum

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clinical signs of vestibular dz

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signs ipsilateral to lesion, asymmetric ataxia, head tilt towards side of lesion, fall towards side of lesion, circle tightly towards side of lesion, spontaneous or positional nystagmus- jerk phase away from side of lesion. Positional strabismus on affected side

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what is important in localizing lesions?

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to differentiate dz in the inner ear or vestobular nerve (Called peripheral vestibular dz) form dz in the rostral medulla affecting vestibular nuclei (called central vestbular dz)

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lameness is caused by

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pain or mechanical factors secondary to inflammatory, degenerative, or traumatic dz of the musculoskeletal system

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how to differentiate lameness from neurologic dz

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based on neuro and orthopedic exams

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paresis is

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decreased muscle activity and strenght caused by impaired motor function

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paralysis/-plegia results from

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complete loss of motor function due to neuro dz

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2 divisions of the UMN systems

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pyramidal and extrapyramidal

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pyramidal system

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composed of neurons located in the motor cortex and whose axons course through the cerebrum, brainstem and spinal cord to synapse on LMN in the spinal cord

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major UMN tracts

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corticospinal, rubrospinal, reticulopsinal, tectospinal, and vestibulospinal

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lesions affected UMN long tracts below the midbrain create clinical signs in

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ipsilateral limbs

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lesions above the midbraine produce signs in the

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contralateral limbs

Front 125

eval UMN?

Back 125

observation of gait and testing postural reactions

Front 126

GSE LMN system

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innervates skeletal muscle and is found in all spinal nerves and CN III, IV, VI and XII.

Front 127

lesion c1-c5

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bilat- tetrapareis/plegia, UMN signs to thoracic and pelvis limbs. Unilat- hemiparesis/plegia, IMN signs to ipsilateral limbs

Front 128

lesion C6-T2

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bilat- tetraparesis/plegia, LMN signs in TL, UMN signs in PL. Unilat- hemiparesis/plegia, LMN signs in ipsilateral TL, UMN signs in ipsilateral pelvic limb

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lesion t3-l3

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bilat-- paraparesis/plegia, UMN signs in PL. unilat- monoparesis./plegia, IMN signs in ipsilateral PL

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lesion L4 to S2

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bilat- paraparesis/plegia, LMN signs to both PL. Unilat- monoparesis/plegia, LMN signs in ipsilateral limb

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lesion S3 to coccygeal

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bilat- minimal limb dysfunction. Urinary incont, paresis or parlysis of the tail and fecal incontinence. Unilat- rare, minimal neuro dysfunction

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brainstem lesion

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creat motor deficits identical to lesions in the cranial cervical spinal cord

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lesions in the forebrain

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cause little gait abnormality

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define pain

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conscious perception of noxious stimuli

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define analgesia

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absence of perception of painful or other stimul

Front 136

how is pain recognized?

Back 136

by behavioral reactions of the patient when painful areas are examined

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dermatome

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area of skin innervated by a pair of spinal nerves

Front 138

panniculus reflex

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useful in localizing lesions affecting spinal cord segments t3-l3. pain rc are stimulated by pin pricking

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trigeminal n

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CN V- provides for perception of noxious stimuli from the face via the maxillary, ophthalmic and mandibular branches. It is the sensory arc of the palpebral and corneal reflexes

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three types of nociceptors

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1) extreme heat 2) excessive mechnical stress 3) chemicals

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types of pain

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acute/physiologic, chronic/clinical

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define lymphadenopathy

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enlargement of lymph nodes

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lymphadeneitis

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inflammation of lymph nodes

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causes of lymphadenopthy are classified by

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the type of cellular response present in the lymph node

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five causes of lymphadenopathy

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reactive hyperplasia, granulomatous lymphadenitis, suppurative lymphadenitis, neoplasia, extramedullary hematopoiesis

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diagnostic plan for lymphadenopathy

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cytologic or histologic exam of enlarged lymph nodes. (aspirate, --> biopsy). CBC,Chem,UA.

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three major types of sudden collapse

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seizures, syncope, and narcolepsy-cataplexy

Front 148

seizures result from

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abnormal electrical discharges in the brain resulting in paraoxysmal abnormal brain function

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one or more of the following occur in a seizure:

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1) loss of consciousness 2) alternation of muscle tone, alteration of sensation 3) disturbance of autonomic functio nand 4) other psychic events

Front 150

syncope is

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sudden loss of consciouness resulting from inadequate oxygen or glucose concentrations in brain.

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three stages of a seizure

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ictus/attack or the actual seizure, the pre-ictal stage, and the post-ictal stage

Front 152

major motion seizures

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animal loses consciousness, develops tonic-clonic movements of the limbs and may urinate and defecate. Ictus usually lasts less than 2 minutes.

Front 153

seizure focus

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paraoxysmal discharge from a group of neurons that may be single or multople. There is a large depolarization of membrane over a longer period of time called the paraoxysmal depolarizing shift.

Front 154

thresohld

Back 154

the electrical level where seizure discharges will occur. Can be lowered by several internal or external factors. Also refers to the summative effects that generate seizure activity

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memory of circuits

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recurrence of seizures increases the probability of additional seizures along the same pathway or circuits of previous seizures. Memory most likely results from synaptic changes that is somewhat similar to those that occur with learning mechanisms

Front 156

classifying seizures

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generalized tonic/clonic (grand mal, major motor), partial (focal motor) and partial seizures with abnormoal or bizarre behavior (psychomotor seizures)

Front 157

cluster seizures

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several within a short period of time

Front 158

status epilepticus

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rapidly recurring seizures wihtout complete recovery between episodes

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DAMNIT-V

Back 159

degenerative - anomaly - metabolic - neoplastic /nutritional - inflammatory/infectious/immune/idiopathic - toxic/traumatic - vascular

Front 160

episodic weakness

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weakness that occurs with exercise and dissipates with rest

Front 161

signs of weakness

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short strided gait with or without ataxia, panting, reluctance to walk to run, lying down, collapse. May be alert or depressed

Front 162

diseases that cause ___ ____ may cause episodic weakness as their primary clinical manifestation

Back 162

electrolyte imbalances

Front 163

myasthenia gravis

Back 163

autoimmune dz affecting ach rc.

Front 164

hyperkalemia

Back 164

decreased intensity due to hypopolarization of membrane, decreased membrane potential. = decreased strength of muscle contraction, block conduction of cardiac impulse

Front 165

hypokalemia

Back 165

membrane hyperpoliarzation = decreased strength of contraction

Front 166

hypocalcemia

Back 166

increased membrane excitability, spontaneous impulses decreased strength of contraction (decreased release of ach at motor end plate)

Front 167

hypercalcemia

Back 167

decreased membrane excitability = increased release of ach = spontaneous contractions/decreased muscle strenght

Front 168

define coughing

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the sudden and noisy expulsion of air from lungs. Normal protective reflex

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cough with upper airway disorders

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loud, dry, harsh cough frequently associated with terminating gag

Front 170

lower airway/CV cough

Back 170

moist, productive coughs

Front 171

upper airway causes of cough

Back 171

pharyngitis, tonsilititis, tracheitis, collapsed trachea, neoplasia, parasites

Front 172

lower airway causes of cough

Back 172

bronchitis, pneumonia, immotile cilia, enlarged hilar lymph nodes, allergic bronchitis, allergic pneumonitis, lungworms, trauma, physical irritation, neoplasia

Front 173

cv causes of cough

Back 173

left sided heart failure, left atrial enlargement, heartworm, pulmonary thrombosis, pulmonary edema

Front 174

dyspnea

Back 174

labored or difficult, uncomfortable breathing.

Front 175

strider

Back 175

dyspnea caused by upper airway obstruction

Front 176

upper airway dz results in

Back 176

Upper airway disease usually gives dypsnea on inspiration with short and effortless expiration, respiratory noise may be loud

Front 177

lower airway / pleural space dz gives both

Back 177

inspiratory and expiratory dypsnea

Front 178

CNS control of respiration

Back 178

medulla/pons, Hering Breuer Reflex (inhibition of inspiration due to stretch receptors in bronchi via vagus nerve to brainstem) is also involved, Carbon dioxide and H+ concentration also stimulate respiration, chemoreceptors in the carotid and aortic bodies sense decrease in oxygen

Front 179

cause of central cyanosis

Back 179

arterial hypoxemia and hemoglobin abnormalities. Both skin and mm are affected

Front 180

peripheral cyanosis causes

Back 180

by slowing or absence of blood flow to an area which provides more time to oxygen extraction (vascular thrombosis, vasoconstriction, polycythemia, low cardiac output)

Front 181

sneezing

Back 181

response to mechanical/chemical stimuli on the receptors in the nasal mucous membranes, innervated by ophthalmic branch of the trigeminal nerve, with several nerves involved in the efferent response, which involves rapid inspirationàvocal folds and epiglottis closeàforceful contraction of expiratory musclesàepiglottis and vocal folds suddenly open allowing entry of air into nasal passages

Front 182

common causes of sneezing

Back 182

Stenotic nares in brachyocephalic breed, neoplasia in long nosed breeds, chronic rhinitis and sinusitis in persian cats, fungal infection

Front 183

causes if bilat nasal discharge

Back 183

upper respiratory viral infection, parasitic disease, allergy, coagulopathy

Front 184

unilateral discharge

Back 184

Foreign body, neoplasia, trauma, fungal infection, dental disease, otitis media, inflammatory polyps