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STEP One > Pathoma 1: Growth and Immune stuff > Flashcards

Pathoma 1: Growth and Immune stuff Flashcards

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1
Q

What are the permanent tissues that only undergo hypertrophy?

A

Skeletal muscle, Cardiac muscle, and Nerves

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2
Q

Osteoblastic bone metastasis

A

prostate cancer, small cell lung ca, hodgkin lymphoma

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3
Q

What symptoms for CO poisoning?

A

Cherry red appearance, confusion.

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4
Q

How to treat CO poisoning?

A

100% O2

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5
Q

How to treat methemoglobinemia

A

methylene blue

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6
Q

What are the irreversible signs of ischemic injury?

A

Membrane damage (plasma, mitochondria, lysosome)

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7
Q

When do you see calcium saponification?

A

Fat necrosis: trauma to fat and fatty acids are released. Can get dystrophic calcification.

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8
Q

What is the outcome of malignant hypertension?

A

Fibrinoid necrosis

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9
Q

What are the causes of fibrinoid necrosis

A

malignant hypertension and vasculitis

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10
Q

Draw the Apoptosis pathways. What are the different pathways and how are they activated? What do they all converge on?

A

Intrinsic: Release of Cytochrome C from the mitochondria is sensed and prevented by Bcl-2. –> Caspases
Extrinsic: FasL on T cells binds FAS R (CD95). Or TNF binds TNF R on target.
CD8 Tcell pathway: Perforins/Granzyme

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11
Q

What are the avenues of free radial injury?

A 
Cytochrome C oxidase (during oxphos)
Ionizing radiation
Inflammation, 
Metals
Acetaminophen (decreased glutathione) 
Carbon Tetrachloride (metabolized by P450, causes decreased apolipoproteins, then fat accumulation--> fatty change in liver)
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12
Q

What are the two types of systemic amyloid protein deposition?

A

Primary: AL from iG light change and is associated with plasma cell dyscrasias (MGUS, MM, Waldenstroms)
Secondary: AA from SAA, which is an acute phase reactant. Associated with chronic inflammatory state or familial mediteranean fever (episodes of fever, serosal inflammation)

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13
Q

When do you suspect and how can you diagnose systemic amyloid deposition?

A

Nephrotic syndrome, Restrictive cardiomyopathy, HSM, tongue enlargement

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14
Q

What are some manifestation of amyloid deposition in tissues?

A

Senile cardiac amyloidosis, NIDDM, Alzheimer’s (AB amyloid on chromosome 21), Dialysis associated (B2 microblogin in joints), Medullary carcinoma of thyroid (C-Cells- tumor cells in amyloid background)

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15
Q

Draw the aracondonic acid pathway? What are the two enzymes that control the first branch?

A

COX: makes prostaglandins which vasodilate, increase permeability in post cap venule. PGE2 produces Fever and Pain.

5-Lipooxygenase: makes Leukotrienes. LTB4 attracts PMNs. LTC4, D4, E4 produce vasoconstriction, bronchospasm, and increase vascular permeability

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16
Q

What attracts PMNs?

A

C5a, LTB4, Bacterial products, IL8

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17
Q

How are Mast cells activated?

A

1) C3a/C5a
2) Cross-linking of IgE by antigen
3) Tissue trauma

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18
Q

What are the immediate and delayed activities of mast cells

A

1) Histamine degranulation

2) Produces aracodonic acid derivatives, particularly leukotrienes

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19
Q

What complements trigger mast cells?

A

C3a and C5a

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20
Q

What complement recruits neutrophils?

A

C5a

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21
Q

What complement serves as an opsonin for phagocytosis?

A

C3b

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22
Q

Where is Hageman factor produced and how is it activated?

A

By the liver and by the endothelium

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23
Q

What does Hageman factor do?

A

It activates coagulation/fibrin, complement, and the kinin system

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24
Q

How does fever work?

A

Macrophages release IL-1 and TNF which promotes hypothalamus to increase COX activity and increase PGE2 levels.

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25
What are Weible Palade bodies and what do they produce?
Produce P selectin and VWF
26
How are E selectins promoted?
TNF and IL-1
27
Chediak Higashi Syndrome Defect. Clinical Syndrome.
Lysosomal trafficking regulator gene --> microtubule problem. Albinism, increased pyogenic infections, peripheral neuropathy, giant granules in leukocytes, defective primary hemostasis.
28
Leukocyte adhesion deficiency Inheritance. Defect. Clinical syndrome.
AR. Decreased integrins (CD18 subunit) Delayed umbilical cord separation, increased ciruclating PMNS, recurrent bacterial infections that lack purulence.
29
Chronic Granulomatous Disease Defect Clinical syndrome What test do you use?
NADPH Ox defect. Catalase + bacteria infections. Staph a., Pseudomonas, Nocardia, Aspergilus NBT test
30
MPO Deficiency
Candida infections | NBT is normal
31
What are the two ways B cells are activated?
1) Antigen binding to surface IgM or IgD | 1) B cell presentation to MHC II and then 2) CD40L to CD40R
32
Formation of granulomas. What cytokines are involved?
MO secrete IL-12 to activate TH1 cells. | TH1 cells secrete INF to activate histiocytes.
33
Digeorge syndrome. chromosome abnormality. Clinical syndrome.
22q11 | Thymus aplasia, no T cells, lack of parathyroids causes hypocalcemia, cardiac outlet? problems
34
Severe Combined Immune Deficiency Etiologies Bugs Tx
Adenosine deaminase deficiency, cytokine receptor defects, MHC class II deficiency. Fungal, viral, bacterial, no live vaccines. Tx: Stem cell transplant
35
X-linked agammaglobulinemia Defect. infections
(Bruton Tyrosine Kinase) bacterial infections (decreased opsonins like IgG), enterovirus (IgA), GIARDIA (IgA) Note: presents after 6 mo old.
36
Common variable immunodeficiency
Low levels of immunoglobulin because of either B or Th1
37
IgA deficiency
associated with celiac
38
Hyper IgM
Mutated CD40 or CD40L
39
Wiskott Aldrich | What is the triad and the inheritance pattern?
Triad of Thrombocytopenia, eczema, Recurrent infections. | X-linked
40
c5-c9 defiency
Neisseria infection
41
C1 inhibitor deficiency
Hereditary angioedema, periorbital edema
42
What are the antiapoptotic signals?
Bcl-2 and Bclx
43
What are the proapoptotic signals?
Bak, Bax, Bim
44
What cytokines to macrophages produce?
IL-1, IL6, IL8, IL12, TNFalpha
45
What cytokines to T cells produce?
IL2, IL3
46
What cytokines do TH1 cells produce?
INF
47
What cytokines do TH2 cells produce?
IL4, IL5, IL10
48
Where are the stem cells of bowel?
Mucosal crypts
49
Keloid has what type of collage?
Type III collagen excess.
50
What surface markers do regulatory T cells express? | What can mutations of these manifest as?
CD4+ (associated with MS, TIDM) CD25+ which is IL-2R Fox P3 (Immune dysfuction polyendocrinopathy, enteropathy, xlinked IPEX)
51
AIRE gene significance and defect?
Autoimmune polyendocrine syndrome. | Triad of hypoparathyroidism, adrenal insufficiency, candida infection
52
What is Leibman Sachs endocarditis
You will see vegetations on boths ides of mitra vale. This is associated with Lupus
53
What are the three anti-phospholipid antibodies of lupus?
Anti cardiolipin Lupus anticoagulant AntiB2 glycoprotein
54
What cancer does Sjogren's put you at risk for?
B cell lymphoma
55
What does CREST stand for?
Calcinosis, Raynaud's, Esophogeal dysmotility, Sclerodactyly, Telangiectasias
56
What is Type I collagen in?
Bone
57
What is Type II collagen in?
Cartilage
58
What is type III collagen in?
Blood vessels, Granulation tissue
59
What is type IV collagen in?
Basement membrane
60
Malignant cells in an amyloid stroma?
Medullary carcinoma of the thyroid

STEP One (20 decks)

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