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Pathobiology > Exam #3 > Flashcards

Exam #3 Flashcards

1
Q

Ischemia

A

deficiency of blood in a part of the body

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2
Q

Hypoxia

A

deficiency of oxygen in the inspired air

leads to hypoxemia

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3
Q

Hypoxemia

A

deficiency of oxygen in the blood

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4
Q

Hypoglycemia

A

deficiency of glucose in the blood

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5
Q

Shock

A

peripheral circulatory failure

circulatory collapse with decreased perfusion of vital organs

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6
Q

Hypotension

A

decreased blood pressure

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7
Q

Atrophy

A

possible consequence when blood supply to an organ or tissue is reduced
still sufficient blood supply for viability

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8
Q

Infarction

A

complete localized loss of effective blood supply leading to coagulative necrosis
seen in ischemia

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9
Q

Neovascularization

A

excessive ingrowth of blood vessels in the limbal vascular lexis

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10
Q

Wateshed/Boundary Zone

A

depend on level of collateral circulation in an organ or tissue

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11
Q

Cyanosis

A

blue discoloration of the skin or mucous membranes
due to hypoxia
indicative of poor oxygenation of blood regardless of the cause

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12
Q

Selective Vulnerability

A

of cells of the nervous system to injury or disease that deprives the brain of nutrients
susceptibility of neurons>olgiodendroglial cells> astrocytes

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13
Q

Insulin/Glucagon

A

controls blood glucose

produced in the pancreatic islets

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14
Q

Pregnancy Toxemia

A

form of hypoglycemia that occurs in small ruminants
blood glucose is disregulated and coupled with the increased energy demands of twin pregnancies
sufficient to cause selective brain damage
only treatment is to terminate pregnancy

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15
Q

Shock:

Hypovolemic

A

develops when there is absolute loss of intravascular blood volume

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16
Q

Shock:

Cardiogenic

A

heart fails to act as an effective pump

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17
Q

Shock:

Maldistributive

A

redistribution of blood to the peripheral circulation due to vasodilation depriving internal vital organs of adequate blood flow

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18
Q

Periventricular Leukomalacia

A

occurs in human infants, similar disorder in animals

likely is multifactoral but has features of ischemia, shock, hypotension

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19
Q

Immune System

A

complex system of defenses against infection

contains proteins and cells with specific functions aimed at identifying and destroying infectious agents in the body

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20
Q

Primary Malnutrition

A

situation in which all or many key nutrients are lacking in the diet
starvation

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21
Q

Secondary malnutrition

A

related to a variety of underlying causes
appetite is suppressed,absorption and utilization are inadequate, increased demand for specific nutrients to meet physiological needs

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22
Q

Inanition/Anorexia

A

failure to eat despite plenty of available food

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23
Q

Primary Protein-Calorie Undernutrition

A

starvation in its truest sense
malnutrition is seldom simple
concurrent disease

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24
Q

Kwashiorkor

A

primary protein-calorie undernutrition
critical lack of protein in diet despite adequate caloric intake
occur sin newborns when breastfeeding and older children being weaned
due to forced subsist on a diet composed almost entirely of carbohydrates
signs are apathy, subcutaneous edema, ascites, enlarged fatty liver, hypoalbuminemia

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25
Q

Marasmus

A

primary protein-calorie undernutrtion
deficiency of protein and carbohydrates in diet
no edema or enlarged liver
children are bright/alert, marked atrophy of skeletal muscle mass, stunted growth

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26
Q

Secondary Protein-Calorie Undernutrition

A

occurs despite availability of a proper diet
due to decreased intake which could be caused by poor dentition, dysphagia, and systemic diseases that lead to poor appetite

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27
Q

Dysphagia

A

difficulty swallowing
impairment of cranial nerve functions
space occupying masses
mechanical injuries

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28
Q

Nigropallidoencephalomalacia

A

dysphagia and starvation are cause of death i horses

due to ingestion of yellow star thistle and Russian knapweed

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29
Q

Malabsorption/ Faulty Utilization

A 
inability to absorb nutrients
secondary protein-calorie undernutrtion
inflammatory disease of the bowel
hepatobiliary
pancreatic disease
intestinal parasitism
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30
Q

Increased Requirements

A

secondary protein-calorie undernutrtion
growth and maintenance
pregnancy and lactation

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31
Q

Ketosis

A

secondary protein-calorie undernutrtion
in high producing dairy cattle
due to demands of lactation and late term pregnancies
negative energy balance
lowered body weight and drop in milk production

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32
Q

Vitamin B12/Cyancobalamin Deficiency

A

essential dietary vitamin
comes almost exclusively from microorganisms
plants/vegetables not good source
can be primary if not in diet or secondary if malabsorption occurs
intestinal parasitism and diverse diseases of the lower small intestine can lead to malabsorption

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33
Q

Intrinsic Factor

A

protein excreted from the parietal epithelial cells of the gastric muscosa as well as hydrochloric acid
binds vitamin B12 in order to be absorbed

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34
Q

Chronic Atrophic Gastritis

A

inflammatory/autoimmune destruction of the epithelial cells, deficiency of intrinsic factor, malabsorption of B12

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35
Q

Vitamin B12 in Relation to Disease

A

1) methylation reaction, requires B12 as cofactor for a methytransferase to synthesize folic acid for DNA synthesis
2) conversion of methylmalomyl-CoA to succinyl-CoA, results in accumulation of methylmalomic acid resulting in defective formation of fatty acids and damage to neuronal membranes such as myelin

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36
Q

Pernicious Anemia

A

decrease in red blood cell count due to Vitamin B12 deficiency

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37
Q

Subacute Combined Degeneration of the Spinal Cord

A

degeneration of the posterior and lateral columns of spinal cord due to vitamin B12 deficiency

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38
Q

Copper Functionality

A

co-factor for many critical enzymatic reactions
ceruloplasmin is the main copper-carrying protein in the blood, also called ferroxidase
enzymatic properties and can catalyze the oxidation of Fe2+ to Fe3+ for heme synthesis

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39
Q

Functions of Enzymes

A

Cytochrome C Oxidase: energy production
Lysyl Oxidase/Collagen: connective tissue integrity
Ceruloplasmin/Ferroxidase: heme synthesis
Monoamine Oxidase: neurotransmission
Cytochrome C Oxidase: myelin formation
Tyrosinase: formation of melanin pigment
Cu, Zn Superoxide Dismutase: antioxidants

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40
Q

Menkes Disease

A

‘Menke’s kinky-hair syndrome’
deficiency is inherited as X-linked recessive trait
absorption of the epithelial cells seems adequate but transport of copper to other tissues is deficient due to defective copper-transporting ATPase

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41
Q

Degenerative Myelopathy

A

associated with copper deficiency
due to degeneration of moto neurons in the spinal cord has late onset
linked to overzealous supplementation with zinc

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42
Q

Falling Disease of Cattle

A

syndrome of sudden death due to heart failure
has been associated with low copper
cardiac failure has been attributed to lack of energy production due to reduced cytochrome C oxidase activity

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43
Q

Aneurysms

A

areas of weakness in the walls of arteries that result in saccular dilations and the potential for rupture
weakness attributed to reduced lysyl oxidase activity necessary for cross-linking and stabilization of collagen and elastin

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44
Q

Hair Abnormalities

A

associated with copper deficiency
includes brittle, kinky, lightly pigmented hair
enzymes involved?

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45
Q

Abnormal Pigmentation

A

associated with copper deficiency

typically most notable as a lighter pigmented hair coat

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46
Q

Enzootic Ataxia/ Swayback

A

associated with copper deficiency
disease of lambs and goat kids
can occur in a more severe congenital form with clinical signs at the time of birth or onset can be delayed
analogies between CNS lesions and Menkes kinky hair disease
degeneration of motor neurons in the spinal cord

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47
Q

Amyotrophic Lateral Sclerosis

A

late onset copper deficiency
similarity with enzootic ataxia/swayback
Cu, Zn-superoxide dismutase abnormalities

48
Q

Thiamine Deficiency

A

vitamin B1
absolute dietary requirement
very little thiamine stored in the body
not required in ruminates as bacteria in their gut synthesize it
deprives the body of high energy phosphates, important intermediates for metaboilic needs, certain neurotransmitters

49
Q

Thiamine as a Co-Enzyme

A

3 metabolic pathways
transketolase-pentose phosphate pathway
pyruvate dehydrogenase-glycotic pathway
a-ketoglutarate dehydrogenase-citric acid cycle

50
Q

Thiamine Deficiency in Humans

A

primary or secondary

inadequate intake, diets high in carbohydrates

51
Q

Secondary Thiamine Deficiency

A 
increased requirement (pregnancy, lactation, hyperthyroidism, ect.)
malabsorption (chronic intestinal disease, alcoholics)
anti-thiamine factors (consumption of tea, coffee, raw shellfish, freshwater fish, ferns)
52
Q

Wet Beriberi

A

due to thiamine deficiency
characteristically a syndrome of congestive heart failure
signs are tachycardia, cardiomegaly, edema, dyspnea

53
Q

Dry Beriberi

A

due to thiamine deficiency
disease of the peripheral nerves
sensory and motor nerves and reflexes are affected
loss of myelin sheaths (demyelation) progresses to axonal degeneration

54
Q

Wernicke’s Encephalopathy

A

due to thiamine deficiency
fairly acute syndrome involving degeneration in multiple discrete areas of the brain
hemorrhage, edema, vascular congestion and prominence, preservation of neurons at early stages

55
Q

Korsakoff Psychosis

A

due to thiamine deficiency
accompanies most cases of Wernicke’s
neuropsychiatric disorder memory deficits involving recent memories

56
Q

Thiamine Deficiency in Carnivores

A

‘Chastek’s paralysis’
typically due to feeding on raw fish containing thiaminase enzymes
lesions similar to Wenicke’s

57
Q

Thiamine Deficiency in Herbivores/Ruminants

A 
enigmatic
lesions preferentially involve the cerebral cortex of the brain rather than the brain stem
ingesting thiaminase-containing plants
acidosis due to overconsumption of grain
use of amprolium
58
Q

Polioencephalomalacia

A

lesions on the cerebral cortex of the brain

seen in thiamine deficiency in herbivores/ruminants

59
Q

Thiaminase-Containing Plants

A

brackenfern

deactivates thiamine made by the normal gut flora in ruminants

60
Q

Amprolium

A

coccidiostat
structural analog of thiamine
causes thiamine deficiency in ruminants

61
Q

Obesity and Related Diseases

A 
ischemic heart disease (heart attack)
hypertension
renal disease
diabetes mellitus
stroke
certain forms of cancer
62
Q

Obesity Survival Rates

A

past heart problems some overweight individuals fair better than lean people experiencing certain medical conditions

63
Q

Kcal Intake vs Kcal Burned

A

1 cause of obesity

availability of foodstuffs
too much food vs too little physical activity

64
Q

Genetics and Neurobiological Mechanisms

A

adopted children still tend to take after their birth parents weight wise

65
Q

Leptin

A

produced mainly by adipose tissue suppresses appetite
most important long term regulator of the body’s fat stores
obese people have high levels of this but seem to have developed a resistance to it

66
Q

Ghrelin

A

produced by cells in the stomach and pancreas

stimulates appetite

67
Q

Orexins

A

‘hypocretins’
produced by neurons in the hypothalamus
stimulate food intake and orexin-producing neurons are inhibited by leptin

68
Q

Adiponectin

A

produced by adipose tissue
complementary to leptin
related to insulin and glucose and fatty acid metabolism

69
Q

Medical and Psychiatric Illnesses

A

hypothyroidism and psychiatric disorders may increase the risk of obesity

70
Q

Socioeconomic Status

A

correlation between status and weight depending on worldly location

71
Q

Hemostasis

A

used synonymously with clotting and coagulation

more strictly refers to the process by which the body attempts to stop bleeding or hemorrhage

72
Q

Postmortem Clots:

Chicken Fat

A

essentially coagulated plasma

never seen by themselves; always form along currant-jelly clots

73
Q

Postmortem Clots:

Currant-Jelly

A

coagulated plasma with red blood cells

commonly only type found

74
Q

Postmortem Clots

A

not to be confused with clots formed prior to death (thrombi)
always have a bright, shiny surface

75
Q

Erythrocyte Sedimentation Rate

A

ESR
based on this in each species that determines which clots appear postmortem.
increased ESR can be a sign of inflammation

76
Q

Antemortem Clotting of Blood

A

balance between maintaining blood in its fluid form necessary for life and stopping unnecessary fluid/blood loss when disease or injury occurs
achieved by anticoagulant factors produced by endothelial cells and proteins circulation in blood and procoagulent factors active in platelets and a different set of proteins in the blood

77
Q

Prostacyclin

A

secreted by endothelial cells
very potent inhibitor of platelet aggregation which is the first step in initiating a blood clot
inhibits secretion of ADP by platelets that prevent attraction of other platelets

78
Q

Endothelins

A

released by endothelial cells
contribute to homeostasis
vasoconstriction to limit bleeding
stimulating proliferation of endothelial and fibroblastic cells to aid in the process of repair

79
Q

Endothelial Cells

A

release prostacyclin and endothelins
release of tissue plasminogen activator that converts a plasma protein, plasminogen to plasmin, to help dissolve the fibrin clot

80
Q

Platelets

A

activated at sight of injury
aggregate and release ADP to attract other platelets
thromboxane to cause vasoconstriction
clcium to participate in clotting cascade

81
Q

Clotting Cascade

A

results in conversion of plasma proteins into fibrin that polymerizes to form the clot
two paths: intrinsic and extrinsic
converge at factor X to form a final common pathway to coagulation

82
Q

Intrinsic Pathway

A

part of clotting cascade

begins inside the vessel with damage to endothelial cells

83
Q

Extrinsic Pathway

A

part of the clotting cascade

begins external to the blood vessels such as from external trauma

84
Q

Antithrombin II

A

protein in the blood

inhibit activation of the clotting cascade

85
Q

Significance of Hemorrhage

A

depends on location, magnitude, whether it is acute or chronic loss of blood
subdural hemorrhage or hematoma in certain tissues can have disastrous effects

86
Q

Faulty Hemostasis

A 
abnormal or delayed clotting of blood
deficiencies in plasma proteins that form the clotting cascade
*look at class notes*
87
Q

Thrombosis

A

formation of a thrombus, typically considered formation of an undesired blood clot within a blood vessels with at least partial obstruction of blood flow

88
Q

Virchow’s Triad

A

leads to thrombosis

  • damage to endothelial cells
  • disordered blood flow
  • hypercoagulable states
89
Q

Propagation

A

fate of thrombosis

spread of thrombus down the length of a blood vessel in the direction of blood flow

90
Q

Embolization

A

fate of thrombosis
detachment of a portion of the thrombus that travels withing a blood vessel to lodge at a more distant site, typically in a blood vessel of smaller caliber

91
Q

Resolution

A

fate of thrombosis

involves the innate process of fibrinolysis with restoration of blood flow

92
Q

Organization and Recanalization

A

fate of thrombosis
fibroblasts can invade the thrombus from the damaged blood vessel walls converting the thrombus to a solid mass of fibrous tissue, permanently creating an occlusion
small blood vessels can invade along with the fibroblasts to form small blood vessels but it is seldom that these establish completely normal blood flow

93
Q

Thromboemolism

A

sequel to thrombosis
‘embolization’
can be disastrous to the formation of emboli
leading to at least partial further vascular occlusion downstream from the site of the original thrombus

94
Q

Ischemia/Infarction

A

sequel to thrombosis
loss of blood supply/coagulative necrosis secondary to ischemia
affected tissue is usually pale, dull, slightly granulated appearance

95
Q

Disseminated Intravascular Coagulation

A 
'DIC'
*look at class notes*
96
Q

Anatomical Barriers

A

not part of the true immune system

  • epidermis resists transfer of bacteria
  • epithelium in trachea and nasal passages contain cilia that beat towards larynx
  • adjoining cells produce a mucin that trap bacteria in trachea
97
Q

Opportunists

A

cause infection in those with impaired immune system

98
Q

True Pathogens

A

cause disease in healthy individuals

99
Q

Inflammation

A

localized, regional, or systemic response of the body to foreign material, perceived foreign material or damaged host tissue
comprises specific inflammatory cells and soluble inflammatory mediators that are directed at destroying and removing the inciting cause

100
Q

Acute

A

sudden onset/ short duration

101
Q

Purpose of Inflammation

A

attempts to destroy disease causing microorganisms and parasites
may lead to encapsulated abscess at localized site if all pathogens aren’t killed
also important ‘cleaning up’ of body’s tissue after injury or death

102
Q

Sequelae of Acute Inflammation

A
  • may rapidly destroy and remove infectious agents, brief chronic inflammation, return to normal state with little scarring
  • considerable level of acute inflammation, tissue damage
  • lead to persistent chronic inflammation
  • acute insufficient to contain local infection, spreads
  • small sites of inflammation at certain locations such abscess in the heart or brain can lead to death
103
Q

Pathologic Process of Acute Inflammation

A

aberrant activation can occur by healthy tissue
result in tissue damage
exp. asthma, immune-mediated hemolytic anemia, flea allergy, systemic lupus erythrematosus

104
Q

Recognizing Acute Inflammation

A 
rubor, tumor, dulor, calor
redness, swelling, pain, heat
nearly always present with acute inflammation
functio laesa
loss of function
105
Q

Mechanisms of Acute Inflammation

A

complement system, antibodies, toll-like receptors initiate this

106
Q

First Phase of Inflammation

A 
vascular response characterized by vasodilation and increased vascular permeability
inflammatory exudate (protein rich fluid leaking unto structure surface)
histamine released by mast cells
nitric oxide produced by endothelial cells and macrophages
107
Q

Second Phase of Inflammation

A

cellular response characterized by migration of neutrophils across blood vessel walls into affected tissue
bone marrow derived cells
pass between two endothelial cells and bind to molecules in the inter-cellular matrix such as fibrin and fibronectin
the protein myeloperoxidase is critical for pathogen killing
lysosomal hydrolases digest bacteria

108
Q

Suppurative Inflammation

A

‘pus’

occurs during the second phase of inflammation when there is a large number of dead neutrophils are present

109
Q

Regional Effect of Inflammation

A

inflammatory mediators withing the tissue fluid in a region of inflammation drain into lymphatics and eventually reach regional lymph nodes where they stimulate a localized lymophcyte proliferation which reslts in the production of antibodies

110
Q

Suppurative Lymphadenitis

A

bacterial infection that lead to regional lymph node abscessation

111
Q

Leukocytosis

A

‘elevated white cell count in blood’
systemic effect of inflammation
inflammatory mediators promote increased proliferation of white blood cells in the bone marrow

112
Q

Acute Phase Response

A

systemic effect of inflammation

changes in the concentration of specific blood proteins that are associated with protection against infection

113
Q

Pyrexia

A

‘fever’
systemic effects of inflammation
pyrogens are substances that promote elevation in body temperature
proteins interleukin 1 and TNF-alpha
enables immune cells, helps destroy infection, can be life threatening

114
Q

Types of Acute Inflammation

A

suppurative inflammation- large number of neutrophils
seous inflammation- low cellularity in exudate
necrotizing inflammation- large amounts of tissue necrosis

115
Q

Chronic Inflammation Key Features

A
  • less swelling and pain
  • significantly fewer neutrophils
  • large numbers of macrophages, lymphocytes, plasma cells
  • fibrosis/ deposition of collagen rich connective tissue
  • tissue destruction/ deformation
116
Q

Macrophages

A

key cell type involved in chronic inflammation
derived from bone marrow precursor cells that release monocytes into the blood
these migrate into tissue and differentiate into macrophages
produce cytokines and prostaglandins that control inflammatory cells
stimulate tissue fibrosis and angiogenesis

Pathobiology (2 decks)

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