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Flashcards in General Path Deck (50)
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1
Q

What is aplasia vs hypoplasia?

A

Aplasia is a lack of cell production in embryogenesis. (absent organs)
Hypoplasia is decreased cell production in embryogenesis (smaller organs)

2
Q

3 general causes of hypoxia

A

Ischemia
Hypoxemia
Decreased O2 carrying capacity

3
Q

What is Methemoglobinemia?

A

When iron in the Hb is oxidized to Fe3+ which cannot bind oxygen
(treatment is methylene blue to get Iron back to Fe2+)

4
Q

Hallmark of reversible cell injury

A

Cell Swelling

5
Q

Hallmark of irreversible cell injury

A

Membrane Damage

6
Q

How does irreversible cell injury result in apoptosis

A

Membrane damage occurs to the mitochondria in the cell which leads to leakage of Cytochrome c and activation of apoptotic enzymes

7
Q

List the 3 nuclear changes that occur in cell death.

A

Pyknosis: condensation (shrinks)
Karyorrhexis: Fragmentation
Karylolysis: dissolution (fading)

8
Q

Necrosis where the tissue is firm and architecture is maintained. Usually due to infarction, pale area.

A

Coagulative necrosis

9
Q

Type of necrosis in brain infarction

A

Liquefactive

10
Q

Coagulative necrosis that resembles mummified tissue.

A

Gangrenous Necrosis

11
Q

Cottage-cheese like appearance necrosis

A

Caseous Necrosis

12
Q

Combination of coagulative and liquifactive necrosis.

A

Caseous necrosis

13
Q

Necrotic damage to blood vessel walls

A

Fibrinoid Necrosis

14
Q

3 enzymes that reduce the amount of free radicals in the body.

A

Superoxide dismutase
Glutathione Peroxidase
Catalase

15
Q

Mechanism of Reperfusion Injury.

A

Ishcemia to a region of tissue causes cell injury. Immediate return of blood to the area brings accumulated oxygen free radicals in high concentration which further damage the tissue.

16
Q

Congo Red Staining with Apple Green birefringence.

A

Amyloidosis: misfolded proteins (from Ig light chains) that deposit in extracellular space

17
Q

Most common organ involved in amyloidosis

A

Kidney: nephrotic syndrome

can also have restrictive cardiomyopathy, or tongue enlargement

18
Q

Arachidonic acid metabolite that mediates pain.

A

PGE2

  • produced from arachidonic acid by COX enzymes
  • primary thing ASA tries to prevent from forming
19
Q

Arachidonic Acid metabolite that is chemotactic

A

LTB4

-made from lipoxygenase enzymes

20
Q

Major mediator from mast cells and what it does.

A

Histamine: increased vascular permeability, vasodilation of arterioles

21
Q

Activators of classical complement pathway

A

IgG and IgM

22
Q

Activators of the alternative complement pathway

A

Microbial products

23
Q

2 complement anaphylatoxins

A

C3a

C5a

24
Q

Complement that is chemotactic for neutrophils

A

C5a

25
Q

Complement that opsonizes bacteria

A

C3b

26
Q

2 inflammatory mediators that induce pain

A

Bradykinin and PGE2

27
Q

2 pyrogen mediators

A

IL-1

TNF

28
Q

Lymphocyte receptor on all T cells for antigen surveillance.

A

CD3

29
Q

Lymphocyte receptor on helper T cells

A

CD4 (recognizes MHCII)

30
Q

Lymphocyte receptor on cytotoxic T cells

A

CD8 (recognizes MHC I)

31
Q

Cells that have MHCII

A

Any antigen presenting cells (APCs)

-usually macrophages, monocytes, dendritic cells, Langerhans cells

32
Q

Cells that have MHCI

A

Any nucleated cells

33
Q

Describe the two types of T helper cells and what each does.

A
Th1: secretes IL-2 for T cells growth
Th2: secretes IL-4 for  Ab class switching, IL-5 for eosinophil chemotaxis and class switching to IgA
34
Q

Mechanism of granulomatous inflammation. (3 steps)

A
  1. Antigen detected by macrophages and is presented to helper T cells on MHCII
  2. Macrophages also secrete IL-12 which makes CD4 cells turn into Th1 cells
  3. Th1 cells secrete INF-gamma converted macrophages into epitheliod histiocytes and giant cells
35
Q

Patient presents with severe susceptibility to fungal, viral,bacterial, protozoan, and opportunistic infections. Treatment is isolation. Describe the problem.

A

SCID

  • cytokine receptor defect
  • adenosine deaminase deficiency
  • MHC II deficiency
36
Q

6 month old baby presents with recurrent bacterial, viral, and Giardia infection. Describe the pathogenesis.

A

X-linked agammaglobulinemia

-mutated Bruton Tyrosine Kinase

37
Q

Patient presents with recurrent viral pharyngitis, nasal infections, conjunctivitis.

A

IgA deficiency

-many mucosal infections

38
Q

Patient develops no Long-term immunity to previously acquired diseases, is able to fight them off in acute states however. What is the pathogenesis.

A

Hyper IgM syndrome

  • Either CD40L mutation on CD4 cells or CD40 mutation on B cells
  • inability to class switch
39
Q

Patient has Thrombocytopenia, eczema, and recurrent infections.

A

Wiskott Aldrich Syndrome

-WASP gene mutation

40
Q

Patient keeps getting N. meningitides infections.

A

Complement deficiency in C5-C9 preventing MAC formation

41
Q

Complement deficiency that results in hereditary angioedema.

A

C1 inhibitor deficiency

-C1 is overactive and creates increased vascular permeability most noticeably at mucosal areas leading to swelling

42
Q

Patient presents with arthritis, rash across the nose and cheeks, and hematuria. What tests would be positive?

A

SLE

-ANA, anti-dsDNA

43
Q

Patient is positive for Antihistone Abs causing SLE symptoms. What is most likely the cause?

A

Drug-Induced: procainamide, hydralazine, isoniazid

44
Q

Patient presents with keratoconunctivitis, zerostomia and recurrent dental carries. What type of Hypersensitivity is this?

A

Sjogren Syndrome

-Type IV: lymphocyte mediated, delayed

45
Q

Patient presents with trouble swallowing, little white nodules on the fingers, and stiff fingers.

A

Scleroderma

-CREST syndrome: calcinosis, raynauds, esophageal dismotility, sclerodactyly, telangiectasia

46
Q

When does repair occur vs. regeneration?

A

Regeneration is mainly in labile cells. However, whenever the regenerative stem cells are damaged, replacement of fibrotic scar tissue occurs.

47
Q

Hallmark of tissue repair and its composition

A

Granulation Tissue

-type III collagen

48
Q

Main two tumor suppressor genes and how they regulate the cell cycle.

A

p53: regulates G1 to S phase
Rb: regulates G1 to S phase (E2F transcription factor)

49
Q

Function of the Bcl gene in apoptosis.

A

Stabilizes the mitochondrial membrane. If Bcl2 is damaged, the apoptotic pathway progresses. In certain cancers, Bcl2 is over-expressed and even if a cell is cancerous it doesn’t undergo apoptosis because the Bcl2 doesn’t let it.

50
Q

How do tumors invade and spread? (4 steps)

A
  1. Downregulation of E-cadherin allows dissolution of cells to one another
  2. Attachment to laminin destroys the basement membrane so the cells can invade.
  3. Cells attach to fibronectin in the ECM
  4. Cells enter lymph or blood and spread