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

Pathoma 1: Growth and Immune stuff Flashcards

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
Q

What are Weible Palade bodies and what do they produce?

A

Produce P selectin and VWF

26
Q

How are E selectins promoted?

A

TNF and IL-1

27
Q

Chediak Higashi Syndrome
Defect.
Clinical Syndrome.

A

Lysosomal trafficking regulator gene –> microtubule problem.
Albinism, increased pyogenic infections, peripheral neuropathy, giant granules in leukocytes, defective primary hemostasis.

28
Q

Leukocyte adhesion deficiency
Inheritance.
Defect.
Clinical syndrome.

A

AR.
Decreased integrins (CD18 subunit)
Delayed umbilical cord separation, increased ciruclating PMNS, recurrent bacterial infections that lack purulence.

29
Q

Chronic Granulomatous Disease
Defect
Clinical syndrome
What test do you use?

A

NADPH Ox defect.
Catalase + bacteria infections. Staph a., Pseudomonas, Nocardia, Aspergilus
NBT test

30
Q

MPO Deficiency

A

Candida infections

NBT is normal

31
Q

What are the two ways B cells are activated?

A

1) Antigen binding to surface IgM or IgD

1) B cell presentation to MHC II and then 2) CD40L to CD40R

32
Q

Formation of granulomas. What cytokines are involved?

A

MO secrete IL-12 to activate TH1 cells.

TH1 cells secrete INF to activate histiocytes.

33
Q

Digeorge syndrome.
chromosome abnormality.
Clinical syndrome.

A

22q11

Thymus aplasia, no T cells, lack of parathyroids causes hypocalcemia, cardiac outlet? problems

34
Q

Severe Combined Immune Deficiency
Etiologies
Bugs
Tx

A

Adenosine deaminase deficiency, cytokine receptor defects, MHC class II deficiency.
Fungal, viral, bacterial, no live vaccines.
Tx: Stem cell transplant

35
Q

X-linked agammaglobulinemia
Defect.
infections

A

(Bruton Tyrosine Kinase)
bacterial infections (decreased opsonins like IgG), enterovirus (IgA), GIARDIA (IgA)
Note: presents after 6 mo old.

36
Q

Common variable immunodeficiency

A

Low levels of immunoglobulin because of either B or Th1

37
Q

IgA deficiency

A

associated with celiac

38
Q

Hyper IgM

A

Mutated CD40 or CD40L

39
Q

Wiskott Aldrich

What is the triad and the inheritance pattern?

A

Triad of Thrombocytopenia, eczema, Recurrent infections.

X-linked

40
Q

c5-c9 defiency

A

Neisseria infection

41
Q

C1 inhibitor deficiency

A

Hereditary angioedema, periorbital edema

42
Q

What are the antiapoptotic signals?

A

Bcl-2 and Bclx

43
Q

What are the proapoptotic signals?

A

Bak, Bax, Bim

44
Q

What cytokines to macrophages produce?

A

IL-1, IL6, IL8, IL12, TNFalpha

45
Q

What cytokines to T cells produce?

A

IL2, IL3

46
Q

What cytokines do TH1 cells produce?

A

INF

47
Q

What cytokines do TH2 cells produce?

A

IL4, IL5, IL10

48
Q

Where are the stem cells of bowel?

A

Mucosal crypts

49
Q

Keloid has what type of collage?

A

Type III collagen excess.

50
Q

What surface markers do regulatory T cells express?

What can mutations of these manifest as?

A

CD4+ (associated with MS, TIDM)
CD25+ which is IL-2R
Fox P3 (Immune dysfuction polyendocrinopathy, enteropathy, xlinked IPEX)

51
Q

AIRE gene significance and defect?

A

Autoimmune polyendocrine syndrome.

Triad of hypoparathyroidism, adrenal insufficiency, candida infection

52
Q

What is Leibman Sachs endocarditis

A

You will see vegetations on boths ides of mitra vale. This is associated with Lupus

53
Q

What are the three anti-phospholipid antibodies of lupus?

A

Anti cardiolipin
Lupus anticoagulant
AntiB2 glycoprotein

54
Q

What cancer does Sjogren’s put you at risk for?

A

B cell lymphoma

55
Q

What does CREST stand for?

A

Calcinosis, Raynaud’s, Esophogeal dysmotility, Sclerodactyly, Telangiectasias

56
Q

What is Type I collagen in?

A

Bone

57
Q

What is Type II collagen in?

A

Cartilage

58
Q

What is type III collagen in?

A

Blood vessels, Granulation tissue

59
Q

What is type IV collagen in?

A

Basement membrane

60
Q

Malignant cells in an amyloid stroma?

A

Medullary carcinoma of the thyroid

STEP One (20 decks)

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