Remaining Patho Flashcards
(130 cards)
1
Q
Being immunocompromised in AIDS allows for what to occur
A
Opportunistic infections and cancers
2
Q
What kind of virus is HIV?
A
retrovirus, converts RNA -> DNA (reverse transcription)
3
Q
What is CD4?
A
Surface receptor on THCs
4
Q
What does HIV1/2 target?
A
THCs
5
Q
How is HIV transmitted?
A
blood and sexual contact, crosses placenta
6
Q
What does the latent period of HIV/AIDS present with?
A
No symptoms, lymphatics damaged, recurrent respiratory infections, fatigue
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
8
Q
If ELISA is positive, what test is done next?
A
Western Blot Assay
measures Abs against specific Ag on HIV
9
Q
What is PCR and what does it measure?
A
Polymerase chain reaction, measures viral RNA
10
Q
What is P24-Ag?
A
Test measuring viral proteins released by HIV
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
12
Q
What is Kaposi’s sarcoma?
A
lesions in skin, mouth, arises in endothelial cells of BVs
13
Q
What kinds of antivirals are given to those with AIDS?
A
Antiretrovirals
14
Q
What are 2 ways to diagnose AIDS?
A
1+ opportunistic infection/CA+ low CD4
OR
20+ opportunistic infections/CAs
15
Q
Dermatoses are caused by which agents?
A
Exogenous and endogenous agents
16
Q
What 2 characteristics of dermatoses?
A
Epidermal edema and separation of epidermal cells
17
Q
Allergic contact dermatitis et
Where does it present?
A
T4HS
Anywhere in body
18
Q
Irritant contact dermatitis et. What subcategories?
A
Caused by chemicals that irritate skin. Can be subjective, acute, chronic, or chemical burns
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
20
Q
Et of nummular eczema? Chronic or acute?
A
idiopathic, chronic
21
Q
What 2 bacteria cause cellulitis?
A
strep progenies, staph aureus
22
Q
What layers does cellulitis affect? Parts of body?
A
Dermis and SC, legs, hands, pinna
23
Q
4 Complications from cellulitis?
A
lymphangitis, gangrene, sepsis, abscess
24
Q
Et psoriasis
A
genetic susceptibility, autoimmunity
25
3 Points patho psoriasis
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
26
Why does nail dystrophy and pitting occur in psoriasis?
abnormal keratinocytes
27
What is a complication from psoriasis?
psoriatic arthritis of the distal joints
28
What does vit D do for those with psoriasis?
modulates Kcytes and regulates T cells
29
What immunosuppressive drug can be given for psoriasis?
cyclosporine
30
What is the pre CA skin lesion called for skin CA?
actinic keratosis
31
What is skin CA prevalence proportional and inversely proportional to?
Age, melanin content
32
What cell origin is basal call carcinoma?
Basal cell of the epidermis
33
What 3 factors lead to a good prognosis in basal cell carcinoma?
No mets, slow advancement, uniform lesion
34
Where do the lesions in basal cell carcinoma occur?
On exposed areas
35
What is the origin of squamous cell carcinoma?
epidermal keratinocyte origin
36
Why is squamous CC hard to diagnose?
Poorly defined and variable lesions
37
What is the origin of malignant melanoma?
melanocyte
38
Where are the lesions in malignant melanoma?
exposed and unexposed areas
39
What is osteoporosis?
Loss of compact bone, porous bone
40
Et OP
ageing, genetic predisposition, endocrine changes
41
Why do post menopausal women have a high risk of having OP?
lowered E levels = less E to limit bone breakdown
42
3 mnfts OP
change in stature, breathing problems, dentition issues
43
Bone density scan. Values and what they mean
T = 1 - 2 1/2
| Closer to 1 = more porous
44
2 drugs and their target cells for OP
```
antiresorptive agents (osteoclasts)
anabolic agents (osteoblasts)
```
45
What kind of tissue does the autoimmune response in Rheumatoid Arthritis target?
Connective tissue
46
The CT targeting in Rheumatoid Arthritis has a pattern. What is it?
Begins in non weight bearing joints and then progresses to CT of heart, BVs, skin, lung, eyes
47
What leads to the release of cytokines in OA?
chondrocytes altered and they release them
48
What does the cytokine release in OA trigger? The effect?
release of proteases which cause destruction of cartilage
49
Why does sclerosis of bone occur in OA? What is the compensation?
Bone makes contact with bone as the cartilage deteriorates.
Subchondral bone increases in density
50
When fluid enters the cracks in the bone in OA what forms?
Cysts and fissures
51
What are osteophytes? What is their effect on joints?
abnormal formations in osteoarthritis. Leads to Joint enlargement and deformity
52
What are cox 2 inhibitors and what do they aim to treat?
cycloxygenase-enzyme inhibitors. They inhibit the cox 2 effects of inflammation and PG formation.
53
What steroid injection is given for severe cases of OA?
intraairticular steroid injections
54
What is RA?
chronic autoimmune connective
55
What is the difference between osteoarthritis and rheumatoid arthritis
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
What is the et for RA?
viral trigger and genetic predisposition (autoimmunity)
57
What do the T cells target in RA?
synovial membrane of non weight bearing joints
58
Patho of B cells in RA. What kind of reaction is this?
B cells are altered, produce Abs (rheumatoid factors) which combine with Ags on membranes (RF+Ag), deposit on membrane = inflammation
T3HS
59
What is a pannus? Which disease is it involved in?
vascular granulation tissu e
| RA
60
4 main points about the pannus formation in RA?
- space occupying
- releases destructive Es that destroy cartilage
- contains inflammatory cells that release mediators
- decreases joint mobility
61
When does the stiffness occur in RA?
after inactivity
62
What extraarticular parts of the body are targeted in RA?
Heart, BVs, skin, lungs, eyes
63
What diagnostic test for RA?
RF measurement
64
What drug can be given to limit progression of RA?
Plaque nil
65
What can be given for pain for RA?
meloxicam
naproxin
NSAIDs
Sulfasalazine + methotrexate
66
What is the main problem in gout?
price acid crystals deposition in joints
67
Primary gout is..
usually in men, metabolic problem
68
Secondary gout is due to
cell destruction, leukaemia, renal problems, chemotherapy
69
What is uric acid soluble and insoluble in?
S: blood
IS: synovial fluid
70
What are the purines?
adenine and guanine
71
What are the pyrimidines?
cytosine, thiamine, and uracil (RNA only)
72
Altered purine metabolism leads to what in gout?
Asymptomatic hyperuricemia
73
When uric acid enters the joints in gout, what happens?
Crystals deposit in synovial joints, leukocytes come, phagocytize, and die. When they die, they lyse and release enzymes which cause inflammatory damage
74
What leads to tophi formation? What is it?
Recurrent acute attacks, a lesion of uric acid
75
5 stages of gout
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
In the acute inflammation phase of gout, when and where does it occur? Why?
overnight (decreased P, inactivity)
| 1 joint, BTJ (colder as it is disease)
77
Why is beer a trigger for the acute inflammatory gout attack?
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
Why would strenuous exercise bring about a gout attack?
This leads to ++ cell damage = increased protein breakdown = increased NWP = increased uric acid
79
What kind of disease is SLE? What organ systems are affected?
chronic inflammatory and rheumatic disease
| every system
80
Who is SLE more common in?
females, african, hispanic and asian
81
How does B cell hyperactivity play a part in the patho of SLE?
BCH = increased production of autoAbs.
| These directly cause damage or combine with Ags to form damaging immune complexes
82
What 2 harmful Abs are produced in SLE? What do they target?
antinuclear Abs and antiDNA Abs
| blood and plasma proteins
83
The development of autoAbs in SLE form from a combination of what factors?
genetics, hormonal, immunologic and environmental (UV, chemicals, food)
84
What are protective factors against SLE? How does this affect the precedence?
Androgens.
| This is why females have a higher incidence rate of SLE.
85
What is a hormonal risk factor for SLE?
Estrogen
86
9 symptoms of SLE
```
arthritis
butterfly rash
GN
nephrotic syndrome
pleural effusion/pleuritis
pericarditis
seizures
psychotic symptoms
low BCs
```
87
What are some diagnostic tests for SLE? What is the most specific?
ANA test, CBC, antiDNA test (most specific)
88
3 drug given for SLE
NSAIDs, corticosteroids, immunosuppressive drugs.
89
What genes contribute to SLE?
HLA-DR and HLA-DQ
90
What is MD?
SKELETAL Muschel degeneration
91
What is pseudo hypertrophy?
Adipose tissue deposited in muscle
92
What 4 things help determine the type of MD?
muscle group, age of onset, rate of progression, mode of inheritance
93
Duchenne MD et
Recessive X-linked trait
94
Where and what is the gene that contributes to Duchenne MD?
Gene on short arm of X chromosome
| Codes for dystrophin
95
What is dystrophin?
Membrane protein on muscle
| Allows for attachment of contractile filaments
96
Patho Duchenne MD
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
When do symptoms occur in MD?
after age 3
98
What 2 systems are affected in MD
respiratory and cardiac
99
2 Dx tests for MD? Pregnancy ones?
Serum CK, biopsy of muscle for pseudohypertriphy & dystrophin
carrier screening for mom, prenatal Dx screen
100
Is primary or secondary bone CA more common?
Secondary
101
Where do primary bone CA tumors mostly originate from?
Metaphysis
102
Most common primary sites for bone CA?
mandible, shoulder, spine, hips, knees
103
Types of primary bone CA and the most common? (6)
```
osteoscarcoma*
chondrosarcoma
Ewing sarcoma
Giant cell tumor
fibrosarcoma
osteoclastoma
```
104
What does the neoplasm in osteosarcoma form?
Bone
105
Where is the most common site for osteosarcoma?
Vicinity of the knee
106
How aggressive is osteosarcoma?
Very. Mets to LUNG
107
What age group does osteosarcoma affect?
108
Where do secondary bone CAs originate from?
Lung, breast, prostate
109
Why are the lesions in secondary bone CA both lytic and blastic?
L: malignant cells release destructive Es to breakdown surrounding tissue
B: must form the malignant bone tumor
110
What is a complication from secondary bone CA?
fractures
111
What are some surgical procedures for bone CA?
block excision and restorative grafting
112
What is a fracture? Et?
BREAK IN THE CONTINUITY OF BONE
| d/t force overload on bone
113
Simple vs compound #
```
simple = closed, skin intact
compound = open, # compromises skin
```
114
Greenstick #
1 broken and 1 bent surface, usually in kids
115
Pathologic #
d/t bone disorder e.g. OP
116
Comminuted #
multiple breaks at 1 site, bone fragmented into smaller pieces, aka burst #
117
Oblique #
break @ 45 degree angle, d/t twisting force
118
Longitudinal #
longitudinal break line
119
Burst #
bone breaks into multiple pics, usually at end of bone
120
Chip #
small fragment near joint
121
Displaced #
bone separates @ # line
122
What soft tissue injuries are associated with #s?
muscle, tendons, ligaments, integument
123
What manifestation is always associated with #? Part of healing
Hemorrhage
124
What are some tx for #s
reduction (realigning bones)
immobilization
PT
125
How long can bone healing take?
6 mo - 2 years
126
4 phases of bone healing
hematoma formation
soft callus formation
bony callus stage
bone remodelling
127
Hematoma formation
Hemorrhaging = hematoma formation
contains fibrous tissue which seals site
provides some alignment and framework for molecular cell signalling
necrosis of bone
128
Soft Callus Formation
fibrocartilage, granulation tissue, angiogenesis, collagen
129
Bony Callus Stage
Replacement of soft callus with spongey bone
| Osteoclasts deposit spongey bone
130
Bone Remodelling
Reshaping bone back to initial formation, removal of necrotic bone, spongey bone -> compact bone
