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Pathology > GIT > Flashcards

GIT Flashcards

1
Q

Developmental anomalies of the oral cavity

A
  • Causes: hereditary factors, maternal nutrition deficiency, teratogenic effects during pregnancy, mechanical interference with embryo
  • Types: Abnormalities in facial bones (aprosopia, brachignatia superior/inferior, diprosopia, dignathia superior/inferior, agnathia) or failure in fusion of facial soft tissue/bone/cleft lip/cleft palate/transverse facial cleft
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2
Q

Developmental anomalies of the teeth

A
  • Dental arch is longer/shorter (prognathia/brachygnathia)
  • Abnormal number (polyodontia/oligodontia/megalodontia)
  • Abnormality of one tooth (torsion, deviation, retention, transposition, dislocation)
  • Abnormal tooth structure (dental fluorosis, cement hypoplasia + caries)
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3
Q

Developmental anomalies of the intestine

A
  • Atresia: Ø/abnormal growing of opening/passage)

- Agnesia: Ø organ part

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4
Q

Enanthema

A

= Local alteration of the mucous membrane

  1. Roseola, erythema
  2. Papula
  3. Vesicle (small) / Bullae (bigger) / Aphta (superficial)
  4. Pustula
  5. Erosion
  6. Ulceration
  7. Necrosis, gangrene
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5
Q

Stomatitis

A

= Inflammatory process of the MM of the oral cavity

  • Classified according to: A. dispersion B. localization C. age of process
  • Forms: according to structure in MM and quality of exudate
  • Viral: FMD, Vesicular stomatitis, Papular stomatitis, SVD, Vesicular exanthema of swine
  • Bacterial: Fusobacterium necrophorum, Actinobacillus lignieresi, A. bovis
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6
Q

Abnormal wearing of teeth

A
  • Brachydont (Hu, Car, Su, enamel only crown) + Hypsodont (Herb, enamel most of root)
  • Enamel-dentin-pulp, cementum, periodontal lig. (w. vessels, nerves, type 1 collagen)
    1. Exsuperantia dentis: overgrowth
    2. Sawtooth 3.Sharp teeth 4. Shear mouth – Incorrect chewing mechanism
    5. Wave complex 6. Step mouth – Structural dev.anom., impacted molar teeth
    7. Crib biting 8. Dentura polita (smooth teeth) – Bad habits
    9. Hooks 10. Ramps – Misalignment of molar arcades
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7
Q

Regressive changes of teeth

A
  1. Enamel hypoplasia/hypomineralization
  2. Chronic fluorine toxicosis
  3. Acquired odontoporosis
  4. Porodontia
  5. Caries
  6. Paradentosis
  7. Pigmentation (extrinsic/intrinsic)
  8. Cementum hyperplasia/-exostosis)
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8
Q

Pulpitis, gingivitis and paradentitis

A
  • Pulpitis: inflam. of pulp, painful, reversible/irreversible, acute/chronic
  • Gingivitis: inflam. of gums, around tooth, primary/secondary, acute/chronic, circum./diffuse
  • Paradentis: inflam. of dental supporting tissues (periodontium, root cement, alveolar bones…), by bacterias, plaque or tartar involved
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9
Q

Esophagus: Stenosis

A

Stenosis: narrowing
1. Stuck on fodder
2. FB, 3.Parasites
4.Tumors
5.Cysts
6. Right Ao arch-Ductus arteriosus Botalli
7. Periesop. inflam.
8.Scar
9.Concretions, Pseudoconcretions, conglobates
10. Hypertrophy
11. Atresia
12. Esophagospasm, cardispasm
-Conseq.:
mild – compensatory hypertrophy of muscle
severe – congestion, cachexia, meterismus, obstructing
FB: necrosis, perforation, arrodation, putrid mediastinitis, pleuritis, periesophageal phlegmone

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10
Q

Esophagus: Dilatation and lesions of continuity in the esophagus

A
  • Dilation: ectasia, dilation, diverticulum, pseudo-diverticulum (traction, pulsion)
  • Lesions of continuity:
    1. Congenital (dev. anomaly: esop-bronchial/tracheal fistula)
    2. Acquired (perforation, arrodation, rupture, laceration, esophagotomy)
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11
Q

Dilatation of forestomachs, their lesions of continuity

A
  • Dilation: due to gases / access amount of feed / stoppage of the motion
    1. Primary/acute tympany – Frothy bloat: foaming of rumen content, often due to composition of feed
      - Stoppage of motion: forestomach atony - dysfunction
    2. Secondary/chronic tympany – Free gas bloat: due to physical/functional defect in eructation
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12
Q

Displacement of forestomachs, their lesions of continuity and consequences

A
  • Displacement: Eventratio proventriculi hernialis/diaphragmatica, torsio ruminis, flexion omasi
  • Lesions of continuity: spontaneous rupture, perforation due to FB
  • Conseq.: acute local fibrinous peritonitis, chronic local peritonitis, traumatic pericarditis
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13
Q

Hyper- and parakeratosis of forestomachs and their consequences

A
  • Hyper- and parakeratosis: abnormal thickening of outer layer of skin (granulation layer)
  • Mode of keratinization characterized by the nuclei in st.corneum
    • Causes: Malnutrition; A-hypo-/a-vitaminosis (aquired/congenital: decr. vitality/dist. of skeletal dev.), rough feed (mechanical irritation) or acidosis
    • Conseq.: locus minoris resistantiae -> Fusobact.necrophorum/pyogenic bact.->abcesses, necrosis in liver
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14
Q

Inflammation of forestomachs

A

-Inflam: degener. epith. -> portal of entry, acute/chronic, supf/deep, local/diffuse
-Rumenitis, Reticulitis, Omasitis
Causes: alimentary problems, malnutrition, infections
-Viral diseases / young calves fed from pail: putrefaction of milk / chemical rumenitis / CH overload: acidosis / trauma from rough feed
-Acute supf. proventriculitis: calves drinking high amount/cold milk, CH overload, urea intox.
-Chronic supf. prov.: chronic rumen atonia, sand in rumen
-Acute/chronic deep prov.: bacteria/fungi colonizing in loose epith.
-Exudative type/longlasting effect of pathogen

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15
Q

Stenosis

A

Stenosis = abnormal narrowing
A. Pyloric stenosis: due to muscular hypertrophy or functional stenosis
B. Gastric outflow obstruction: due to neoplasia, FBs, polyps, ulcers, sand accum., zootrichobezoars

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16
Q

Dilatation and lesions of continuity of the stomach

A
  1. Primary acute extension: aerophagia, pylorus spasm, decr. function of gastric muscles -> suffocation, circ. and resp. problems
  2. Secondary acute dilation: insuff. peristalsis, reflux from intestines
    - > (both 1. And 2. lead to) Chronic: long lasting effect, pronounced distention, muscle hypertrophy, fermentation
    - Lesions of continuity:
  3. Non-penetrating (erosion-supf, ulcer-deep, gastropexy)
  4. Penetrating (perforation, rupture, arrodation)
17
Q

Regressive changes in the stomach

A

Regressive changes:

  1. Circulatory disturbances: hyperemia, edema, hemorrhages
  2. Necrosis of gastric mucosa: Colliquation (bacterial) or coagulation (infarct), due to circ. disturb., bacterias, toxins, acids, chemicals
  3. Dystrophic calcification of mm.:
  4. Peptic erosion and peptic ulcers
18
Q

Pathogenesis of gastric ulceration

A
  • Forms: round, oval, cone shaped, stages, terraced
  • Low pH of stomach content + injury of mucosa/decr. defence mech. -> autodigestion -> formation of peptic erosions+ulcers
  • Necrotized ulcers need 1 day to extend to muscle layer, peptic 3-4 d.
  • Causes: Mechanical, circ. dist., nervous regul., chemical, pathogens, previous gastritis, metabolic dist., stressors, duodenogastric bile reflex
  • Fate: 1. Healing, 2. Arrodation, 3.Digestion in surrounding tissue, 4.Gastrorrhagia (haemorrhage from stomach)-anaemia-shock
19
Q

Gastritis

A
  • Causes: Alimentary (freq.), swallowing irritating materials/chemicals, disease symptom, conseq. of other diseases
  • Negative effect: decr. gastric juice prod., decr. stomach movement after transient incr., maldigestion, abnorm. decomp. of food, instead of digestion – fermentation
  • Types: 1.Acute / 2. Chronic atrohpic/hypertrophic catarrhal, 3.Hemorrhagic, 4. Gastritis w. pesudomembrane formation - crupous/diphteric, 5. Purulent, 6. Emphysematous, 7. Gastritis w. granuloma form., 8.Lymphomatic, 10.Eosinophilic granulocytic, 11. Scirrhotic, 11. Reactive/chemical gastropathy/gastritis
20
Q

Intestinal torsions, flexion, intussusception, (invagination), prolapsus, eventration

A
  • Torsion: intestine twist around it´s longitudinal axis/mesenterium – SI/LI
    • Causes: fast movement, differences in amount of content, spastic peristalsis, tumor, inflam.
    • Conseq.: suffocation -> intox. -> death
  • Flexion: intestine+attachement are bent
    • Conseq.: stenosis, circ. dist.
  • Intussusception: intestine folds into the section immediately ahead of it, simple/multiple
    • Intussescipient (recipient, outside) or Intussesceptum (protrude, inside)
    • Causes: adhesions, tumors, parasites, parvoviral enteritis
  • Prolaps: Prolapsus recti (due to incr. abd. pressure, loose lig´s.) or P. ani (permanent protrusion of rectal mucosa)
  • Eventration: protrusion trough a (cong./acquired) weakness/defect of abd. wall
21
Q

Hernias

A
  • Hernia: intestine get out from abd. cavity through anatomical/acquired opening
    • External: visible; H.umbilicalis, H.inguinalkis, H.scrotalis, H.femoralis, H.pectoralis
    • Internal: not-visible; H.foraminis epiploici Winslowii, H.spatii renolienalis, H.mesenterialis, H.diaphragmatica
    • Conseq.: incarceration, suffocation, circ. dist.
22
Q

Intestinal stenosis and obstruction (ileus)

A
  • Stenosis:
    • Obturation (decr. in diameter from outside) – tumor, hematoma, abscess, torsion, incarceration of hernia
  • Obstruction (-from inside) – FB, fodder, parasites, concretions, pseudoconc., inflam. of perianal glands, tumor, invagination, constipation, flexion/stricture due to scar formation
    • Ileus: ceased passage of intestinal content – Malposition, stricture, compression, abnormal content (impaction), FBs, dynamic (paralytic, symp. N. inhib.)
23
Q

Intestinal dilatation and constipation

A
  • Dilation: congenital/acquired (ectasia, diverticulum), usually due to accum. of gases or food, or FB´s
  • Constipation: accum. and conc. of content – feed composition, hair balls (fe), inflam. of perianal gl. (dogs), lack of exercise, dehydration, atony, intestinal spasm
    • Location: often last portion of ileum/caecum, Eq: chronic caecal impaction
    • Conseq.: ileus, autointox., bowel wall rupture, peritonitis
24
Q

Circulatory disturbances in the intestine.

A
  • Circ.dist.:
    1. Hyperemia
    2. Congestion
    3. Edema
    4. Thrombosis, emboli
    5. Hemorrhaes
  • Hyperemia: Active (physiologic during ingestion, inflammatory) / Passive (congestion)
  • Congestion: malpositions, thromboembolism, shock
25
Q

Thrombosis in the intestine

A

-Thrombosis in intestines: blood clot in vessels supplying intestines
- Neonates: Omphalophlebitis
- Ru: liver flukes
- Eq: Strongylus vulgaris larvae
-Conseq: ischemia, hypoxia, local tissue necrosis
-Hemorrhages:
A. Intraparietal:
-Rhexis (rupture of blood vessel) – trauma, parasites, FBs
-Diapedesis (RBC´s go through vessel wall) – toxicosis, enteritis, congestion, septicaemia -> into lumen = melena
B. Free hemorrhages: Rectic or Diapedic – Incarceration, hemorrhagic enteritis, toxicosis/septicaemia
-Lymphangiectasia intestinal: dilation of lymph vessels in dog

26
Q

Enteritides, basic forms

A
  • Location: Duodenitis, jejunitis, ileitis, typhlitis (caecum), colitis, proctitis (rectum)
  • Superficialis/Profunda/Perienteritis (tissue next to intestine)
  • Endogenous: viral, bacterial, fungal, parasitic, FB, drugs, toxins, low quality food
  • Exogenous: infection, intoxication, gastritis, stagnating ingesta, dysbacteriosis, metabolic disorders, anaphylaxis, chronic ingestion
  • Basic forms: 1. Acute catarrhal (fast, fatal w/in 24h, hyperaemia) 2. Chronic catarrhal (follows acute/slow, no hyperaemia) – both excessive prod. of thick mucus
  • Ultimate forms: 3. Hemorrhagic 4. Crupous/Diphteric (fibrin on surface/deep) 5. Necrotic 6. Suppurative 7. Proliferative 8. Mucomembranous (allergy)
  • Colitis: -cystica profunda, Idiopathic mucosal
  • Typhlitis: Trichuris, Entamoeba histolytica, Histoplasma, Leishmania, Parvovirus, Coronavirus, Spirochetes, Campylobacter

Pathology (11 decks)

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