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Patho 2nd Semester > Remaining Patho > Flashcards

Remaining Patho Flashcards

1
Q

Being immunocompromised in AIDS allows for what to occur

A

Opportunistic infections and cancers

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2
Q

What kind of virus is HIV?

A

retrovirus, converts RNA -> DNA (reverse transcription)

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3
Q

What is CD4?

A

Surface receptor on THCs

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4
Q

What does HIV1/2 target?

A

THCs

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5
Q

How is HIV transmitted?

A

blood and sexual contact, crosses placenta

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6
Q

What does the latent period of HIV/AIDS present with?

A

No symptoms, lymphatics damaged, recurrent respiratory infections, fatigue

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7
Q

What is the ELISA test?

A

enzyme linked immunosorbent assay
Measures Abs against HIV
Not all those with a positive result have HIV as viral proteins of HIV can be similar to those of other viruses

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8
Q

If ELISA is positive, what test is done next?

A

Western Blot Assay

measures Abs against specific Ag on HIV

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9
Q

What is PCR and what does it measure?

A

Polymerase chain reaction, measures viral RNA

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10
Q

What is P24-Ag?

A

Test measuring viral proteins released by HIV

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11
Q

What are some respiratory, NS, and CAs that occur with AIDS?

A

TB/pneumonia
encephalopathy, dementia
Kaposi’s sarcoma, non hodgkins lymphoma, cervical CA

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12
Q

What is Kaposi’s sarcoma?

A

lesions in skin, mouth, arises in endothelial cells of BVs

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13
Q

What kinds of antivirals are given to those with AIDS?

A

Antiretrovirals

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14
Q

What are 2 ways to diagnose AIDS?

A

1+ opportunistic infection/CA+ low CD4

OR

20+ opportunistic infections/CAs

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15
Q

Dermatoses are caused by which agents?

A

Exogenous and endogenous agents

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16
Q

What 2 characteristics of dermatoses?

A

Epidermal edema and separation of epidermal cells

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17
Q

Allergic contact dermatitis et

Where does it present?

A

T4HS

Anywhere in body

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18
Q

Irritant contact dermatitis et. What subcategories?

A

Caused by chemicals that irritate skin. Can be subjective, acute, chronic, or chemical burns

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19
Q

What causes atopic eczema? Where does it occur?

A

Ig-E mediated HS (T1HS)

Anywhere on body, doesn’t have to have been in contact with the allergen

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20
Q

Et of nummular eczema? Chronic or acute?

A

idiopathic, chronic

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21
Q

What 2 bacteria cause cellulitis?

A

strep progenies, staph aureus

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22
Q

What layers does cellulitis affect? Parts of body?

A

Dermis and SC, legs, hands, pinna

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23
Q

4 Complications from cellulitis?

A

lymphangitis, gangrene, sepsis, abscess

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24
Q

Et psoriasis

A

genetic susceptibility, autoimmunity

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25
Q

3 Points patho psoriasis

A

Accelerated epidermal cell cycle
T cell autoimmunity response triggered by trauma = mediators released = stimulation of abnormal keratinocyte AND BV growth
patterns of remission and exacerbation

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26
Q

Why does nail dystrophy and pitting occur in psoriasis?

A

abnormal keratinocytes

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27
Q

What is a complication from psoriasis?

A

psoriatic arthritis of the distal joints

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28
Q

What does vit D do for those with psoriasis?

A

modulates Kcytes and regulates T cells

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29
Q

What immunosuppressive drug can be given for psoriasis?

A

cyclosporine

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30
Q

What is the pre CA skin lesion called for skin CA?

A

actinic keratosis

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31
Q

What is skin CA prevalence proportional and inversely proportional to?

A

Age, melanin content

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32
Q

What cell origin is basal call carcinoma?

A

Basal cell of the epidermis

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33
Q

What 3 factors lead to a good prognosis in basal cell carcinoma?

A

No mets, slow advancement, uniform lesion

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34
Q

Where do the lesions in basal cell carcinoma occur?

A

On exposed areas

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35
Q

What is the origin of squamous cell carcinoma?

A

epidermal keratinocyte origin

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36
Q

Why is squamous CC hard to diagnose?

A

Poorly defined and variable lesions

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37
Q

What is the origin of malignant melanoma?

A

melanocyte

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38
Q

Where are the lesions in malignant melanoma?

A

exposed and unexposed areas

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39
Q

What is osteoporosis?

A

Loss of compact bone, porous bone

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40
Q

Et OP

A

ageing, genetic predisposition, endocrine changes

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41
Q

Why do post menopausal women have a high risk of having OP?

A

lowered E levels = less E to limit bone breakdown

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42
Q

3 mnfts OP

A

change in stature, breathing problems, dentition issues

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43
Q

Bone density scan. Values and what they mean

A

T = 1 - 2 1/2

Closer to 1 = more porous

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44
Q

2 drugs and their target cells for OP

A 
antiresorptive agents (osteoclasts)
anabolic agents (osteoblasts)
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45
Q

What kind of tissue does the autoimmune response in Rheumatoid Arthritis target?

A

Connective tissue

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46
Q

The CT targeting in Rheumatoid Arthritis has a pattern. What is it?

A

Begins in non weight bearing joints and then progresses to CT of heart, BVs, skin, lung, eyes

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47
Q

What leads to the release of cytokines in OA?

A

chondrocytes altered and they release them

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48
Q

What does the cytokine release in OA trigger? The effect?

A

release of proteases which cause destruction of cartilage

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49
Q

Why does sclerosis of bone occur in OA? What is the compensation?

A

Bone makes contact with bone as the cartilage deteriorates.

Subchondral bone increases in density

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50
Q

When fluid enters the cracks in the bone in OA what forms?

A

Cysts and fissures

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51
Q

What are osteophytes? What is their effect on joints?

A

abnormal formations in osteoarthritis. Leads to Joint enlargement and deformity

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52
Q

What are cox 2 inhibitors and what do they aim to treat?

A

cycloxygenase-enzyme inhibitors. They inhibit the cox 2 effects of inflammation and PG formation.

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53
Q

What steroid injection is given for severe cases of OA?

A

intraairticular steroid injections

54
Q

What is RA?

A

chronic autoimmune connective

55
Q

What is the difference between osteoarthritis and rheumatoid arthritis

A

OA

  • degenerative joint disease
  • WEIGHT BEARING JOINTS
  • chondrocytes are main sources of destruction
  • sclerosis of bone & osteophytes

RA

  • autoimmune joint disease
  • AI targets connective tissue
  • NON WEIGHT BEARING JOINTS
  • T & B cell mediated destruction
  • targeting of synovial membrane NOT cartilage
56
Q

What is the et for RA?

A

viral trigger and genetic predisposition (autoimmunity)

57
Q

What do the T cells target in RA?

A

synovial membrane of non weight bearing joints

58
Q

Patho of B cells in RA. What kind of reaction is this?

A

B cells are altered, produce Abs (rheumatoid factors) which combine with Ags on membranes (RF+Ag), deposit on membrane = inflammation

T3HS

59
Q

What is a pannus? Which disease is it involved in?

A

vascular granulation tissu e

RA

60
Q

4 main points about the pannus formation in RA?

A
  • space occupying
  • releases destructive Es that destroy cartilage
  • contains inflammatory cells that release mediators
  • decreases joint mobility
61
Q

When does the stiffness occur in RA?

A

after inactivity

62
Q

What extraarticular parts of the body are targeted in RA?

A

Heart, BVs, skin, lungs, eyes

63
Q

What diagnostic test for RA?

A

RF measurement

64
Q

What drug can be given to limit progression of RA?

A

Plaque nil

65
Q

What can be given for pain for RA?

A

meloxicam
naproxin
NSAIDs
Sulfasalazine + methotrexate

66
Q

What is the main problem in gout?

A

price acid crystals deposition in joints

67
Q

Primary gout is..

A

usually in men, metabolic problem

68
Q

Secondary gout is due to

A

cell destruction, leukaemia, renal problems, chemotherapy

69
Q

What is uric acid soluble and insoluble in?

A

S: blood
IS: synovial fluid

70
Q

What are the purines?

A

adenine and guanine

71
Q

What are the pyrimidines?

A

cytosine, thiamine, and uracil (RNA only)

72
Q

Altered purine metabolism leads to what in gout?

A

Asymptomatic hyperuricemia

73
Q

When uric acid enters the joints in gout, what happens?

A

Crystals deposit in synovial joints, leukocytes come, phagocytize, and die. When they die, they lyse and release enzymes which cause inflammatory damage

74
Q

What leads to tophi formation? What is it?

A

Recurrent acute attacks, a lesion of uric acid

75
Q

5 stages of gout

A
  1. asymptomatic hyperuricemia
  2. acute inflammation
  3. subsides in 1 week
  4. asymptomatic hyperuricemia
  5. recurrent attack to more joints leading to permanent damage
76
Q

In the acute inflammation phase of gout, when and where does it occur? Why?

A

overnight (decreased P, inactivity)

1 joint, BTJ (colder as it is disease)

77
Q

Why is beer a trigger for the acute inflammatory gout attack?

A

Beer is high in purines. When purines are broken down, so are the proteins that make up those nitrogenous bases. Those lead to the buildup of uric acid in the body

78
Q

Why would strenuous exercise bring about a gout attack?

A

This leads to ++ cell damage = increased protein breakdown = increased NWP = increased uric acid

79
Q

What kind of disease is SLE? What organ systems are affected?

A

chronic inflammatory and rheumatic disease

every system

80
Q

Who is SLE more common in?

A

females, african, hispanic and asian

81
Q

How does B cell hyperactivity play a part in the patho of SLE?

A

BCH = increased production of autoAbs.

These directly cause damage or combine with Ags to form damaging immune complexes

82
Q

What 2 harmful Abs are produced in SLE? What do they target?

A

antinuclear Abs and antiDNA Abs

blood and plasma proteins

83
Q

The development of autoAbs in SLE form from a combination of what factors?

A

genetics, hormonal, immunologic and environmental (UV, chemicals, food)

84
Q

What are protective factors against SLE? How does this affect the precedence?

A

Androgens.

This is why females have a higher incidence rate of SLE.

85
Q

What is a hormonal risk factor for SLE?

86
Q

9 symptoms of SLE

A 
arthritis
butterfly rash 
GN
nephrotic syndrome
pleural effusion/pleuritis
pericarditis
seizures
psychotic symptoms
low BCs
87
Q

What are some diagnostic tests for SLE? What is the most specific?

A

ANA test, CBC, antiDNA test (most specific)

88
Q

3 drug given for SLE

A

NSAIDs, corticosteroids, immunosuppressive drugs.

89
Q

What genes contribute to SLE?

A

HLA-DR and HLA-DQ

90
Q

What is MD?

A

SKELETAL Muschel degeneration

91
Q

What is pseudo hypertrophy?

A

Adipose tissue deposited in muscle

92
Q

What 4 things help determine the type of MD?

A

muscle group, age of onset, rate of progression, mode of inheritance

93
Q

Duchenne MD et

A

Recessive X-linked trait

94
Q

Where and what is the gene that contributes to Duchenne MD?

A

Gene on short arm of X chromosome

Codes for dystrophin

95
Q

What is dystrophin?

A

Membrane protein on muscle

Allows for attachment of contractile filaments

96
Q

Patho Duchenne MD

A

altered dystrophin = poor contractile protein attachment = fibre necrosis with use

poor repair and regeneration = further necrosis

membrane altered = Ca+ influx and enzyme release (CK_

Fibrofatty CT replaces muscle (pseudo hypertrophy)

97
Q

When do symptoms occur in MD?

A

after age 3

98
Q

What 2 systems are affected in MD

A

respiratory and cardiac

99
Q

2 Dx tests for MD? Pregnancy ones?

A

Serum CK, biopsy of muscle for pseudohypertriphy & dystrophin

carrier screening for mom, prenatal Dx screen

100
Q

Is primary or secondary bone CA more common?

101
Q

Where do primary bone CA tumors mostly originate from?

A

Metaphysis

102
Q

Most common primary sites for bone CA?

A

mandible, shoulder, spine, hips, knees

103
Q

Types of primary bone CA and the most common? (6)

A 
osteoscarcoma*
chondrosarcoma
Ewing sarcoma
Giant cell tumor 
fibrosarcoma 
osteoclastoma
104
Q

What does the neoplasm in osteosarcoma form?

105
Q

Where is the most common site for osteosarcoma?

A

Vicinity of the knee

106
Q

How aggressive is osteosarcoma?

A

Very. Mets to LUNG

107
Q

What age group does osteosarcoma affect?

108
Q

Where do secondary bone CAs originate from?

A

Lung, breast, prostate

109
Q

Why are the lesions in secondary bone CA both lytic and blastic?

A

L: malignant cells release destructive Es to breakdown surrounding tissue
B: must form the malignant bone tumor

110
Q

What is a complication from secondary bone CA?

111
Q

What are some surgical procedures for bone CA?

A

block excision and restorative grafting

112
Q

What is a fracture? Et?

A

BREAK IN THE CONTINUITY OF BONE

d/t force overload on bone

113
Q

Simple vs compound #

A 
simple = closed, skin intact
compound = open, # compromises skin
114
Q

Greenstick #

A

1 broken and 1 bent surface, usually in kids

115
Q

Pathologic #

A

d/t bone disorder e.g. OP

116
Q

Comminuted #

A

multiple breaks at 1 site, bone fragmented into smaller pieces, aka burst #

117
Q

Oblique #

A

break @ 45 degree angle, d/t twisting force

118
Q

Longitudinal #

A

longitudinal break line

119
Q

Burst #

A

bone breaks into multiple pics, usually at end of bone

120
Q

Chip #

A

small fragment near joint

121
Q

Displaced #

A

bone separates @ # line

122
Q

What soft tissue injuries are associated with #s?

A

muscle, tendons, ligaments, integument

123
Q

What manifestation is always associated with #? Part of healing

A

Hemorrhage

124
Q

What are some tx for #s

A

reduction (realigning bones)
immobilization
PT

125
Q

How long can bone healing take?

A

6 mo - 2 years

126
Q

4 phases of bone healing

A

hematoma formation
soft callus formation
bony callus stage
bone remodelling

127
Q

Hematoma formation

A

Hemorrhaging = hematoma formation
contains fibrous tissue which seals site
provides some alignment and framework for molecular cell signalling
necrosis of bone

128
Q

Soft Callus Formation

A

fibrocartilage, granulation tissue, angiogenesis, collagen

129
Q

Bony Callus Stage

A

Replacement of soft callus with spongey bone

Osteoclasts deposit spongey bone

130
Q

Bone Remodelling

A

Reshaping bone back to initial formation, removal of necrotic bone, spongey bone -> compact bone

Patho 2nd Semester (6 decks)

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