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Path I > first section > Flashcards

first section Flashcards

1
Q

pathology is

A

the bridge between clinical science and basic science

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2
Q

pathos means

A

suffering

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3
Q

define etiology

A

cause of disease

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4
Q

infectious inflammation of lungs

A

influenza pneumonia

black pneumonia

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5
Q

influenza is an etiological agent of

A

influenza pneumonia

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6
Q

dramatic inflammation of the bladder

A

acute cystitis

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7
Q

gram negative bacilli that causes acute cyctitis

A

E. coli

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8
Q

E.coli is an etiological agent for

A

acute cystitis

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9
Q

what is an idiopathic disease

A

diseases with unknown cause

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10
Q

what percent of disease has a known etiology

A

25%

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11
Q

Idiopathic ankylosing spondylitis aka

A

bamboo spine

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12
Q

autoimmune
idiopathic
inflammation of joints leads to vertebral body fusion
severe back pain- do not adjust

A

idiopathic ankylosing spondylitis

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13
Q

DISH

Forestier’s disease

A

Hyperostosis

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14
Q

non inflammatory ossification of the ALL

A

DISH
Hypterostosis
Forestiers

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15
Q

Categories of etiology

A

Genetic
Congenital
Aquired

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16
Q

individuals genes are responsible for the structural or functional defect

A

genetic etiology

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17
Q

chorea form syndrome

A

huntingtons disease

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18
Q 
onset 30-35 years
death 10-15 years following
loss of motor function due to loss of striatal nuclei in the midbrain
dementia
chorea
A

huntingtons disease

genetic etiology

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19
Q

rapid jerkky involuntary movements of face and extremities

A

chorea

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20
Q 
trisomy 21
characteristic appearance
greater chance of having a child with syndrome if older than 35 yrs
no cervical adjustments
chromosomal abnormality
A

downs syndrome

genetic etiology

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21
Q

Genetic information is intact but other factors in the embryo’s intrauterine environment interfere with normal development.

A

Congenital etiology

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22
Q

What is a teratogen?

A

Agent that causes physical abnormality in a developing embryo

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23
Q

What causes toxoplasmosis?

A

Protozoan toxoplasma Gondi

Cat poop

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24
Q

What is a good example of teratogenic effect?

A

Rubella

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25
Q

What is recommended for women who have rubella

A

Abortion

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26
Q

Birth defect resulting from high alcohol consumption by mother

A

Fetal alcohol syndrome

congenital etiology

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27
Q

What time is highest teratogenic effect for fetal development

A

First three days

First trimester

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28
Q

Alcohol effects what process of cells

A

Mitosis

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29
Q

What sleeping drug created by Pfizer was give top regnant women to prevent morning sickness

A

Thalidomide

congenital etiology

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30
Q

What is the teratogenic effect of thalidomide?

A

Babies born with one eye and only limb buds

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31
Q

What are acquired etiological effects

A

Herpetic rash
Emphysema
Parameningeal infection

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32
Q

What causes shingles

A

Varicella-zoster virus

33
Q

Lung consolidation due to rupture and damage of alveoli

A

Emphysema

34
Q

Brain abscess due to improper popping of pimples

A

Parameningeal infection

35
Q

What bacteria is responsible for parameningeal infection

A

Staphylococcus aureus

S. Pyogens

36
Q

Who does infection get into the brain

A

Communication of veins for the face and brain

37
Q

Parameningeal infection can result in

A

Death
Spread of infection
Damage scarring

38
Q

What is a symptom

A

Subjective findings

Pain, nausea, HA

39
Q

What is a sign

A

Objective finding

High bp, rash

40
Q

Collection/group of signs and symptoms associated with particular disease

A

Syndrome

41
Q

Vasospastic contractions of distal vessels

A

Raynaud’s syndrome

42
Q

Order of raynauds syndrome

A

1–>contract arteries–> fingers/toes appear WHITE
2–>contract veins–>fingers/toes appear BLUE
3–> relax of vessels–> finger/toes appear RED

43
Q

Autoimmune
Middle Ages women (over 35)
Totally dryness of mucous membranes due to damage of exocrine glands
Bilateral parotitis

A

Sjögren’s syndrome

44
Q

Typical manifestation of Sjögren’s syndrome

A 
Xerostomia= dry mouth-->damage of sublingual gland teeth rot 
Xerophthalmia= dry eyes --> damage of lacrimal gland corneal ulcer
45
Q

What is bilateral parotitis?

A

Inflamed parotid glands (largest salivary gland)

46
Q

Pattern of disease development

A

Pathogenesis

47
Q

an illness that develops rapidlly
short duration (5-7 Days)
virus or cold

A

acute disease

48
Q

slow and serious development
symptoms persist for a long time
duration is greater than 6 weeks
TB

A

chronic disease

49
Q

confined to one organ/region of the body

ie stomach cancer

A

local disease

50
Q

involves multiple organs or systems

ie metastasized stomach cancer

A

systemic disease

51
Q

limited to one or more distant sites within a diseased organ
ie on tumor in stomach
on bite of an apple

A

focal damage

52
Q

uniformly distributed damage within a diseased organ
ie entire stomach is cancerous
half eaten apple

A

diffuse disease

53
Q

ID of patients specific disease

A

diagnosis

54
Q

prediction of a particular disease’s outcome

A

prognosis

55
Q

cause of cell injury

A

deficiency
intoxification
trauma

56
Q

types of deficient cell injury

A

primary nutrient

secondary nutrient

57
Q

lack of substances to the cell

A

deficiency cell injury

58
Q

simple absence of nutrient components in food
pellagra
casels necklace deratitis

A

primary nutrient deficiency

59
Q

vitamin B3 deficiency

A

pellagra

60
Q

components are in the food but cannot be absorbed

A

secondary nutrient deficiency

61
Q

normal RBC production in bone marrow and normal nerve cell metabolism requries

A

B12

62
Q

B12 must be combined with what to be carried into the blood

A

intrinsic factor

63
Q

presence of substance that interferes with cell function

A

intoxification

64
Q

types of intoxification

A 
exogenous
endogenous
genetic
ionizing
accumulation
65
Q

gets into the body from the outside

A

exogenous

66
Q

types of exogenous intoxification

A

microbes
chemicals
overdose

67
Q

toxins produced within the body

A

endogenous toxins

68
Q

if a normal metabolic reaction is disrupted what can happen

A

intermediate can accumulate because of missing enzyme and becomes toxic
intermediate can be used in an alternate pathway because of missing enzyme which the product can be toxic

69
Q

accumulation of a normal metabolite within the body can cause

A

alkaptonuria

homogentisic acid

70
Q

activation of an alternate pathway in a metabolic cycle

A

phenylketonuria

71
Q

normally phenylalanine is converted to tyrosine
however oxidase is not produced causing the intermediate homogentisic acid (aka alkapton) not to be converted
homogentisic acid accumulates and is excreted in urine causing it to turn black

A

alkaptonuria

72
Q

if homogentisic acid accumulates in specific tissues it is called

A

onchronosis

73
Q

where is the common site of accumulation of homogentisic acid

A

cartilage

74
Q

what happens when there is an extreme excess of homogentisic acid in cartilage

A

leads to OA and severe degeneration

75
Q

if alkapton (homogentisic acid) is deposited in the ears

A

ears appear blue

76
Q

calcification of IVD is common with

A

accumulation of homogentisic acid (alkapton)

77
Q

normally 50% of phenylalanine is used and 50% converted to tyrosine
nonprod of enzyme hydroxylase results in a switch to alt pathway–> production of phenylpyruvic acid, phenyllactic acid and phenylacetic acid
results in serious mental underdev
low IQ

A

phenylketonuria

78
Q

can result in free radicals that can destroy cell membranes

A

ionizing radiation

79
Q

3 major factors of gout

A

gouty arthritis
deposition of uric acid salts in joints
deposition of salts in kidneys= renal failure

Path I (5 decks)

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