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INTERNAL MEDICINE > LIVER > Flashcards

LIVER Flashcards

1
Q

HEPATIC INSUFFICIENCY SYNDROME: Definition

A

impairment of the liver f(x) as a result of severe aggression afecting 70 - 80% of the hepatic functional area

  • F(x) of liver
  • Role of liver in Carbohydrate Metab
  • In lipid metab
  • Fat volatile acids
  • In proteic metab
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2
Q

HEPATIC INSUFFICIENCY SYNDROME: F(x) of liver

A
  1. Metab regulation: glu, lip, prot
  2. In metab of hmnes
  3. Urea synthesis, uric acid
  4. Biliary secretion
  5. Detox of various metabolites
  6. Blood reservoir
  7. Deposit for vitamins and minerals
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3
Q

HEPATIC INSUFFICIENCY SYNDROME: Carb Metab

A
  • Glicogen transformation
  • Krebs cycle -> pyruvic ac -> lactic ac_ CO2 + H20+ ATP
  • Penthose pathway -> lipid converting pathway
  • Uronic ac pathways
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4
Q

HEPATIC INSUFFICIENCY SYNDROME: FVA

A
  • acetic ac: energy resource
  • propionic ac: gluconeogenesis
  • ac butiric: transforms at the mucosa levels in the rumen in betahidroxibutirate
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5
Q

HEPATIC INSUFFICIENCY SYNDROME: lipid metab

A

Lipid -> port vein -> liver -> betaoxidation -> acetyl coa -> acetato acetate -> energy prod -> netahidroxibutirate

2acetylcoa …. cumulative energy-> betahid= ketone bodies

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6
Q

HEPATIC INSUFFICIENCY SYNDROME: prot metab

A
  • Sinthesize plasmic prot: albumin, globulin, fibrinogen, prothrombin
  • NH3 resulting from the deamination from aa and the absorbed from colon / rumen are transformated into urea/uric ac in birds in the liver
  • Permanent exchange of aa w blood and tissues
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7
Q

HEPATIC INSUFFICIENCY SYNDROME: ETIOLOGY

A

Toxic:

  1. wasp/bee venom, carbon tetrachloride, metals (Cu, Zn, P, Fe), organochlorine pesticides
  2. paracetamol, aspirin, ketocolazole (dog/cat), just cat glucocorticosteroids, big animals are alcohol and isoflurane and ALL halotane

Biotic agents:

  • Viral (PIF, Parvo, Calicivirus, Infectious Anemia…)
  • Bact (Salmonelisos, Lepto, Tularemia)
  • Parasites (babesia, fasciola, dirofilaria, erlichia)

Others:
- Shock, insomnia, hepaic traumas, organopathies, neoplasm, adquired/genetic portosystemic

COWS: assoc w hepatocellular osteoarthritis due to fatty hepatosis (en dof pregnancty of immediately postp) w fatty cow sdr and lipod mobilization sdr

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8
Q

HEPATIC INSUFFICIENCY SYNDROME: Pathogenesis

A

Causal factors act on the vascular and parechimatose systems-> tissue and cel chnges + infiltration + necrosis + dystrophy and lately; a conjuctival reaction characteristic of fibrosis/cirrhosis

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9
Q

SMALL HEPATIC INSUFFICIENCY SYNDROME: Clinical Signs

A

F(x) disturb w/out visible lesions macroscopically and detectable by means of usual examination

Symptoms:

  • Reduced voice: weak apetite, weakening, asyhenia
  • Low productive capacity
  • Increased irritability
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10
Q

BIG HEPATIC INSUFFICIENCY SYNDROME: Clinical signs

A

Major clinical disorders w dramatic evol expressed by exitation crises

General : tachy/bradi cardia
Digestive: vomiting, diarrhea , melen
Neurological: disorientation, coma syncope, phtialism in cats, irritability
Renal: PDPU, bilirrubinuria
Hematological: petechia, bruising, hematoma
Hepato/Splenomgaly´
Jaundie, microhepatitis
Pruritus
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11
Q

HEPATIC INSUFFICIENCY SYNDROME: Species symptoms

A

Horse: sleepingness/excitatiability (empty mastications), constipation, jauncice, fotodermatosis

Bov: Cortical deprrssion (ataxia, astenia, bruxism, icteric mucosa, coma ,even death), Hepatic coma may be due hepatic steatosis, assoc w ketosis + parturition + fatty cow sdr

Ov: Cortical depression, tightening teeth, paresis of preestomach, photodermatosis, jaundice

Car: Dig (vomiting, diarrhea, anorexia), nerve disorders, epileptiform seizures

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12
Q

HEPATIC INSUFFICIENCY SYNDROME: Treatment

A

Dietetic

  • Proteins that contaic essential aa
  • No indicated FAT
  • Carbs to protect their metab
  • Fermentable fibers can reduce signs of portal encephalopaty
  • Non fermentable for constipation avoidance
  • Zn , Vit E (antioxidants)+ K (antihemorrag)
  • Vit C assoc w Fe and Cu + Vit B complex

Medicaments

  • Restore biliary f(x) Na Bicarb NaMg
  • Restore electrolytes KCl
  • Restore lipids (lipotrotoc factors)
  • For accum of Cu -> penicillamine

Antiinf therapy: NOT for chronic hepatitis, Yes for autoinmune hepatitis, PREDNISON + DEXAMETHASONE ( if E ascitis / edema)

Antifibrotic tto: corticosteroids, interferon , interlukins (immunomodulator), Vit E (antioxidant)

Tto of ascitis and hemorrag cond: Furosemid, Vit K, prepared w Ca

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13
Q

JAUNDICE SDR: Definition

A

Morbid state: coloring in various yellow shades of the mucus mbs and or the skin as a result of excessivie acumulation of bile pigments in plasma and tissues.

Pseudoicter in case of caroteinemia

Jaundiec of Newborn: mechanical, hepatocelular, helotitic, and newborns or congenitall

Source of bilirrubin: destruction of (mature) erytrocytes in the resticuloendotelial system of bone marrow

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14
Q

JAUNDICE SDR: Bile Components

A

The bile is produced by the liver and contains a SECRETION product (BILIARY ACID) and an excretion product (BILIARY PIGMENTS)

BILIARY PIGMENTS result from the degradation of Hb in the reticulo-endothelial system (bilirubin and biliverdin) which in the intestine are degraded by the bacterial flora into stercobilin and urobilin which are eliminated by feces

BILIARY ACID derives from Colanic ac. and is represented by COLIC AC. which by CONJUGATION with TAURINE AND GLYCOCOL determines the synthesis of TAUROCHOLIC AND GLYCOLIC AC which forms the basis of the production of BILIARY SALTS

COLESTEROL- is a precursor for ac biliary

Bilirubin is transported in the blood to the liver bound to ALBUMIN and in the liver cell it detaches from this protein and is conjugated with AC GLUCURONIC causing the appearance of hepatic bilirubin

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15
Q

JAUNDICE SDR: Mecanic Icter

A

Reduction or suppression of bile transit in the extrahepatic bile ducts: obstructions;

  • Biliary calculus or stones
  • Intrahepatic and intestinal parasitic infestations, fasciola hepatica (gigantica most of the herbivores) or dicrocoelium in swines
  • Extrahepatic biliary tract spasms
  • Pancreatitis, duodenitis
  • Scars, tumors, abdominal adenopathies

Clinical Manifestation

  • Yellowing of mucous membranes and tegument
  • Disorexy/selective appetite
  • Tendency to constipation
  • Uncoloured feces , bad smell
  • Colurie
  • Colalurie

HUMORAL: bilirubin ↑, PA ↑, VSH ↓ , normal transaminases

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16
Q

JAUNDICE SDR: Hepatocelular Icter

A

Hepatocyte lesions caused by infectious (bacterial, virals) and toxic etiological agents, letting so the bile go into the blood and causing icter

In other cases, blocking intrahepatic bile ducts occurs, in which case the sub pressure-accumulated ,the bile passes through the hepatocytes causing jaundice by “burglary”

Clinical Manifestation

  • Mucous coloration in reddish-orange /yellow
  • Inappetence to anorexia, asthenia, vomiting
  • The sensitive and enlarged liver area
  • Initially fever, then hypothermia
  • Due to the passage of pigments and bile salts into bradycardia.
  • Nervous disorders manifested by excitation or depression, even going to hepatic coma
  • Feces are of normal color
  • Coluria, collauria, proteinuria
  • Liver tests are positive
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17
Q

JAUNDICE SDR: Hemolitic Icter

A

Hemolytic intensive process with excess of bilirubin formation. It occurs after the destruction of erythrocytes in the vascular bed

Causes
- Poisoning with copper, phenothiazine, arsenic, saponin-rich plants
- Due to the resorption of large hematomas after hemotherapy
- Phosphorus deficiency (postpartum hemoglobinuria at bovines)
- water intoxication
- Hemosporidiosis, infectious processes with leptospira, streptococcus, staphylococcus, clostridium
(Clostridium haemoliticus) infections.

Clinical Manifestations
- Anemia of mucous membranes and skin in white-yellow nuance
- Feces and urine are a more intensely colored, big functions are accelerated
- Hematologic: decrease in hematocrit, hemoglobin, erythrocytes and VEM and VSH increase
- In the case of microscopic hemosporidiosis endo globular parasites and Joly corpuscles (chromatin
residues = regenerative anemia)

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18
Q

JAUNDICE SDR: Neonatal Icter

A

Can be mechanically due to meconium that it expands at the intestinal level, umbilical infections that can spread in to the bile ducts Toxic (cuprum, plumb) and infectious hepatocellular (viral hepatitis, leptospirosis)

Hemolytic jaundice is the result of incompatibility of the blood group with the fetus by isomic factors derived from the male reproductive system.

In pigs this jaundice can appear in case of repeating too much sexual acts with the same male, for reproduction purpouses .

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19
Q

JAUNDICE SDR: TTO

A

Higienic:

  • Avoiding altered food, moldy, high fat qanitat
  • In large animals: feeding of green fodder in summer, good quality winter hay
  • In pet: administering low fat soups, sweet cow’s cheese, avoiding spicy foods.
  • Administration of sugar beet or fodder beet to large animals and carrots in small animals

Biliary function: stimulates cholagogue and choleretic drugs: Colebil

Glyco-regulating function: stimulate with iso- or hypertonic glucose solutions, calcium chloride, vitamin complex B (B1, B6, B2) and vitamin C

Lipido regulator function : preparations containing lipotropic factors (choline, methionine)

Function proteine reglatoare: arginine, tryptophan, sorbitol,

Combating hemorrhagic conditions : Vitamins K and C. Calcium therapy will also be done

Combating nervous and agitation status : administration of sedatives and tranquilizer

Combating dehydration: Fluid therapy

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20
Q

ACTIVE HEPATIC CONGESTION: DEFINITION

A

Increased blood flow in the liver, being physiological in intensive efforts / digestion and pathology in poisoning, overheating, direct trauma, infections and at low temperatures

Blood flow causes irritation to the hepatocyte by activating various functions, and when a certain limit is exceeded, it can cause bleeding or leukocyte infiltration, edema, hepatitis, or hepatosis.

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21
Q

ACTIVE HEPATIC CONGESTION: Clinical Symptoms

A
  • Colic, superficial breathing.
  • Signs of primary illness, coloration of the feces sometimes greenish, often diarrhea.
  • The physical examination of the liver area reveals increased sensitivity, increased size of the liver .
  • If there is an infection- subfebrile.
  • Poisoning - Hypothermia.
  • Paraclinical hyperazotemia, hyperglycaemia, sometimes glycosuria
22
Q

ACTIVE HEPATIC CONGESTION: Pathological Anatomy

A

The liver is enlarged in volume, with reddish brown edges, tense capsules, and a large amount of blood drains across the section

23
Q

ACTIVE HEPATIC CONGESTION: Treatment

A

Cold compressions with cold water , introduction of the animal during summer in water or cold water spraying; in their absence, frictions, massages;

Soothing; the best results are given by magnesium sulfate, procaine adm. intravenous (opioids, tranquilizers, barbiturates, as in all liver diseases, will be avoided);

Alkalis prevents the complications that arise from the administration of painkillers, while helping liver functions.

24
Q

PASSIVE HEPATIC CONGESTION: DEFINITION

A

It is a morbid state in which blood circulation is slowed down, causing hepatic dysfunction through tissue anoxia

25
Q

PASSIVE HEPATIC CONGESTION: ETIOLOGY

A

The consequence of a general circulatory disorder and more rarely local circulatory disorders;

Major causes – cardiac insufficiency(endocarditis, pericarditis, myocarditis) because the liver is considered to be a “heart valve defense” in case of partial or global insufficiency;

Alongside cardiac disorders will be mediastinal syndromes, pulmonary disorders (pleurisy), compressions of large vessels in which a stasis occurs and liver have an important role;

Passive congestion also occurs in the hepatic artery aneurysms, when blood due to lack of pressure and speed stagnates in the liver.

26
Q

PASSIVE HEPATIC CONGESTION: Pathogenesis

A

Blood stasis causes circulatory disturbances, local trophic hypoxia, hepatic insufficiency, hepatosis, and even cirrhosis when the stasis lasts longer

27
Q

PASSIVE HEPATIC CONGESTION: Clinical Manifestations

A

Are masked by the primary illness circulatory insufficiency - acute or chronic cardiomyopathy, pericarditis, pleurisy, mediastinal disorders

The presence of somnolence that occurs immediately after eating, selective appetite, sometimes even the inappetence, alternations of constipation and diarrhea with soft faces with a foul odor, coluria and collauria.

The apparent mucous → subicter / secondary anemia (hemolisis) or reduction of hematopoiesis, in which the liver also competes

In the case of compressions on caval caudal vein, pelvic limb edema occurs which disappear in reduced movement and accentuates the effor

Sometimes there is an increase in the projection area without a particular algal state.

Portal Hypertension

  • Portal Thrombosis hyperechogenic fibrosis at the level of the portal vein walls, the total confer VP to a cavernous aspect
  • Cardiac liver = passive congestion
28
Q

PASSIVE HEPATIC CONGESTION: Morphopathological

A

Hepatomegaly, the liver having dark brownish color (stasis or heart liver).

By aging the process, conjugative reactions of proliferative and even ascitic type may occur;

Myocardial damage, mediastinitis, pneumopathy, etc.

29
Q

PASSIVE HEPATIC CONGESTION: TTO

A

Treating the primary disease, requiring rest, dietary nutrition mentioned in case of hepatic insufficiency;

It will be considered to stimulate hepatic and cardiac hepatoprotective and cardiotonic activity.

30
Q

SUPPURATIVE HEPATITIS (purulent or apostomatotic) : Definition

A

Septic process characterized by fever and presence of a single abscess or of many abscesses at the liver. It is particularly common for cattle subject to fattening and calves

31
Q

SUPPURATIVE HEPATITIS: Etiology

A

Migration of foreign bodies from the gastric compartiments ;
Metastatic sowing through general circulation at the level of suppurative outbreaks (metrites, mastitis, arthritis) is rare but not excluded;

Concomitantly with hepatic metastases, metastases occur in the lungs, spleen, kidneys

In young cattle fatteners, liver abscesses are a disease of concentrated feeds, when liver abscesses occur after acute ruminants or rumen parakeratosis;

At the level of pre-existing degenerative or inflammatory liver processes, of a parasitic nature (hydatid cyst), actinobacillary, tuberculous, et

32
Q

SUPPURATIVE HEPATITIS: Clinical Symptoms

A

Acute septicemic episode with fever, then the clinical manifestations decrease in intensity, corresponding to the isolation and encapsulation of the necrotic-purulent focus;

Fever may occur remitting or intermittently, the animal moans during urination and defecation;

In the case of abscesses located closer to the surface of the liver, the palpation of the projection area shows increased sensitivity;

Signs of primary disease (reticuloperitonitis, pneumonia, etc.);

Cachexia, symptoms of Hoflund’s syndrome and even subicterus. Symptoms of omphalophlebitis also occur in calves.

Hematologically, there is a neutrophilic leukocytosis, with the Arneth index deviating to the left.

33
Q

SUPPURATIVE HEPATITIS: Anato-pathological lesions

A

The liver is enlarged in volume, showing single, usually unique abscesses or multiple low volume abscesses;

The abscess can drain into the vein cavity, causing the occurrence of edema and pulmonary congestion, or in the abdominal cavity causing peritonitis;

Lesions of primary disease, sometimes angiocholitis

34
Q

SUPPURATIVE HEPATITIS: TTO

A

Antibiotics: (Tylosin, )

Curative - ineffective treatment, even if massive antibiotic therapy is used;

Small abscess - surgery, followed by postoperative treatment.

35
Q

HEPATIC STEATOSIS: Definition

A

Hepatic steatosis is the fatty infiltration of hepatocytes and lipids deposition intra and extracellular.

The process is irreversible, lipid degeneration being included in the group of civilization diseases

The disease is more common in highly productive lactating cows (Fatty liver syndrome), in laying hens (hemorrhagic fatty liver syndrome), broiler chickens (kidney liver steatosis syndrome) in geese (fat liver), in rats and infant piglets.

36
Q

HEPATIC STEATOSIS: Ethiopatogenesis

A

Chronic hepatitis, parasitic infestations, intoxication with P and Cu and even the consequence of anemia, favored by reduced liver glycogen, gestation and productive force through fattening; the dystrophic process is also aggravated by the lack of lipotropic factors (methionine, choline), etc.

37
Q

HEPATIC STEATOSIS: Clinical symptoms

A

Cortical excitatory states, especially in the horse and pig, sometimes reaching the meninges, followed by a cortical inhibition with adynamics, asthenia, disorrexia, accelerating major functions, cardiac

Arrhythmias, dyspnoea, pulmonary edema.

In ruminants the paresis of the stomach occurs, signs of ketosis (hyperketonemia, hyperketonuria, hypercholesterolemia) sometimes jaundice

Hepatic sensitivity, hepatomegaly,

Oliguria
- Coluria, collauria.

38
Q

HEPATIC STEATOSIS: Treatment

A

Hygiene-diet will correct deficiencies of comfort, avoiding high-fat fodder, and especially those with peroxides;

Quality feed rich in vitamins and lipotropic factors will be provided

Medicaments high doses of vitamin C corticoids, glucose, amino acids (methionine, choline), hepatic extracts (Vitogepat, Sirepar), insulin etc. can be given

39
Q

ACUTE PARENCHYMAL HEPATITIS: DEFINITION

A

Acute or subacute yellow atrophy involves mesenchymal inflammation, accompanied by a parenchymal degeneration that can progress to the stage of necrotizing.

40
Q

ACUTE PARENCHYMAL HEPATITIS: Ethiopatogenesis

A

In ruminants, secondary hepatitis frequently occurs in ketosis, in paresis, acidosis, poisoning with
copper, phosphorus, arsenic, carbon tetrachloride, some viruses, parasites and some mycotoxicosis.
- In horses, infectious rhinotracheitis, contagious pleuropneumonia, infectious anemia, and some
mycotoxicosis.
In dogs, the disease occurs in case of Rubarth viral hepatitis, in Carre’s disease, various intoxications.

In poultry, the disease occurs in most septicemic diseases, and in duck blooms in case of infectious hepatitis.

The initial hepatocytes has hyperemia, infiltration, and the mesenchymal inflammatory reaction;

These processes may occur predominantly in certain areas, in relation to the pathway of the causal factor (hepatic, umbilical, vaginal);

Hepatic insufficiency of varying degrees - hepatitis outbreaks

41
Q

ACUTE PARENCHYMAL HEPATITIS: Clinical Symptoms

A

Initially prevalent signs of primary disease, then symptoms of jaundice syndrome occur; sometimes in horses and cattle the disease evolves anichetically

general clinical signs consist of loss of appetite, fever, constipation, atony of preemia, fecal discolouration, but intense colored urine.

Hepatomegaly with diffuse sensitivity, and paraclinic liver tests are positive;

The big accelerated functions, animals are apathetic, asthenic, adynamic, ataxic and prefer decubitus;

Nerve signs of hyperexcitability (tetaniform) or inhibition (hepatic coma);

Signs of nervous excitation occur frequently in hematoencephalic syndrome;

In depressive, comatose forms, hypothermia occurs especially in cattle.

42
Q

ACUTE PARENCHYMAL HEPATITIS: Treatment

A

Hygienic-dietary, providing conditions of comfort, diet, low volume diet with frequent high; food and feed rich in lipids and fats, glucide will be easily assimilable.

The water will preferably be provided with a slightly saline or
alkalized water. In cortical excitations, a thick bedding will be provided to minimize possible trauma.

Medicamentos: sedative analgesia in the forms of cortical excitation and analeptic in the depressive forms;
recovery and stimulation of liver function (see major liver failure).

43
Q

CHRONIC HEPATITIS: LIVER CIRRHOSIS (DEF)

A

Chronic hepatitis develops with a process of the liver and replacement of liver tissue with conjunctival tissue when the dystrophic process is localized dominantly on the vascular system of the liver, generates asciteogenic cirrhosis, and when the secretory canalic network is affected, it will generate icterogenic cirrhosis

44
Q

CHRONIC HEPATITIS: LIVER CIRRHOSIS (Etiology)

A

Chronic hepatitis - liver cirrhosis may be a continuation of various hepatopathy, degenerative, circulatory and inflammatory hepatopathy, or appear as such, when infectious, toxic and parasitic factors interfere with moderate intensity but for a long time

Specific hepatobiliary parasitic infestation, prolonged food deficiencies, dismetabolites, maternal toxicity, especially by aflatoxins, neoplastic processes, hepatic and extrahepatic bile stasis, lack of lipotropic factors in the diet, autoimmune hepatic lesions (systemic lupus erythematosus), prolonged cholestasis, chronic cardiac insufficiency that causes chronic hepatocellular anoxia.

45
Q

CHRONIC HEPATITIS: LIVER CIRRHOSIS (Clinical Symptoms)

A

PRE ASCITICAL PHASE
- There are general symptoms: capricious or selective appetite, alternation ofconstipation with diarrhea, often confusing with digestive states or even with chronic gastroenteritis;

In horses in the pre-ascitical phase there are symptoms of mild and repeated colic;

The color of the mucous membranes is unchanged in this form of evolution; on the contrary, the animals are progressively weakening, tired of effort and lacking in force.

THE ASCITIS PHASE
Clinical signs are particularly evident in small animals (dogs and pigs), with increased abdomen in volume, ptozate, pyriform printing the appearance of “abdomen of the batrachian”;

Major functions are accelerated, dyspnea, sometimes hepatic syndrome;

Edema declive, ectasia of superficial and paraumbilical veins (jellyfish appearance), pale palatability of the skin and mucous membranes. The animal is normothermic, progressively weakening, and may experience symptoms of spike syndrome.

There is also vomiting, the alternation of constipation with diarrhea, the feces is colored and with a ugly odor

Oliguria is accompanied by colluria and collauria and possible to appear the filtration albuminuria;

Palpation of the liver, especially in small animals, shows tough consistency, hepatomegaly, easily noticeable in weakened animals. There is also generalized pruritus and intolerance to some foods

46
Q

CHRONIC HEPATITIS: LIVER CIRRHOSIS (TTO)

A

Hygienic-dietetic, is to provide comfort conditions in the shelter, feeding with easily digestible feeds, energizing with lipotropic factors and vitamins (beetroot, fresh cow’s cheese to carnivores); the protein and lipid intake will be restricted and compensated for the easily assimilable carbohydrate, and anorexic subjects will use artificial feeding

Treatment medicamentos: recovery of large functions of the liver and nervous system, the digestive system according to the therapy of the hepatic failure

47
Q

ANGIOCHOLITIS AND CHOLECYSTITIS (DEF)

A

Inflammation of intrahepatic and extrahepatic bile ducts, and cholecystitis of gallbladder inflammation. The disease occurs more frequently in ruminants but also in dogs.

48
Q

ANGIOCHOLITIS AND CHOLECYSTITIS: Ethiopatogenesis

A

Ascending movement channels to the cholecyst, being represented by parasites (Fasciolla spp., Dicrocoelium spp.) of bile calculus or due to duodenitis and descending, hematogenic by metastatic transport;

E. coli and some pyogenes germs;

In dogs, cholecystitis - Giardia spp;

Angiocholitis in carnivores may be followed by hepatitis coexisting under the name of cholangiohepatitis

49
Q

ANGIOCHOLITIS AND CHOLECYSTITIS: Clinical Symptoms

A

Acute form: severe colic, tachycardia, superficial breathing, dyspeptic syndrome, tendency to constipation with discolored feces and bad smells, then greenish diarrhea, and ruminant atonia;

1-2 days after the onset of jaundice, the mucus is orange yellow, fever and leukocyte reflux reaction;

In half the cases with acute form of the disease appear nervous depression, decubitus, dehydration;

In the event of tearing of the gallbladder will appear the post-haemorrhagic shock and frequently exitus
shock occurs.

Frequently this disease evolving asymptomatically, with non-characteristic digestive and general signs, decreased productive yield, anemia, sub-cyst, and positivity of liver tests;

In more frequent carnivores is the chronic form manifested by bilious vomiting, the state of subicter sometimes slight colic, often the tendency of constipation.

50
Q

ANGIOCHOLITIS AND CHOLECYSTITIS: TTO

A

In ruminants it is necessary to periodically the antiparasitic treatment;

Cholecystectomy in pets

In small animals are recommended to use choleretics and colagoses drugs for human use, Anghirol and even purgatives.

INTERNAL MEDICINE (4 decks)

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