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General Pathology final examination > B List > Flashcards

B List Flashcards

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
Q

What are consequences of autotoxemia

A

all the ones mentioned plus

DIC and microthrombus

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26
Q

BActeria viruses and fungi, parasites

A

infectios routes of entry
oronasal, urogenital, venereal, urinary or genital
omphalogen
Transplacental
Ovogen
Latrogenic
Locus minoris resistentia

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27
Q

bacteria, funghi, viruses influecing factors

A

infectivity
pathogenicity
Virulence
Host specifity (PRRSV in pigs, aujeszky disease
Invasiveness
Contagiousness
Host defense mechanisms

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28
Q

Pathological aspects of immunology, innate and adaptive

A

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

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29
Q

Adaptive immunity

A

Self and non self recognition
Humoral B
-extracelkluar
-toxins

Celluar T
intracelluar
-antigen binding to MHC

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30
Q

cells of the immune system

A

innate system
macrophage
natural killer cell
neurophil
eosinophil
Basophil
dendritic cell

Adaptive Immunity
B-cell
Antibodies
T-cell
CD4+ Tcell
CD8+ Tcell

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31
Q

MPS

A

Mononuclear phagocytic system
- immunity inflammation, tissue remodeling repair
-circulation= monocyte
-tissue: histiocytes
-resident macrophages: Kupffer cells in liver, alveolar macrophages in lung

32
Q

Cytokines= messenger o fimmune system

A

low molecular weight, soluble glycoproteins
local action, or systemic fever
Direct the immune system response
cytokine storm= oversecretion- death

33
Q

Disorders of the immune system
hypersensitivity

A

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
Q

Autoimmune system disease

A

specific resposnse to antigens
multifactorial
autoantibodies
t, b lymphocytes

leading to tissue damage and inflammation
AIHA: autoimmune hemolytic anemia

35
Q

immunodeficiency syndromes

A

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
Q

FIV

A

Feline immunodefciency
decreased CD4, alteration of CD$ and CD8
decrease antigen presentation
decrease Ne adhesion and migration
increase IgG

37
Q

Disturbances in water balance of the organism EDEMA

A

water balanceand regulation by:
nervous sytem
hormonal regulation
physical chemical factors

38
Q

increase Water retention

A

=filtration (arterioles)
-increase tissue oncotic pressure
increase capillary hydrostatib pressure
increase vascular permeability

39
Q

decrease water retention

A

increase in plasma oncotic pressure
starvation
increase in electrolyte in blood leading to kidney failure

40
Q

anasarca

A

excess of water in skin or subcutis all over the body

41
Q

hydrops

A

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
Q

types of hydrops

A

Hydrops hemorrhagic acutus: congestion
Hydrops adiposus: fatty transudate
Hydrops chylosus: turbid transudate, mixed with lymph, mesenteric lnn rupture

43
Q

EDEMA

A

intercelluar water accumulation

44
Q

classification of edema types

A

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
Q

Microscopic appearances of edem

A

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
Q

Dehydration and Exsiccation

A

tissue becomes dry
caused by increased fluid loss
, sweating, diarrhea, vomiting, renal failure

47
Q

pathology off dehydration and exsiccation

A

eyes are sunken
skin decrease in turgor
mucous membranes are dry

48
Q

casue of disturbances in water balance of cells

A

hypoxia
lps endotoxins
autotoxemia
Bruns, frostbites
Alkalosis, acidosis
Conns disease
Water toxicosis
Hypoproteinemia

49
Q

Cell swelling

A

swollen mitochondria, sodium pump stops

Hypoosmotic hypovolemia

Hypotonic hypervolemia (water toxicosis)
-increased water retnetion

50
Q

Vascular degenration

A

big vaculoses in cytoplasm
-increased cell swelling

51
Q

Hydropic degenration

A

Reticulated degenration:small vacuoles
Balloning degenration: reticulated in epithelium -desmosome break- rounded cells

52
Q

Vesicular degenration

A

swollen cell, pyknotic nucleus
cytoplasm cavernous, full of vacuoles

53
Q

Disturbances in fat metabolism

A

LPIDS
Simple fats
Compound Fats
Fat investigation
Fat deposition
Liver Fatty degeneration
Obesistas- adipositas
Lipoidoses

54
Q

simples fats of fat metabolism

A

in cells as depots
stable structure and transport
-neutral fats =rttyglycerides,
-USFA: linoleic, linolenic, arachidonic
Lipoprotein lipase
Waxes=cholesterol

55
Q

Compound fats and llipoids

A

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
Q

Fat investigation

A

Physical:
sudan 3, tellowihs -orange, scarlet red=sudan 4
Sudan black
Oil-red O

Chemical staining
Nile blue
PAS schiffs reagent
Schulltz method

57
Q

Fat deposition

A

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
Q

liver and Fatty degeneration

A

physiological is at the perophery
pathological the centrolobular diffuse

2 types
simple
necrobiotic

59
Q

causes of liver fatty degenration

A

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
Q

Lipoidoses

A

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
Q

Disturbances of carbohydrate metabolsim

A

Glycogenesis
GNG
Glycolysis

62
Q

regulation of carb metabolism

A

Hormonal:
insulin
growth hormones
GLucagon
GC hormones, STH,ACTH,TSH,LTH
Adrenaline

Neural:
MO, hypothalamus

63
Q

Glycogen

A

Storage fomr physiological and pathological, labile, stabile

demonstration of glycogen with lugol, best carmine
PAS, reaction
PAS+ diastase and no coloration

64
Q

increase production of glycogen and reduction

A

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
Q

Diabetius melitus

A

Type 1
decrease insulin prod. insulin dependant
-sign of ketoacidosis thin

Type 2
insulin resistant (receptor)
non insulin dependant cats, dogs, obesity

66
Q

Hyperglyecmia, hypertiglyceridemia

A

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
Q

DM consequences

A

Ketoacidosis
diabetic coma
glycogen accumulation in renal tubules
ALopecia
Microangiopathi
Neuropathia
Cataracta diabetica

68
Q

Disturbances of keratinization
and steps

A

keratinization,cells become enucleated, flattened, filled with secretory produce keratin
-Prekeratine
Keratohyaline granuloma
Odlands granula
Digestion of organelles

69
Q

Soft and Hard keratin

A

majority of epidermis mucous membranes

feather hoof horn

70
Q

Hyperkeratosis

A

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
Q

Hypokeratosis

A

rare, cachexia, wasting disease

72
Q

parakeratosis

A

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
Q

Keratinization Steps

A

-Prekeratine
-Keratohyaline granula
-Odlands granula
-digestion of organelles- keratinocytes

74
Q

Amyloidosis

A

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
Q

Amyloid Characteristics

A

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
Q

Amyloidosis and recognition, types

A

extracelluar deposition
Bloacks normal transfer of materials
loss of fiunction, regressive changes in tissues

77
Q
A

General Pathology final examination (2 decks)

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