Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

STEP1 > Pathoma--Chapter 2 > Flashcards

Pathoma--Chapter 2 Flashcards

1
Q

what are the key mediators of pain?

A

PGE2 and bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the four cardinal signs of inflammation?

A
  1. redness-rubor & warmth calor
  2. swelling
  3. pain
  4. fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the mechanism behind redness in acute inflammation?

A

vasodilation and increased blood flow

  • mediated by prostaglandins, bradykinin, and histamine*
  • lead to vasodilation of the arteriole bed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the mechanism behind pain in acute inflammation?

A

sensitization of nerve endings

-caused by bradykinin and PGE2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what two things mediate pain in the inflammatory response?

A

PGE2 and bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the mechanism of fever?

A

macrophages release IL-1 & TNF–> perivascular cells of hypothalmaus ( increase in COX–> PGE2)
-increase in set point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 5 mediators of acute inflammation?

A
  1. TLR (toll-like receptors)
  2. Arachdonic acid metabolites
  3. Mast cells
  4. Complement
  5. Hagemen factor (Factor XII)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What factor is associated with DIC?

A

Hagemen factor (factor XII)
(inactive proinflammatory protein produced in liver that is activated upon exposure to subendothelial or tissue collagen)
-activates coagulation and fibrinolytic systems
-activates complement
-activates kinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is an inactive inflammatory protein produced in the liver?

A 
Hageman factor (factor XII)
-associated with DIC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What 3 ways is complement activated?

A
  1. classically
  2. alternative pathway
  3. mannose binding lectin pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the classic activation of complement?

A

C1 binds to IgG or IgM that is bound to antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the alternative activation of complement?

A

microbial produces directly activate complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does the MBL pathways activate complement?

A

MBL binds to mannose on microrganisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens once complement is activated?

A
  1. C3 convertase (C3–> C3a & C3b)
  2. C5 convertase ( C5–> C5a & C5b)
  3. C5b complezes with C6-C9 to form MAC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the fxn of C3a & C5a?

A

trigger mast cell degranulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is an additional fxn of C5a?

A

chemotactic for neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the fxn of C3b?

A

opsonin for phagocytosis

-protein that tags things that neutrophils need to eat up!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the fxn of MAC?

A

MAC (membrane attack complex)

-lyses microbes by creating holes in the cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What 3 things activate mast cells?

A
  1. tissue trauma
  2. complement proteins C3a & C5a
  3. Cross linking of cell surface IgE by antigen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the 4 key mediators that attract and activate neutrophils?

A
  1. LTB4
  2. C5a
  3. IL-8
  4. bacterial products
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is arachadonic acid released from cell membranes?

A

phospholipaseA2

-two pathways–> enzymes cyclooxygenase (prostaglandins) OR 5-lipoxygenase (leukotrienes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What happens when a mast cell is activated?

A

release of preformed histamine

  • immediate response: vasodilation and increased vascular permeability
  • maintaince: production of leukotrienes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do prostaglandins do?

A

PGI2, PGD2, PGE2 –> mediate vasodilation and increased vascular permeability

-PGE2–also mediates pain and fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What do leukotrienes do?

A

mediate vasoconstriction, bronchospasm, increased vascular permeability
(2/2 to smooth muscle contraction)

  • LTC4, LTD4, LTE4
  • LTB4–attracts neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how are TLR activated?

A

PAMP (pathogen asoscated molecular patterns)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is CD14?

A

TLR that recognizes LPS (PAMP) on gram - bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does TLR activation cause?

A

upregulation of NF-KB (nuclear transcription factor)

-activates immune response genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Do TLR play a role in acute or chronic inflammation?

A

both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What chromsome mutation is associated with DiGeorge Syndrome?

A

22q11 microdeletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Developmental failure of the 3rd and 4th pharyngeal pouch leads to what immunodeficiency?

A

DiGeorge Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the presentation of DiGeorge syndrome?

A

things derived from 3/4 pharyngeal pouch

  • lack of thymus–T cell deficiency (problems fighting viruses & fungal infection)
  • lack of parathyroid–issues with Ca (hypocalcemia)
  • great vessels, lower face, superior aspect of heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What type of immune deficiency occurs in SCID?

A

both cell mediated (tcell) & humoral (B cell) immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are the etiologies of SCID?

A
  1. cytokine receptor defect
  2. adenosine deaminase deficiency
  3. MHC II deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

characteristics of SCID

what is the tx–temporary and long term

A
  • increased risk of opportunistic infections, fungal, parasitic, viral, and bacterial infection
  • avoid live vaccines
  • temporary measure: bubble baby!
  • long term tx: stem cell transplant–> now they can develop normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

X linked agammaglobuinemia is characterized by

A

complete lack of ig in blood

2/2 to defective B cell maturation–> plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is the mutation in X linked agammaglobuinemia?

A

bryton tryosine kinase mutation (BTK)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is the typical presentation of Xlinked agammaglobuinemia? what are these patients at risk for developing?

A

bacterial , enterovirus , giardia
IgG allows for opsonination
IgA protective against mucosal infections
typically presents after 6 mths

38
Q

CVID characterized by?

symptoms?

A

low immunoglobin
2/2 to B cell or helper T cell defect (both required to produce immunoglobin
-typically asymptomatic

39
Q

Patients with CVID are at increased risk for what as they get older?

A

autoimmune disease and lymphoma

40
Q

what three types of infections are people without immunoglobins (low Ig) at risk for developing?

A

bacterial, entervirus, giardia

41
Q

What is the most common cause of Ig deficiency?

A

IgA deficiency

42
Q

What does IgA protect you from?

A

mucosal infections–particuarly viral

43
Q

Patients with what GI disease commonly have IgA deficiency?

A

Celiac disease–low IgA

44
Q

hyper IgM syndrome is characterized by?

mutations in what leads to this disease?

A

characterized by too much IgM

2/2 to mutations in CD40

45
Q

Class switching is required to produce what Igs?

A

IgA, IgG, IgE

-pt will have high IgM

46
Q

Wiskott Aldrich syndrome characterized by triad of

It is caused by a defect in what protein?

A

thrombocytopenia (petechiae, gum bleeding)
ecezma
recurrent infections

2/2 to defect in Wiskott Aldrich syndrome protein (X linked)

47
Q

deficiencys in any complement C5-C9 they are at increased risk for developing what infections?

A

Neisseria

48
Q

deficiency in C1 inhibitor lead to

A

herediatry angioedema

-edma of skin and mucosal lining (particularly periorbital)

49
Q

what are the three types of tissues based on regenerative capabilities?

what are examples of each?

A
  • labile: bowel (SC in crypts), skin (SC in basal layer), bone marrow
  • stable: liver or proximal renal tubule
  • permanent: myocardium, skeletal muscle, neurons
50
Q

what is the difference between regeneration and repair?

A

regeneration: requires SC
repair: scar formation

51
Q

what is the inital tissue type in scar formation? what are the three things characteristically found in it?

A

granulation tissue

  • myofibroblasts
  • fibroblasts
  • blood vessels
52
Q

what type of collagen is granulation tissue compromised of?

A

type III

53
Q

which of the four types of collagen is strongest? where can each class of collagen classically be seen?

A

type I has high tensile strength (bone)
type II-cartiledge
type III-pliable (granulation tissue, embryonic tissue)
type IV-basement membrane

54
Q

what is the fxn of TGF-alpha?

A

epithelial and fibroblast growth factor

55
Q

what is the fxn of TGF-beta?

A

STOp inflammation and initate repair along with IL-10

-fibroblast growth factor

56
Q

fxn of PDGF

A

platlet derived growth factor

GF for endothelium, smooth muscle, and fibroblasts

57
Q

fxn of FGF

A

fibrobast growth factor
-angiogenesis
skeletal development

58
Q

fxn of VEGF

A

vascular endothelial growth factor

-angiogenesis

59
Q

what is the difference between primary and secondary intention wound healing?

A

1- realign the edges–ex) suturing

2- edges not reapproximated (space fills with granulation tissue–big scar, can contract 2/2 to myofibroblasts)

60
Q

what is the most common cause of delayed wound healing?

A

infection

61
Q

Deficiency of what three cofactors can independently cause delayed wound healing?

A 
vitamin C (cofactor in hydroxylation of proline-lysine in procollagen--neccessary for crosslinking)
Cu (cofactor for lysyl oxidase enzyme that plays a role in cross linking of collagen)
Zinc (cofactor for collagenase--replaces type III--> type I collagen)
62
Q

Hypertrophic scar is caused be excess of what type of collagen?

A

Type I

63
Q

Keloid is caused by excess of what type of collagen? what population is most at risk? where are they most commonly seen?

A

type III, AA, ear

64
Q

what population is at greatest risk of AI disease? why?

A

women of reproductive age

-increased estrogen–>decreased apoptosis

65
Q

what are the three types of self tolerance that are meant to protect against getting AI disease?

what three markers identify Treg?

A
  • central tolerance (occurs where lymphocytes generated)
  • peripheral tolerance
  • Treg (CD4, CD25, FOXP3)
66
Q

Patients with SLE can have damage to what layers of their heart?

A

ALL THREE

67
Q

Patients with SLE can develop Libman-Sacks endocarditis–what is this characterized by?

A

small vegetations on both sides of the mitral valve

68
Q

SLE is characterized by what type of HSR?

A

type III–ag/ab deposition in tissues–> complement activation and tissue destruction

69
Q

Pts with SLE typically have deficiencies in what part of the complement cascade?

A

early part of the classical complement cascade–helps remove ag/ab complexes and be taken up directly by macrophages or taken by erythrocytes to the spleen where they are then taken up by macrophages

70
Q

What characterizes a discoid rash?

A

circular, erythematous, scaling rash that can scar

71
Q

In SLE diffuse proliferative glomerulonephritis presents with…

A

nephritic syndrome

72
Q

In SLE membranous glomerulonephritis presents with

A

nephrotic syndrome

73
Q

What types of renal disease can patients with SLE develop?

A

both nephritis and nephrotic syndrome

74
Q

What ab are specific for lupus?

A

anti-dsDNA and anti-Sm

75
Q

Is antiphospholipid syndrome more commonly seen 2/2 to lupus or on its own?

A

on its own

76
Q

what are the three antiphospholipid ab?

A 
cardiolipin (false positive for VLDRL or RPR)
anti-B2 glycoprotein I
lupus anticoagulant (falsely elevated PTT)
77
Q

what ab is characteristic of drug induced lupus?

A

antihistone ab

78
Q

what drugs commonly cause drug induced lupus?

A

hydralazine, procainaminde, isoniazaid

79
Q

what ab are positive in patients with sjogren syndrome?

A

anti-SSA, anti-SSB (antiribonucletide)

80
Q

what other AI disease is sjogrens syndrome typically seen with?

A

RA

81
Q

which ab in sjogrens or lupus is concerning for the fetus?

A

anti-SSA

-can lead to neonatal lupus–> congential heart block

82
Q

what is characteristic of sjogrens on biospy?

A

lymphocytic sialadenitis

83
Q

what type of HSR is sjogrens characterized by?

A

type IV–lymphocyte mediated damage w/ fibrosis

84
Q

2 of these 3 criteria need to be met for a patient to be diagnosed with sjogrens syndrome

A
  • dry eyes
  • ana AND anti-ssa, ssb, OR rheumatoid factor
  • lymphocytic sialadentis
85
Q

patients with sjogrens who present with unilateral enlargement of the parotid gland are at increased risk for developing what?

A

B-cell (marginal zone) lymphoma

86
Q

scleroderma is characterized by

A

perivascular fibrosis!!

87
Q

limited type of scleroderma is characterized by

A

CREST

  • calcinosis (anticentromere)
  • reynods (can present years before any other symptom)
  • esophageal dysmotility (2/2 to fibrosis of lower esophagus)
  • sclerodactyly
  • telangiectasias of skin
88
Q

diffuse type of scleroderma

A

skin involvement w/ early visceral involvement

  • any organ can be involved
  • lung–pulmonary HTN and interstital fibrosis–kills
  • kidneys–scleroderma renal crisis–sudden onset ARF and htn tx w/ ACEi
  • GI tract
  • anti-DNA topoisomerase I
89
Q

antiDNAtopoisomerase I is assocaited with what disease

A

diffuse scleroderma

90
Q

mixed connective tissue disease is characterized by

A

features of sle, sjogrens, and polymyosititis

-ANA + serum ab U1 ribonucleoprotein

STEP1 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions