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General Pathology final examination > B List > Flashcards

B List Flashcards

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1
Q

causes of high temp as cause of a disease

A

radiant heat
hot liquid
steam, gas
solid substances

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2
Q

burn can be either catgory

A

external or internal

internal inhalational

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3
Q

on severeity of lesion by heat category

A

severety of lesion determined by temperature, duration, quality, extension and age of the animal is important
1st degree combustion erythematosa
-hyperemic shock, dialted vessels and edema

2nd degree C. bullosa
-vesication, denaturatio, precipitation of proteins , pain

3rd degree C. Escharotica
coagulation necrosis of tissues
hemostasis- thrombosis, pale and insensible

4th degree Carbonisation
charred

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4
Q

General effects of burning

A

GRAPH

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5
Q

Pathological findings of hyperthermia

A

quick rigor mortis
incompletly clotted blood
hemostasis
Brain edema
Meningeal hypermia
Hypothalamus hemorrhages

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6
Q

Lesions hyperthermia

A

Heat spasm
Heat distress
Heat stroke

sunstroke is rare in animals:
vasodilation, brain and meningeal edema leading to death

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7
Q

Local effect of hypothermia or low temperature

A

Contractionof vessels, local ischemia
increased metabolites
hemostasis

Frostbite and Congelatio

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8
Q

degrees of low temperature

A

1st C. erythematosa
blueish, red swollen

2nd C. bullosa- vesication, edema

3rd C. escharotica- necrosis

4th C. gangrenosa- gangrene

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9
Q

general effects of hypothermia

A

gengrenous lesions

below 35 degress animals sensitive , newporn piglets
caused by weather, exhaustion, starving and predisposing factors
27-30 vital functions standstill
20-25 death

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10
Q

Mechanism against cold

A

newborn have brown fatty tissue
shivering
metabolism is increased
vasoconstriction
shallow and quick respiration

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11
Q

sensitive animlas to cold

A

piglets disease: acute hypoglycaemia of the newboorn pigs (anemia) -cold and starvation

newborns in general sensitive, large body surface, not perfect heat regulation

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12
Q

inadequate oxygen water supply

A
  1. SUFFOCATION/ asphyxia meaning lack of air
  2. HYPOXEMIA/ hb saturation is low
    -not enough O2 in the air, cause by altitude, embolism or brisket disease in cattle
    -HB cant take up O2, decrease Hb O2 affinity, carbonone monoxide poisoning , cherry red blood, ROOS, Fenton reaction iHB-Fe3) chocolate brown colour, nitrite poisoning pesticides in water dark brown chocolate blood
    -. decreased HB, anemia hemolysis- BM damage
    -. intracelluar respiration decrease : cyanide poisoning
    -. respiratory center paralysis: bacterial toxins, poisons, hyperemia
    -. Vasomotor center paralysis
    -. Obstavle to breathing and circulation
    3.HYPOXIA: decreased O2 tissues supple
  3. Hypercapnia increased CO2 in tissue
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13
Q

pathology of suffocation

A

Dar unclotted blood
petechial hemorrhages
Acute lung hyperemia and edema
Acute heart Dilation
Acute emphysema

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14
Q

Disturbances of the water balance

A

Exsiccosis and dehydration
-insufficient water intake
increased electrolyte concentration, ph shift
increased fluid loss leading to vomiting and diarrhea, persipitation

Hyperhydration
-leading to polyuria- minerals electrolyte loss

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15
Q

Disturbances of the nutrient supply

A

1.total starvation - inanitio completa
no food intake, energy from own body, protein degradation leading to ketone bodies. young animals are sensitive, Cachexia is 40% weight loss
Fat is gelatinous PM

2.Partial starvation -inanitio incompleta
decreased quantity, quality feed
inadequate food intake, GIT lesions, maldigestions, malabsorption,
deficiency disease

  1. obesity, overfeeding- obesitas
    too much food compared to needs
    continuous oroccasionla
    Dilation or rupture of stomach
    neural disorders
    hormonal causes, hypothyroidism
    decreased physical activity
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16
Q

Autointoxication

A

Autointoxication is poisoning with endogenous toxins

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17
Q

types of autointoxication

A

Diabetic
Retention
Hepatic
Putrid
Abnormal direction of metabolism
Enterogenic
Resorption

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18
Q

Diabetic autointoxication

A

ketone bodies, acetoacetate, b hydroxybutyrate, acetone
Ketosis
Ketoacidosis , animals with type 1 DM

leading to dehydration, tachycardia and cerebral edema

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19
Q

Retention autointoxication

A

Uricosis - uric acid
Icterus- bilirubin and bile acids
Kidney failure- uremia

increased ceratinine creatine urea , uric acid= uremic toxins

leading to vascular damage, MOF multiorgan failure seizures, coma, death

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20
Q

hepatic retention

A

damage of the liver, hepatitis, hepatosis tumor, fibrosis cirrhosis
impaired detoxification
phase 1: oxidation, reduction, hydrolysis
phase 2:conjugation
increased bilirubin

casued by exposure of toxins, viral infections, hyperthyroidism, gilberts syndrome, cholestasis and decreased liver supply

consequences are chronic fatigue, depression, constipation and mental confusion

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21
Q

putrid autoiintoxication

A

gangrene: type of necrosis leading to ichorus inflammation- putrefecation of tissues
wet bacterial infection - toxic products

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22
Q

abnormal direction of metabolism autointoxication

A

Porpgyrias, accumulation of porphyrins, rare

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23
Q

Enterogenic autointoxication

A

absoprbed decomposition products from GIT
Clostridium perfrigens, Cl. botulism , grass fever
Intestines: indol, scatol, phenol, methylmercaptan, urobilin, NH3, cadaverinRe

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24
Q

Resorption

A

Ruptured, perforated eroded, stomach, intestine, urinary bladder

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25
What are consequences of autotoxemia
all the ones mentioned plus DIC and microthrombus
26
BActeria viruses and fungi, parasites
infectios routes of entry oronasal, urogenital, venereal, urinary or genital omphalogen Transplacental Ovogen Latrogenic Locus minoris resistentia
27
bacteria, funghi, viruses influecing factors
infectivity pathogenicity Virulence Host specifity (PRRSV in pigs, aujeszky disease Invasiveness Contagiousness Host defense mechanisms
28
Pathological aspects of immunology, innate and adaptive
Innate -non specific -immediate - no memory anatomic barriers such as skin and mucos physiological properties Phagocytosis Complement Adaptive -specific for Ags -slower last ing days weeks memory, vaccination humoral (b lymph cellular (t lymph
29
Adaptive immunity
Self and non self recognition Humoral B -extracelkluar -toxins Celluar T intracelluar -antigen binding to MHC
30
cells of the immune system
innate system macrophage natural killer cell neurophil eosinophil Basophil dendritic cell Adaptive Immunity B-cell Antibodies T-cell CD4+ Tcell CD8+ Tcell
31
MPS
Mononuclear phagocytic system - immunity inflammation, tissue remodeling repair -circulation= monocyte -tissue: histiocytes -resident macrophages: Kupffer cells in liver, alveolar macrophages in lung
32
Cytokines= messenger o fimmune system
low molecular weight, soluble glycoproteins local action, or systemic fever Direct the immune system response cytokine storm= oversecretion- death
33
Disorders of the immune system hypersensitivity
type 1 - immediate IGE-mediated : allergies and anaphylaxis type 2 - cytotoxic: hemplytic anemias type 3 - immune complex type 4 - delayed: tuberculin test, contact dermatitis, Crohn's disease, rheumatoid arthritis
34
Autoimmune system disease
specific resposnse to antigens multifactorial autoantibodies t, b lymphocytes leading to tissue damage and inflammation AIHA: autoimmune hemolytic anemia
35
immunodeficiency syndromes
failure of immune system congenital or acquired -severe combined immunodeficiency SCID, affects humoral and cellular -secondary immunodeficiency malnutrition, chronic disease, tumors, aging, viral infection, immunosuppressive agents, stress
36
FIV
Feline immunodefciency decreased CD4, alteration of CD$ and CD8 decrease antigen presentation decrease Ne adhesion and migration increase IgG
37
Disturbances in water balance of the organism EDEMA
water balanceand regulation by: nervous sytem hormonal regulation physical chemical factors
38
increase Water retention
=filtration (arterioles) -increase tissue oncotic pressure increase capillary hydrostatib pressure increase vascular permeability
39
decrease water retention
increase in plasma oncotic pressure starvation increase in electrolyte in blood leading to kidney failure
40
anasarca
excess of water in skin or subcutis all over the body
41
hydrops
fluid accumulation in interstices or serous cavities ascites inabdominal cavity hydrothorax hydropericardium fluids can be: transudate-watery, yellowish, congestion modified transudate, secondary inflammation exudate: turbid, fibrinflakes, inflammation- septic and non septic
42
types of hydrops
Hydrops hemorrhagic acutus: congestion Hydrops adiposus: fatty transudate Hydrops chylosus: turbid transudate, mixed with lymph, mesenteric lnn rupture
43
EDEMA
intercelluar water accumulation
44
classification of edema types
Oe. Stagnatosis: increase in bp no filtration or resoprtion leading to edema Oe. dysoricum: inflammatorium toxicum, allergicum, angioneuroticum Oe. Hypopretieinemia: cacheticum, renale+edema Oe. lymphangioticum: stagnation, increase of Bp inhibitslymphatic drainage Oe. hormonal: myzedema and hypothyroidism, piglet hypofunction
45
Microscopic appearances of edem
skin swelling jelly fish like cut surfaces mucous membranes are bulky and fluctuating Parenchymal organs have rigidity, swelling and congestion Body cavities, transudate and exudate
46
Dehydration and Exsiccation
tissue becomes dry caused by increased fluid loss , sweating, diarrhea, vomiting, renal failure
47
pathology off dehydration and exsiccation
eyes are sunken skin decrease in turgor mucous membranes are dry
48
casue of disturbances in water balance of cells
hypoxia lps endotoxins autotoxemia Bruns, frostbites Alkalosis, acidosis Conns disease Water toxicosis Hypoproteinemia
49
Cell swelling
swollen mitochondria, sodium pump stops Hypoosmotic hypovolemia Hypotonic hypervolemia (water toxicosis) -increased water retnetion
50
Vascular degenration
big vaculoses in cytoplasm -increased cell swelling
51
Hydropic degenration
Reticulated degenration:small vacuoles Balloning degenration: reticulated in epithelium -desmosome break- rounded cells
52
Vesicular degenration
swollen cell, pyknotic nucleus cytoplasm cavernous, full of vacuoles
53
Disturbances in fat metabolism
LPIDS Simple fats Compound Fats Fat investigation Fat deposition Liver Fatty degeneration Obesistas- adipositas Lipoidoses
54
simples fats of fat metabolism
in cells as depots stable structure and transport -neutral fats =rttyglycerides, -USFA: linoleic, linolenic, arachidonic Lipoprotein lipase Waxes=cholesterol
55
Compound fats and llipoids
Phospholipids: Fa, glycerol, phosphoric acid (H3PO4) -lechitins, cephalins, shingomyeling Glycolipids: lipids=sugar: cerebrosides, suphatides, gangliosides Steroids: corticosteroids (AG), cholesterol Caratenoids: alpha, gamma, beta, carotenes, lipochromes, yellow color to lipids
56
Fat investigation
Physical: sudan 3, tellowihs -orange, scarlet red=sudan 4 Sudan black Oil-red O Chemical staining Nile blue PAS schiffs reagent Schulltz method
57
Fat deposition
physiological fatty infiltraion of the: Liver, depot of cholesterol Kidneys: in cats ++ BM Mammary galnds, sebaceous glands- neutral fats Adrenal cortex, bile GB mucosa, corpus luteum, Leidig cells, CNS-cholesterol Pathological fatty infiltration -excessive entry from liver decrease metabolizing capacity lack of essential substances
58
liver and Fatty degeneration
physiological is at the perophery pathological the centrolobular diffuse 2 types simple necrobiotic
59
causes of liver fatty degenration
overfeeding increase mobilization accumulation hypoxia toxins lack of lipotrophic factors CH metabolism disturbances Vitamin defiecny Protein metabolism disturbances , chang in ionic balance NUTMEG LIVER
60
Lipoidoses
lpod thesarisomoses, accumulation of fat in abnomral places local or systemic local cholesterol granuloma, on pleura systemic: Sphingomyelin- liver tay sachs schaffer disease Ganglioside- Vogt spielmeyer Kerazine - Gauchers disease
61
Disturbances of carbohydrate metabolsim
Glycogenesis GNG Glycolysis
62
regulation of carb metabolism
Hormonal: insulin growth hormones GLucagon GC hormones, STH,ACTH,TSH,LTH Adrenaline Neural: MO, hypothalamus
63
Glycogen
Storage fomr physiological and pathological, labile, stabile demonstration of glycogen with lugol, best carmine PAS, reaction PAS+ diastase and no coloration
64
increase production of glycogen and reduction
increase: overfeeding with CH increase activity from inflammation, irritation, malignant tumours glycogen storage disease decease: prdoctuin wither chemical (strychnine, chloroform) or bacterial mobilization increase with starvation, piglet disease, cold, fever
65
Diabetius melitus
Type 1 decrease insulin prod. insulin dependant -sign of ketoacidosis thin Type 2 insulin resistant (receptor) non insulin dependant cats, dogs, obesity
66
Hyperglyecmia, hypertiglyceridemia
increase glucos in body, glucosuria: diabetes insipidus increase in glucose fermenting microorganisms- emphysematous cystitis glycogen accumulation overweight of metabolic pathway -increase starvation increase in ketone bodies decrease in glucose uptake glycation fo proteins microvascular macrovascular lenses- cataract impaired leukocytes function, decrease resistance to infection
67
DM consequences
Ketoacidosis diabetic coma glycogen accumulation in renal tubules ALopecia Microangiopathi Neuropathia Cataracta diabetica
68
Disturbances of keratinization and steps
keratinization,cells become enucleated, flattened, filled with secretory produce keratin -Prekeratine Keratohyaline granuloma Odlands granula Digestion of organelles
69
Soft and Hard keratin
majority of epidermis mucous membranes feather hoof horn
70
Hyperkeratosis
Local hyperkeratosis -mechanical irritation -long chronic inflammation circulatory disturbances- pachyderma -malformation- cutaneous horn -trophoneurotic disturbance- hard pad systemic hyperkeratosis -vitamin a def biotin def toxicosis, asphalt primary seborrhea ichthyosis congentia
71
Hypokeratosis
rare, cachexia, wasting disease
72
parakeratosis
imperfect keratinization on skin -zn def -acanthosis nigricans -chronic inflammation on rumen chronic inflammation, willow leaf like hyper and parakeratosis in rumen -cattle liver abscessation Dyskeratosis (rare)
73
Keratinization Steps
-Prekeratine -Keratohyaline granula -Odlands granula -digestion of organelles- keratinocytes
74
Amyloidosis
no inflammatory activity amyloid= starch like, aggregat of proteins amyloidosis+tissue damage die to amyloid depot , extracellular on collagen and reticular fibers, non inflammatory
75
Amyloid Characteristics
x-ray diffraction -fibrils composed of filaments, protofilaments beta sheet fiber network not soluble in water staining lugol methyl violet, toluidine blue PAS congo red Van gieson Immunofluo
76
Amyloidosis and recognition, types
extracelluar deposition Bloacks normal transfer of materials loss of fiunction, regressive changes in tissues
77

General Pathology final examination (2 decks)

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