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Flashcards in HY Deck (621):
1

pyknosis?

karyorrhexis?

karyolysis?

pyknosis: ink dot, nuclear condensation

karyorrhexis: fragmentation

karyolysis: disolution

2

Virchow Triad

dirupt in blood flow: stasis activates coag cascade

endothelial cell dmg: endothe protects collagen and tissue factor, prod PGI2 blocks platellet, secrete heparin like molecules > activate antithrombin

 

hypercoag state

3

Positive and negative selection of T cells

 

T cells in bone marrow -> Thymus

->positive->can yopu bond to self antigen -> yes good

Negative -> bind too tight? -> yes -> destroyed to avoid autoimmune apoptosis (FAS ligand binds FAS receptor)

4

Fat necrosis 

 

supponification Ca boinds fatty acids turns chalky

breast due to trauma MVA

contains Giant cells 

 

5

MI-> cardiac enzymes inc-> cath lab -> CE keep increasing why?

 

 

reperfusion injury O2 enter in large amount creating free radicals and causing DMG

6

Protein C and S do what?

 

inactivates factor 5 and 8, deficiency lead to hypercoag state

7

hallamrk of IRReversible injury
 

Membrane DMG

> enzymes leak (like MI troponin leaks) & Ca entering

8

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9

Homocysteine elevated in

B12 and folate def.

cannot convert homocysteine > methionine

10

caspases intrinsic pathway

injury -> DNA dmg/ loss hormonal stimulus -> lowers Bcl2 -> cytochrome c leak00s -> activates caspases

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11

characteristics of thrombus vs postmortum

lines of Zahn

attachment to vessel wall

12

antioxidant vitamins?

Vit A, C, E,Gluthiopne

13

dystropic calcification vs metastatic calcifications

dystrophic calcification: normal Ca/ P, deposits in necrotic tissue

Meta: high Ca/P and deposits in normal tissue

14

every organ type of necrosis?

 

Coag necrosis

except Brain > liquifactive because microglial  > enzymes released

15

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16

39 yo female presets with preclampsia, + protinuria? mst likely

Fibrinoid necrosis of placeta -> necrotic dmg to vessel -> malignatn htn and vasculitis

17

ubiquitin

destroys cytoskeleton

18

Prothrombin 20210A

point mutation that increases prothrombin ( thrombin goal fibrinogen to fibrin) > thrmbus formation 

19

Caseous necrosis

 

cottage cheese

combination of Coag and Liqui

TB or fungals infect

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20

how oral contraceptives affect coagulation

 

estrogen increases prod of COag factors.

21

which metaplasia doesnt progress into CA

Apocrine metaplasia of breast

is a change in fibrolytic

22

Fentox Rx

Fe2+ -> OH- (hydroxyl) antiox (Gluthione)

23

Cytochrome C does what

 

activates apoptosis

inside inner mitochondrial memb

24

how B12 and folate interact

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25

free radical by neutrophil?

 

O2 -1e-> O2- ( superoxide) antioxidant superoxide dismutase

26

gangrenous necrosis

coag necrosis that looks mummified dry

lower limb popletial A. and GI tract

27

free radicals generation

 

during ox phospho by Cytochrome C which transfer electrons

28

barrets esophagus type of

metaplasia squamous epi to clolumnar nonciliated mucinus epi may progress into ADENOCARCINOMA

29

factor 5 Leiden

mutated factor 5 that cannot be deactivated by protein C/S > hypercoag state

most common inherited

30

endothelium prevents clot by

  1. protect collagen and tissue factor
  2. prod PGI2 (opposite of thrmboxane) and NO
  3. secrete heparin like molecule
  4. secrete tPA > converta plasminogen into pasmin > cleaves fibrin and fibrinogen,and destroys coag fact
  5. secrete thrombomodulin > makes thrombin ( normally coverts fibrinogen to fibrin) instead activates protein C > inactivates factor 5 and 8

31

How oxygen transf to blood

 

FiO2 -> PAO2 -> Pa O2 -> SaO2

high alt -- hihg PACO2--intersti fibrosis --

32

Bud Chiarri by

1 Polycythemia Vera: thick blood

2 Lupus coag state

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33

 increased warfarin skin necrosis with 

warfarin block epoxide reductase > cant activate vit K > factors 2, 7, 9, 10, Prot C and S wont work

protein c and S(inactivates factors preventing coag) degrade first so 2, 7, 9 , 10 increase risk for activation 

thats why heaprin also given untill window whe 2, 7, 9, 10 also degrade

 

protein C or S def even more concers cuz cause warfarin skin necrosis

34

homocystinuria

problem

causes what

cannot convert homocystine into Cystathionine

incresed lvls of homocystine( causes endothelial dmg)

CF: vessel thrombosis, mental retardation, lens dislocation, long sledner fingers

 

35

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36

night blindness by

 

15, 17 dislocation -> Vit A DEF

37

Liquifactive Necrosis on

 

Brain microglial

abscess by neutrophils

pancreatitits by enzymes

38

radicals with antioxidant

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39

hallamrk of reversible injury

swelling

-> loss of microvilli and membrane blebbing

>RER losses ribosomes, decreases prot synth

40

Carbon monoxide posioning know

 

norm PaO2 but low SaO2 ( bound to Hb)

Cherry face

** early sign headache -> coma -> death

41

role of caspases?

caspases -> proteases/ endonucleases -> break cytoskeleton/ break DNA

42

pt expressed to CHM laundry cleaning agent. what exposed to?

 

CCL4-p450->CCL3-> cells swelling-> ER swelling decreasing prot synth->decreasing apolipoprotein prod decreasing carrying of cholesterol---> Fatty Liver

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43

whats hemochromatosis

increase Fe l- liver dmg by free radical production thats why iron is tightly bound in physiology

44

ATIII def

antithrmbin 3 made by endothelioum aka heparin like molecule

if given heparin ptt wont rise because it cannot activate ATIII, need to give high dose  of heparin and coumadin to maintain anticoag state

45

MEthemoglobimia

Fe2 -> Fe3 which cant bind to o2

Sao2 decreased

oxidant stress ( sulfa and nitrate drugs

newborns

chocolate color blood cyanosis

tx methylene blue -> fe2

46

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47

whats  an  amyloid

misfolded protein that deposits extracellualrlly d causing dmg to tissues

48

stain for amyloidosis

congo and apple green birefringance, beta plated config

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49

PRimary amyloidosis is?

over profd of Ig light chain that deposits

r/t plasma cell dyscresias ie: multiple myeloma

50

secondary amylydoisis

derived form serum amyloid associated proteins, acute rx increased in chronic stated

51

FMF familial medit fever

dysfucntion of neutrophils

autosomal recessive, fever, acute serosal inflamation( ,i,ics append, arthitis, Mi depending where

52

most common organ for amylidoisis

kidney-> mimics nephgrotic syndrome 

followed by heart -> cardiac myopathy decrease wall reflex decrease CO

 

organs need to be transplanted

53

derivative of insulin that causes amylidoisis?

amylin-> deposists in islets of pancreas

54

alzheimer precursor gene which?

 

Chromosome 21 beta amyloid precursos-> alphabeta amyloid deposits in brain

common with Downs syndrome(21) by 40 yo

55

dialisis amyloidosis

beta 2 microgobulin(opart of MHCI structure ) deposists in joints

56

medullaryt carcinoma thyroid how related to amyloids

calcitonin (protein)prod by tumor  deposits within tuymor

57

cells in acute vs chronic inflamation

acute neut edema, due to infection or necrosis

chronic lymphocytes

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58

all gram - outter contain?

 

LPS (lipipolysacharide) like a PAMP ( apthogen associated moleculat patterns

recognized by cd14

59

CD14 

recognizes?

on?

 

recognized LPS on G- bact

on macrophages

60

NF-kb role?

TLR activates NK-> activated immune mediators

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61

Arachnoid acid from?

cascade?

Phospholipiod membrane by phospholipase a2

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62

products of arachnoid acid

Cyclooxyganase and 5 lipoxygenase

63

cyclooxygenase products what they do

prostaglandins

vasoconstricts (artiriole)

increase permeability( post cap venule)

especially PGE2- causes fEver

64

mast cells activated by?

trauma, C3A and C5a, or cross link surface IgE by antigen

65

mast response when activated?

 

release histamine

66

effects of histamine?

vasodialtion artirioles

increase permeability

production of arachnoid acid metabolite particularly LEukotrines

67

complement classical pathway

 

GM Makes Great Cars

bacteria->> IgG/M->>C1 = classic pathway

68

C3A/C5A TRIGGER?

 

C3A/C5A (ANAPHALATOXINS) ->MAST CELL DEGRANULATION -> HISTAMINE RELEASE -> INCREASE PERM -> DELAY RESPONSE ARACHNOID ACID -> * LEUKOTRINES

69

WHAT BRINGS NEUTROPHIL

LTB4

C5A

IL8

BACTERIA PRODUCTS

70

HAGEMAN FACTOR IMPORTANT IN?

PRODUCED BY LIVER

ACTIVATED BY EXPOSURE TO SUBENDOTHELIAL/COLLAGEN

CAUSE ACUTE INFLAMATION

In DIC w/ severe G- sepsis-> also activates Hageman f. -? coag, fibrinolytic, kinin syst activated-> bradykin -> vasodilation. increas eperm, pain

71

G- sepis -> DIC how

In DIC w/ severe G- sepsis-> also activates Hageman f. -? coag, fibrinolytic, kinin syst activated-> bradykin -> vasodilation. increas eperm, pain

72

what mediated pain?

 

PGE2 (pain and fever)

Bradykinin

 

73

C3 to MAC how?

c3- c3 convertase-> C3a, C3b-C5 convertase-> C5a, C5b-C6 C9->MAC

74

fever occurs by?

LPS(pyrogens) cause macrophage-release-> IL1 and TNF-> increase COX in perivascular of hypothalamus -> increase PGE2--> increase temp set point

75

whats neutrophil margination?

when large molecules like neutrophils enter vasodilated vessels get closer to border at post cap venule -> produce selectin which are speed bumps

76

p selectin vs e selectin

P from Weibel Palade bodies

w: vonWillerbrand

p: P-selectin

E-selectin induced by TNF and IL!

77

what binds to selectins

sialyl Lewis X on leukocyted

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78

adhesions molecules (after rolling) regulated by?

ICAM and VCAM regulated by TNF and IL1

CAMs interactions with integrins causes adhesions of leukocytes

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79

4 molecules that bring neutrphils?

 

C5a

LTB4

IL8

Bacteria prod

80

delay separation of umbilical cord?

Leukocytes adhesion deficiency , defect CD18 (autosomal recesive)

delay separation of umbilical cord

normally necrosis but since neutrophils cant destroy it it wont separate

 

81

Leukocyte adhesion deficiency

Defect of integrins (CD18  subunit)

=delay umbilical cord separation: Neut can destroy the tissue

=increase lvl of neutrophils because normally neutrophils are stroed in lung but impaired adhesion of marginated pools

=recurrent bacterial infections that lack pus

82

where leukocytes transmigrate?

 

psot capillary venules where vasodilation

83

phagocytosis enhanced by?

 

opsonins ( IgG and C3b )

attach to bacteria and easier to recognize

84

Chediak Higashi Syndrome

Autosonal recessive  defective protein traffic

prevents phagosome railroad(microtubules) to lysosome

=increase infections

=neutropenia: neut cant divide so die

=histo:  giant granules next to golgi

=defective 1ry hemostasis (abnorml dense granules in plate)

=Albinism: melanocytes cant move melanin to adjecent kratinocytes

=Peripheral neuropathy: toe nuclues in spine microtubules wont work

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85

best method of destruction

 

o2 dependent best 

HOCL-gen by oxidative burst 

86

oxidative burst how it works

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87

Chronic granulomatous disease is?

NADPH oxidase defect

recurrent infection unable to prod blech ( HOCL-)

x link defect

test nitro blue : if colorless and not blue = +

**infections with S Aureus, P Cepacia S Marcescens Nocardia Aspergillus**

88

Chronic granulomatous disease caused by which microbes

nfections with

S Aureus,

P Cepacia

S Marcescens

Nocardia

Aspergillus*

Nitro blue test if colorless and not blue = +

89

Nitroblue tetrazolium to test for?

chronic granulomatous disease

nfections with S Aureus, P Cepacia S Marcescens Nocardia Aspergillus*

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90

1. NADPH oxidase defect vs 2.myeloperoxidase deficiency

 

1. cannot convert 02 -nadph ox-> o2-

2. cannot convert h2o2 -MPO->HOClp( bleach) last product

1. tested with nitro blue tetrazolium, colorless = + for x link defect

2. increase risk for candida

91

02 independent vs dependent

independent less effective

lysosome in macrophages

major basic protein in eosinophils

 

92

macrophages destroy with

o2 independent

lysosomes in secondaty granules

93

healing induced by 

macrophages:

IL10, TGF beta

both anti inflamatories

94

TGF-Beta and IL10 do what

 

antiinflamatories and induce 

95

with acute inflamation what are the outcomes

 

1. healing by macrophages -> IL10, TGF beta

2 cont acute infla- pus formation, macrophages ->IL8 to bring neut

3. abscess, acute infla surrounded by fibrosis, macrophages -> fibronogenic GF and cytokines

4. chronic inflamation, macropha ->present antigent(ingested virus MHC II) to CD4+ helper ->cytokines that induce chronic inflammation

96

what causes chroninc inflamation

persistent infection

virus

mycobacteria

parasites

fungi

autoimmune

foreign cancers

97

t cells cycle

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98

MHC II present on

AP cells

like macrophages on the outside

99

CD4 activation

 

1st signal binds MHC complex with antigen

2nd signal B7 binds CD28

then secreted cytokines -> inflammation

th1 and th2 subsets

7/28=4= cd4

100

Th1 and Th2 

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101

CD8 activation

MHC I on all nucleated 

and IL2 from CD4 Th1 

causes to secrete perforins and granzymes

granzymes enters proes and activates apoptosis

102

enzyme that activates apoptosis

Caspases

3 ways

1: intrinsic: mitochondrial: cytochrome c leak

2: extrinsic: fas ligans  expresion-> binds fas on target cells activate it

3: CD* -> granzymes 

 

103

naive B cells expess what

IgM and IgD

104

b cell activation

1: antigen bindind by surface IgM or Ig D indices plasma cell that secretes that Igm or IgD

2: b cell present to CD4 helper via MHC II, CD40 on B cell binds CD40L on helpter -> activates CD4 to secrete IL4 and IL5  -> cause B cell isotope swithc and maturation to plasma cells

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105

key characteristic of granuloma

epithelial histiocyte

macrophages with abundant pink cytoplasm

106

non caseating granuloma

lack of central necrosis 

rx to foerign body( implant broken)

sarcoidosis( tiny collections of granulomas)

beryllium

chron's

cat scratch ( neck stallae shape

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107

caseating granulomas

by: TB : AFB stain

fungal

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108

DiGeorge Syndrome fail of what?

what DNA change?

3rd and 4th pharyngeal pouch

22q11

lack structure related to : thymus -> T cell def

lack parathyroid-> hypocalcemia

abnormal great vessels, heart and face

109

SCID etologies

sever immnodeficiency

defective cell and humoral immunity

1. adenosine deaminase def  (ADA needed to deaminate adenosine and other toxic products to lymphocytes

2. cytokine receptor defect((prolif and mature B/T cells)

3. MHC ii def: needed for CD$ activationa and cytokine prod

 

110

SCID 

no T cells ->

no B cells ->

tx?

no T cells -> fungal, viral

no B cells -> bact, protozoa

worst than aids for opport inf ** no live vaccines**

tx? stem transplant

111

x linked Agammaglobulinemia is?

mutation?

decrease immunoglobulins leads to what infection?

when start showing

 

b cells cannot mature into plasma due to Bruton tyrosine kinase

Brutons tyrosine kinase X linked

bacteria ( no IgG - cannot opsonize)

enterovirus and Giardia (decrease IgA GI virus )

shows after 6 months moms ab end, no live vaccines to be given

 

112

CVID is?

risks?

 

Common variable immune def

low immunoglobulins

decrease b cells and cd4 help both needed for immunoglob prod

risk? autoimmune disorder and lymphoma

113

GI disease with IgA Def?

Celiac Disease

increased mucosal infection

114

Why IgM increase in hyper IgM syndrome?

the forst way of the B cell activation not affected but with CD40L on Cd4 or CD4) receptor on B cell, mutation prevent class swithing. cytoknes necessayr for swithing not produced. low IgA, G, E result in recurrent pyogenic infection

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115

Wiskott aldrich syndrome

thrombocytopenia, eczema, recurrent infection

wasp gene mutaion X linked

116

C5-C9 deficiencies risk for 

increased risk for Neisseria gono and menin

117

C1 inhibitor defi

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118

automimmune diaseses affect more?

 

women in child bearing age  30-50

119

SLE type of hypersensitivity?

type 2 - cytotoxic

and type 3 - antigen antivbody complex

120

SLE common in 

ss

AA females 

chronic inflamation: fever and weight loss, butterfly rash when exposed to sunlight, arthritits, pleuriritis, 

121

most common SLE lesion?

 

diffuse proliferative Glomurelonephritits 

122

SLE cardiac problems

 

endocarditits, myocardititis, pericarditits, any layer

 

123

Libman-Saks endocarditis

classical finding with SLE, sterile depositson both sides of mitral valve 

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124

SLE common cause of death?

renal proliferative glomerulonephritits -> infections

125

SLE dx test?

ANA sensitive but not specific

anti dsDNA-> highly specific> DX

126

Drug induced SLE

drugs?

antibody?

drugs: hydrolazine, procainamide, isoniazid

antihistone antibody

removal of rx -> remision

127

antiphospholipid antibody syndrome?

30% of SLE

anticardiolipin antibody interferes with PTT false elevated 

pt actually hypercoagu: DVT, heaptic vein throb (vod chiarri, polycythemiavera) infection, stroje, tx lifelong anticoag

 

128

Sjogren hypersensitivity type?

type 4: lymphocyte mediated dmg

129

cant chew cracker, dirt in eye, frequent caries dx?

Sjogren syndrome

keratoconjunctivits, xerostomia

130

Sjogren synd test

related to what diseases?

test: antiSS-a and antiSS-b both target ribonucleoprotein antibody

Rheumatid arthritis is associated with it

131

Pt with sjogren s/s bilat enlarged parotid. pt says unilateral growth. Dx? 

B cell lymphoma complication of Sjogren unilatera enlarge late . in the course of the disease

132

Diffuse Scleroderma test?

ANA positive antiDNA topoisomerase SCL70 

 

diffuse involved skin and visceral involment ( esophagus: dysphagia)

activation of fibroblast deposit collagen-> fibrosis

133

Scleroderma Localized

local skin and late visceral

CREST

Calcinosis/anti Centromere ab

Raynaud phenomenom

esophageal dysmotility

telangiectasias of the skin

134

Raynaud;s phenomenon 

ud's phenomenon is a condition resulting in discoloration of the fingers and/or the toes after exposure to changes in temperature (cold or hot)

135

Pt with multiple s/s

trouble up stairs, combing hair, SLE like s/s, systemic sclerosis

mixed CT disease

ab against U1 ribonucleoprotein

136

labile tissues

labile have stem cells= constantly regenarating 

bowel(crypts), skin(basal), rbc(bone marrow marker CD34), wbc, pt, lung(type 2 pneumocyte)

137

Stable tissues

Quiescent (G0) but can enter cell cycle

liver, proximal renal tubules( acute tubular necrosis they can regenerate, dialysis till then)

138

Permanent tissues

lack of regenerative potential

myocardium, skeletal muscle, neurons

heal by repair (fibrous scar) MI

139

scar deep enough-

loss of basal layer(stem) -> fibrous scar

140

component granulation tissue

fibroblast ( type 3 collagen)

141

granulation vs granulation tissue

granuloma -> subtype of chronic inflammation

hallmak *** epithelial histiocyte***

IL12(macrophages) CD+ -> CD4 THI -> secrete interference gamma

turns macrophages to Epithelial like

142

granulation turns into

Granulation -> scar

Collagen 3 (pliable) -> collagen 1 ( strong)

uses collagenease (zinc cofactor)

143

types of collagen

 

I: ONE, bONE, high tensile strength

II: carTWOlage

III: reTHREEcular, blood vessel, granulation(pliable)

iV: basement membrane

144

TGF alpha

TGF beta

PDGF

FGF

VEGF

TGF alpha : epithelial and fibroblast growth factor 

TGF beta : by macrophages if no more inf to heal, inhibits inflammation, is a fibroblast GH 

PDGF:  platellet seal -> PDGF -> GH for endothelium, smooth muscle, and fibroblast

FGF(fibroblast growth factor) : angiogenesis, skeletal development

VEGF( vascular endothelial growth factor):  angiogenesis

145

1ry vs 2ry intention

1ry: a pproximated with suture to avoid scar

2ry: not approximaed-> granulation formed fills defect -> myofibrolblast contracts the wounds forming the scar

146

pt with wound heal with secondary and has reduced in size how?

myofibroblast 

granulation has 3 : capillaries, fibroblast, myofibroblast ( contracts)

147

delayed wound healing most common  with?

infections: S aureus 

148

vitamin C role in collagen

Vit C hydroxylation of proline and  lysine -> crosslinking 

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149

Cooper deficiency affects collagen by?

collagen 

cooper is a cofactor of lysyl oxidase which crosslinks Lysine and hydrolysine to form collagen

150

Zinc deficiency affects collagen by?

Zinc is a cofactor for collagen collagenase 3 of granulation tissue-> stronger type 1 

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151

whats is a Keliod?

out of proportion scar tissue

increase type 3 

genetic predispistion AA

affects earlobes, face, upper ext

152

collagen + zinc 

type 3 to 1

153

dicyclomine

anticholinergic used with IBS

154

characteristics of neoplasia

unregulated

irriversible

monoclonal : from single mother cell

155

clonality determined by

G6PD enzyme isoforms

multiple isforms exist only one is inherited from each parent present on X chromosome, on women inactivated in each cell by lyonization random

normal ratio 1:1 maintained in hyperplasia, which is polyclonal (from multiple cells)

in neoplasia only one isoform is present

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156

mononoclonacity produced by?

G6PD *a in all cells instead of different = neoplasm

157

clonality lymphocytes

determined by immunoglobulin Ig light chain either Kappa or lambda normal 3:1, maintained in hyperplasia

in neoplasm only one poliferates either increase like 6:1 or inverst 1:3

158

normal Ig light chain ratio

3kappa : 1 lambda

159

lymp node enlargement possibilities?

a: metastatic CA

b: reactive hyperplasia( infection)

c: lymphoma: biopsy proliferation of lymphocytes w/ 20:1 Ig normal 3:1 K:L

160

benign tumor

do not metastasize

161

malignant tumor

invade local and potential to metastasize

162

tumor of epithelium

benign adenoma (gland), Papilloma (fingerlike) 

malig adenocarcinoma, Papillary carcinoma

163

tumor of mesenchyme

ct: fat bone, vessek, cartilage

benign: lipoma, osteoma, chondroma, angioma

malignant: liposarcoma...

164

tumor of lymphocyte

NEVER BENIGN

malignant: lymphoma, leukemia

165

tumor of melanocyte

 

benign: nevus ( mole)

malignant: melanoma

166

leading cause of death 

adult children

adult: 1st cardio 2nd cancer 3rd cva

children 1st accidents 2nd cancer 3rd congenital

167

most common ca in adults? 123

1 breat/prostate

2 lung

3 colorectal

168

most common causes of ca mortality 123

1 lung

2 breast/prost

3 colorectal

169

how many cancer divisions for symtomps 

30 divisions

170

goal of screening?

catch dysplasia (reversible) or detect carcinoma before clinical s/s

171

mamography goals?

detect cancer in situ( 1cm), usually calcifies before invades or before clinically palpable ( 2cm), larger tumor = more mutationsand chances for metastasis

172

prostate cancer grows  where?

BPH where?

prostate ca grows in posterior peripheral of prostate: silent no symptoms, digital rectal excam close to posterior

BPH:  grows in center of prostate causing s/s

173

benefits of colonoscopy?

catch adenoma before adenocarcinoma or carcinoma before clinical sympt.

174

Aflatoxins

Associated cancer

 

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hepatocellular carcinoma, from Aspergillus from stored grains, 

175

Alkylating agents,  

Associated cancer

Leukemia lymphoma, s/e of chemo

176

alcohol, 

Associated cancer

Squamous cell carcinoma of oropharynx and upper esophagus,

pancreatic carcinoma

hepatocellular carcinoma

177

Arsenic

Associated cancer

women that worked in the field would apply arsenic to whitening back in the days. Present in cigarrette smoke

Squamous cell carcinoma of skin

lung cancer

angiosarcoma

 

178

Asbestos 

Associated cancer

Lung carcinoma and mesothelioma

exposure to asbestos is more likely to lead to lung cancer than mesothelioma

179

exposure to asbestos is more likely to lead to             than         

lung cancer, mesothelioma

180

Cigaretter smoke

Associated cancer

carcinoma of oropharynx, esophagus, lungs, kidneys and bladder

polycyclic hydrocarbons are particulary carcinogenic

181

Nitrosamines

Associated cancer

Stomach carcinoma

on smoked food, responsible for high rate of stomach CA in japan

stomach cancer 2 types : Intestinal carcinoma (nitrosamine), diffuse of carcinoma

182

Naphthylamine

Associated cancer

urothelial carcinoma of bladder

derived from cigarette smoke

183

Vinyl chloride

Associated cancer

angiosarcoma of liver

occupational exp to PVC pipes

184

Nickel, Chromium, Beryllium, or silica

Associated cancer

Lung carcinoma

occupational exp

185

EBV 

Associated cancer

most likely 1 chinese male 2 african infividual present with necj mass

nasopharyngeal carcinoma

burkitt lymphoma

CNS lymphoma in AIDS

186

HHV-8 

Associated cancer

human herpes virus

kaposi sarcoma

tumor of endothelial

187

pt present with purplelish lesion on skin

3 types

1: older eastern european males, skin tx excise

2: AIDS Tx: treat virus w/ antiretroviral and will boost CD4+

3: transplant: tx with reduce immuno suppresion slightly

188

HBV and HCV 

type of cancer

hepatocellular carcinoma

HBV DNA

HCV RNA

189

HBV vs HCN type of virus

HBV DNA

HCV RNA

190

HTLV-1

type of cancer

human T lymphotropic virus

adult t cell lymphoma/leukemia

191

High risk HPV 16, 18, 31, 33

type of cancer

Squamous cell carcinoma of vulva, vagina, anus, and cervic, adenocarcinoma of cervix

192

Ionizing (nuclear reactor accidents and radiotherapy)

type of cancer

generates what free radical

AML, CML, papillary carcinoma of the thyriod

hydroxyl free radical

193

non ionizing ( UVB sunlight most common

results in?

Basal cell carcinoma, squamous cell carcinoma, melanoma of skin

results in formation of pyrimidine dimers in dna excised by restriction endonucleases

seraderma pigments -> high risj skin CA

194

p 53 role?

regulates cell growth, suppresses risk of tumor formation

G1 --> S phase

p53 checks DNA, if dmged,  repair or brings BAX

BAX destroys BCL@ ( stabilizes mito mem) and cytochrome C leaks -> activates caspases -> apoptosis

195

tumor suppresors classic examples

p53

Rb retinoblastoma

196

P53 what is needed for tumors to grow?

both copies need to be knocked out

Knudson two hit hypothesis

197

PDGFB

function

mechanism

tumor associated

its a growth factor problem

platelelet derived GF :

overexpression ( PDGFB) of autocrine loop

Astrocytoma

 

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198

ERBB2 ( HER2/neu)

function

mechanism

tumor associated

growth factor receptor problem

epidermal growth factor receptor

amplification 

subset of breast carcinomas

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199

pt come w/ hx of breast ca, she read new tx designed against HER2. what new test needed?

HER2 new receptor

progesterone recepto

estrogen receptor

200

RET

function

mechanism

tumor associated

 

neural growth factor receptor

point mutation

MEN 2A, MEN 2B and sporadic medullary carcinoma of thyroid

201

trastuzumab

designed against HER2/neu

breast carcinoma where increase of receptor

202

pt develop multiple tumors in endocrine organs. Tx

if suspect MEN2A, 2B

do RET study 

if + thyrodectomy

203

KIT 

function

mechanism

tumor associated

stem cell growth factor receptor

point mutation

gastrointestinal stromal tumor

204

RAS gene family 

function

mechanism

tumor associated

SIGNAL TRANDUCER

GTP binding prot

point mutation

carcinomas, melanoma, lymphoma

70-80% tumors 

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205

ABL

function

mechanism

tumor associated

SIGNAL TRANDUCER

tyrosine kinase

t( 9;22) with BCR

defines CML, also seen in ALL ( adult) ( usually . children. poor prognosis

206

B C- MYC

function

mechanism

tumor associated

Nuclear Regulator: over prod of growth promoting proteins

transcription factor

t(8;14) involving igH

Burkitt Lymphoma: lymphoma of B cells, jey Histology: starry sky appearance blue and white

 

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207

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starry sky appearance = burkitts lymphoma, b calls 

c-MYC , transcriptio factor, t(8;14) involving IgH

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208

N-MYC

function

mechanism

tumor associated

nuclear regulatior

transcription factor

amplification

neuroblastoma N-MYC

209

L_MYC

function

mechanism

tumor associated

nuclear regulator

transcription factor

amplification

Lung cell carcinoma (snall cell)

210

CCND1 
( cyclin D1)

function

mechanism

tumor associated

cell cycle regulators

cyclin

t(11;14) involving IgH

Mantle cell Lymphoma

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211

CDK4

function

mechanism

tumor associated

 

cell cycle regulators

cyclin-dependent kinase

amplification 

Melanoma

212

where is Ig heavy chain

chromosome 14

213

Role of Retinol Blastoma Rb

G1 ---> S phase

needs E2F. Rb holds the E2F transcription factor, when Rb is phosphorylated by cyclinD/cyclin-dependent kinase 4 (CDK4) 

mutation of Rb allows for free E2F, and progression through cell cycle

both copies of Rb must be knocked out

214

Sporadic mutation

both hits are somatic, unilateral retinoblastoma

215

Germline mutation

familial retinoblastoma (2nd hit is somatic) bilateral retinoblastoma and osteosarcoma

216

unilateral vs bilateral retinoblastoma

unilateral: both hits are somatic

bilateral: familia retinoblastoma and 2nd hit is somatic, retinoblastoma and osteosarcoma

217

BCL@ over expressed in?

Follicular Lymphoma t (14:18)

BCL2 OVEREXP LEAD TO SUPER STABILIZED MITOCHONDRIA AND PREVENTS APOTOSIS

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218

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219

tumor factors for angiogenesis

FGF/ VEGF

angiogenic factors

220

Immune survelleance of tumor by? 

MHCI and CD8

mutations -> misfolded proteins -> expressed on MHCI -> CD* recognized abanormal proteins

tumors can regulated MHCI to avoid immune surveillance

221

Epithelial cells attached to ea other by?

E-cadherin, prevents metastasis

downregulation of E-cadherin -> dissociation of attached cells

cells attch to laminin and destroy basement membrane ( collagen type IV) cia collagenase

222

tumor invasion and spread progression

1. downregulation of  e-cadherin ( attch to each epi)

2. attch to lamina

3. destroy basement membrane w/ collagenase IV

4. attach fibronectin in ECF & spread locally

5. enter vascular /lymp -> metastasis

223

carcinoma spread to 

breast->

except

regional lymph 

breast -> axillary lymph

except:

renal cell carcinoma -> invades renal vein 

hepatocellular -> hep vein

Follicular carcinnoma of thyroid

Choriocarcinoma

 

224

sarcomas spreds via?

heamatogenous -> lungs

225

omental caking is ?

seeding of cavities of ovarian carcinoma -> peritoneum 

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227

characteristics of bening vs malignant tumors

benigng: slow growing, well circumscribed, distinct, mobile,  organized growwth, uniform nuclei, low molecular to cytoplasmic ratio, minimal mitotic activity, lack of invasion basement, no metastatic potential, benign NEVER invade

malignant: rapid growing, poorly cirm, infiltrative, fixed to surrounding, poorly differentiated, disorganized growth ( loss polarity), nuclear pleomorphism and hyperchromasia, hugh nuclear to cytoplamic ratio, highly mitotic and atypical. invasion of basement membrane

228

absolute diff between benign and malignant 

benign never metastasizes

229

immunohistochemical stain for 

epthelium

kerratin, for carcinoma

230

immunohistochemical stain for 

mesenchyme

Vimentin

for sarcoma

231

immunohistochemical stain for 

muscle

DEsmin

 

232

immunohistochemical stain for 

neuroglia

GFAP

233

immunohistochemical stain for 

neurons

neurofilaments

234

immunohistochemical stain for 

prostatic epi

PSA

235

immunohistochemical stain for 

Breast epi

ER

estrogen receptor

236

immunohistochemical stain for 

thyroid follicular cells

thyroglobulin

237

immunohistochemical stain for 

Neuroendocrine cell

chromogranin

for small cell carcinoma of lung and carcinoid tumors

238

stain for small cell carcinoma of lung and carcinoid tumors

Chromogranin

239

immunohistochemical stain for 

melanoma

S-100

240

tumor biopsy report keratin + cells

carcinoma (from epithelium)

241

Pt PSA elevatetd PSA next step?

biopsy, only way . to dx

242

grading of cancer measures?

differentiation  how much resembles tissue 

well diff= low grade, better prognosis

poor diff= high grade

243

stagin  measires?

based on size and spread more important than grade , determined after final sx

244

TNM system is?

T: tumor size

N:  *nodes* spread (lmph)( second most important)

M: metastasis ( most important

245

1ry hemostasis is?

platellet plug ( weak) (platellet vessel)

246

2ry hemostasis

stabilizes platellet plugs by coag cascade

247

steps in 1ry hemostasis

1:  transient vasoconstriction ( by  neural reflex and endothelium released-> vasoconstriction)

2: vWF binds subendo collagen ( links to platellet (GP1b). vWF comes from platellet and endothelial cells. wndothelial cells hace Weibel(vWF) Pladadel bodies( (P-selectin speed bumps) 

3: Platellete degranulate -> release ADP and TXA2. ADP: from granules promotes GPIIb/IIIa aggregation. TXA2: synthe by COX promotes aggregation

4: aggregation via GPIIb/IIIa using fibrinogen and link molecules -> platellet plug

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248

pt w/ primary hemostatis disorders present w/

mucosal and skin bleed .most common  is epistaxis, also gi , hemoptosis, hematuria, menorrhagia,

249

severe thrombocytopenia sign

intrcranial bleed

250

Petichiae vs ecchymoses vs purpura

Petichiae : 1-2mm

ecchymoses >1mm

purpura >3cm

more likely quantitative and not qualitative disorders.

 

251

immune thrombocytopenia purpura caused by?

IgG against platetellet antigens GPIIb/IIIa

252

most common thrombocytopenia in child and adults?

immune thrombocytopenia purpura ITP

autoimmune prod IgG against platelet antigens.

 

253

acute ITP common in ?

childre weeks after viral infection/immunization resolve in week just support

254

chronic ITP common in

adult women in child bearing 

primary or secondary like SLE

if pregnant -> corss placenta cause short lived thrombocytopenia in offspring since IgG can cross placenta

255

ITP labs 

decrease pt count <50K,  increased megakaryicytes

Pt/PTT not affected because cascade is not affected

256

ITP tx

1: corticosteroids: child respond well but adult relapse

2: IVIG : spleen would destroy these instead of those bound to platelet, temporary giving them time while symptomatics bleeding but it is short lived.

3: splenectomy : removes both source and site of destruction only in refractory cases

 

257

what is microangiopathic hemolytic anemia? 

microthrombi insmall vessels causing dmg to RBC -> hemolytic anemia with SChistiocytes

caused by TTP  & HUS

=seen TTP thrombotic thrompocytopenia purpura ( decrease ADAMTS13 enzymes which normally cleaves vWF into smaller monomers for degradation

HUS hemolytic urimic syndrome: bydrugs or  infection, E coli O157:H7  classically affects childreen eating undercooked beef, verotoxin dmg endothelium -> microthrombi 

258

TP t

hrombotic thrompocytopenia purpura ( antibody decreases ADAMTS13 enzymes which normally cleaves vWF into smaller monomers for degradation

259

HUS

hemolytic urimic syndrome: bydrugs or  infection, E coli O157:H7  classically affects childreen eating undercooked beef, verotoxin dmg endothelium -> microthrombi 

260

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261

microangiopathic hemolytic anemia tx

plasmapherisis and corticosteroid 

remove AB protetin

262

Bernard Soulier syndrome is ?

GPIv deficiency : where vWF binds

blood smear shows:

-mild thrombocytopenia,  destroyed

- and enlarged platellet, immature

BS Big Sucker

263

Glanzman thrombasthenia is?

genetic def of GPIIb/IIIa receptor -> normally cause aggregation to ea other linked by fibrinogen

264

aspirin inactivates

cox

the lack of TXA2 (causes aggregation)  decreases aggregation

265

uremia when? what

decrease kidney functiuon

build up of nitrogenous prod disrupt platellet functiion affecting qualitative platellets disorders

266

2ry hemostasis 

stabilizes plug

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267

where is . phosholipirequired for coag from?

surface platellet

268

prod of coag cascade are prod iin? required what?

in liveer and required activation 

requires:

1: tissue thromboplastin activates VII extrinsic thways, subendothelial collalgen activates XII (ntrinsic paathway

2: phospholiipid surfaceof platellets

3: calcium platellet dense granules

 

269

clinical manifestation of 2ry hemostasis disorders?

labs?

 muscle and joint hemathrosis and rebleeding sx such as circumcisiona nd wisdom tooth extractions

labs: pt and ptt

270

goals of cascade coag

produce factor 10

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271

hemophilia A factor and cause?

deficiency in factor 8 ( hemophilia 8, can be de novo( new mutation), X link

presents with deep tissue joint and postsurgical bleeding classic like 2ry hemostasis disorders

272

deficiency in factor 8 cause ptt?

increase ptt and factor 8 decrease

273

Hemophilia A tx

hemophilia a ''8'' 

recombinant factor 8

mixing normal plasma will correct ptt which would be low and this defferentiates from Coag factor Inhibitor

274

Hemophilia B (christmas disease) factor def

factor 9. one step back from hemophilia A ''8''

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275

most common factor affected by coag inhibitor? 

factor 8, acquired antibody  against coag factor, clinically similar to hemophilia A

mixing study: mixing normal plasma with pt plasma wont correct ptt due to inhibitor , ptt corrects in hemophilia A

276

most commoninherited coag disorder?

vW disease

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von Willerbrand disease clinical manisf? labs? tx?

clinical: mucosal and skin bleeding ( 1ry hemostasis disorder) afects adhesion

labs : increae bleeding time, increase ptt: need vWF to stabilize factor 8, normal PT, abnormal Ristocetin tttest : which induces platellet aggregation by causing vWF to bind GPIb, lack of vWF -> impaired aggregation -> abnormal test

 

Tx: desmopression ADH analog whihc causes release of vWF from Weibel Palade bodies of endothelia cells

278

Vitamin K needed for ?

gamma carboxylation needed for function of factors 2, 7, 9, 10, protein C, S

279

Vitamin K activated by 

epoxide reductase in liver 

280

coumadin blocks?

epoxide reductase, wont activae vitamin K ->  decreases factor 2, 7, 9, 10, C, S

281

Vitamin K def in?

newborns: no bacteria, vit k inhection prophylactically to all newborn

long term ABx

Malabsorption: leads to def of fat soluble vitamins,  including vit k

282

liver failure why 2ry hemostasis problems

decrease coag factor product, decrease epoxide reductase  check PT

283

Heparin induced thrombocytopenia affects platellets by? 

Hep- PF4 complex (factor 4 on platellet: develop IgG to this complex -> decreases platellet count ->  if fragments leave spleen can cause thrombosis

 

tx: STOP HEPARIn but dont give coumadin can cause coumadin skin necrosis

284

DIC progression

start widespread clot which -> ischemia/infarction then all coag factor used -> bleeding from IV/mucosa

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DIC caused by? 

labs?

Tx

always 2ry 

-amniotic fluid has tissue thrmboplastin -> coag 

- sepsis (Ecoli) endotoxins

-adenocarcinoma: mucin activate coag

*rattle snake venom -> coag coag

Labs decrease pt count, fibrinogen, increase pt/ptt, microangiopathic anemia ( rbc breaks with small thrombi)

Tx: underlying cause, transfuse, Cryoprecipritate (has coag factor)

 

286

microangiopathic anemia

( rbc breaks with small thrombi)

287

fibrinlolysis?

removal thrombus by plasmin

plasminogen -> plasmin ---tPA-> cleaces fibrin and serum fibrinogen, destroy coag factors , block pt aggregation

288

fibrinolysis how

which medication?

converts plasminogen to plasmin-> cleasves fibrin and fibrinogen, destroys coag factors and blocks pt aggreagtion

tPA tissue plasminogen 

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289

what inactivates plasmin?

 

alpha 2 antiplasmin

290

Cirrhosis how it affects fibrinolysis?

In liver cirrhosis, there is decreased production of alpha 2-antiplasmin, leading to decreased inactivation of plasmin and an increase in fibrinolysis. This is associated with an increase risk of bleeding in liver disease

Individuals with α2-plasmin inhibitor deficiency exhibit a hemorrhagic tendency caused by reduced inhibition of plasmin, accompanied by resultant increased fibrinolytic activity

Clots that are formed are not rapidly soluble in 5-mol/L urea because normal factor XIII activity is retained. However, whole blood and euglobulin lysis times are markedly accelerated. Definite diagnosis requires a specific α2-plasmin inhibitor assay.

291

plasmin overactovity caused by which diseases?

-radical prostatectomy: release of urokinase activates plasmin

-cirrhosis of liver:  reduced prod of alplha2 antiplasmin

292

DIC v. Disorder of fibrinolysis. Tx?

fibrinogen split prod increase but no DDimers ( no fibrin to cleave) cuz no clot formed ( like in DIC) But instead overactive plasminogen

tx: aminocrapoic acid -> blocks activation of plasminogen

293

thrombosis most common are

charectirized by

DVT, legs

lines of Zahn, autopsy of MI 

294

before death clots vs after

before, lines of Zahn and attachment to vessels

295

endothelial protects by

1 protects exposure of syb endothelial collagen and tissue factor

2. produce prostaglandin I2 and NO -> vasodilation

3. secrete heparin like molecules III (ATIII) which inactivates thrombin and coag factors

4. secretes tPA tissue plasminogen activator, converts plasminogen to plasmin that cleaves fibrin and fibrinogen destroyg coag fact, and block platelet aggregation

5. secrete thrmbomodulin. redirects thrombin to activate protein cwhich inactivates factor 5 and 7

296

elevated levels of homocystine caused by:, causes?

1 .Vit b12/ folate def

2. cystathionine beta synthade deficiency. CBS, ( other mental retard, lens dislocation, long slender fingers

 

causes vascular endothiliad dmg -> thrombosis

 

297

Pt with mental retard, lens dislocation, long slender fingers what test?

2. cystathionine beta synthade deficiency. CBS, ( other mental retard, lens dislocation, long slender fingers

 

might have homocystenuria genetic

298

protein X and S def?

risk for?

C: inhibits V and VII

S: inhibts VIII

leads to hypercoag state

increased risk for warfaarin for skin necrosis

pt  with normal levels of those you give warfarin -. decreases new fators, but some old still present however C/S have shortest halflive so will degrade faster -> so 2.7.9.10 still around without C/S -> hypercoag state -> thats why also started with heparin along till factors degrade, 

with deficiency even more so

299

warfarin skin necrosis

warfarin is epoxide reductase in liver -> cannot activate vit K -> 2.7.9.10 c.s. wont produced propperly ->

pt  with normal levels of those you give warfarin -. decreases new fators, but some old still present however C/S have shortest halflive so will degrade faster -> so 2.7.9.10 still around without C/S -> hypercoag state -> thats why also started with heparin along till factors degrade, 

300

Factor V Leiden

Mutated V that cannot be cleaved, cannot be shut off by prot C/S,

most common inherited 

301

ATIII deficeincy

decreases effect heparin loike molecules so wont activate

heparin given at normal dose wont increase ptt

302

pt administered normal heparin dose but ptt wont incrase likely?

 

ATIII def, 

high heaparin and then coumadin given to maintain anticoag state

303

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atherosclerotic embulus charaterized by cholesterol clefts in center

304

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fat embulus 

clinical m

after fracture , trauma

duspnea lungs, petechia of chest

305

pt with dyspnea and petechia on chest ?

fat embolism r/t to bone fracture due to trauma

306

Caisson disease

chrnoic gas emboli by  multifocal ischemic necrosis of bone 

307

pt given birht SOB, neurologic sympt, DIC what caused

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DIC due to thrombogeneic nature of amniotic fluid ( loaded with tissue thrmboplastin) with squamous cell and keratin debris from fetal skin 

characte

308

why PE is normally clinically silent

lung has dual blood supply, 

309

chronic emboli can cause

pulmonary htn

310

pale conjuctiva and skin, headache, angina s/s of 

hypoxia like in anemia

311

anemia parameters

Hb < 13.5 males, < 12.5 females

MCV: microcytic MCV <80, normocytic 80-100, macrocytic > 100 (size of rbc)

312

microcytic anemia how it begins? 

why?

erythroblast divides to form small RBCs normally but in microcytic there is one extra divisions.

because decrease prod of Hb to maintain the concentration of Hb in it " it would not be as red if it doesnt divide more"

 

hemoglobin is made of Fe + protoporphyrin, if one component is missing it causes microcytic, 

313

types of microcytic anemia and why? 

1. Iron def: not enough iron to make Hb -> microcytic

2. anemia of chronic dis: there is iron but cannot be used stored in macrophages, 

3. sideroblastic anemia: decrease of protoporphorin (component of Hb)

4. thalassemia: decrease prod globin chain

Hb= heme (Fe+proto) + globulin

314

Iron def anemia causes

most common type anemia

dietary or blood loss

infants- breast feeding -> little iron in milk

children- poor diet

adults - peptic ulcer males, ,menorrhagia/ pregnancy females

elderly: colon polyps/carcinoma, Hookworm

malnutrition, malabsorption( Celiac), Gastrectomy ( Fe2 easier form to absorp, acid maintain iron in 2+ sate, with gastrectomy less acid = more Fe3+ state = harder to absorp 

315

Iron cosumed types

where absorbed

in Heme ( meat) and non Heme( vegetable)

Enterocytes in duodenum regulate intake of iron via ferroportin (transporter). enterocyte absorbs but ferroportin only allows it to enter systemic but there is no way of getting rid off it

316

iron cycle into system

GI -> duodenom enterocytes -> ferroportin allows it to enter system -> bound as Trasferrin-> to liver or bone macrophages to store -> store intracellular bound to ferritin

not unbound or creates freeradicals -> hydroxyl : gluthione (Fentyl react)

317

Labs for Iron status

Serum iron : bound to transferrin, 1 out 3 transferrin is bound to iron, 

TIBC: total amount of transferrin in blood bound and unbound

% saturation: measures bound iron

Serum ferritin: how much present in bone marrow macrophages and liver

318

stages of iron def and labs

1st stored iron depletion:  serum ferratin decreases/ increase TIBC ( measures traferrin)

2nd serum iron decrease and percent saturation goes down 

3rd normocytic anemia : not enough iron but would still make normal RBC in lower amount

4th so severe that forced to go extra division and would be Microcytic ( smaller) and hypochromic ( less red color)

319

clinical findings of Iron def, labs findings

anemia

Koilonychia. spoon shapes nails

Pica: chew on ice, dirt

 

Labs: microcytic, hypochromic anemia, increase RDW  ( RBC distribution width) spectrum: wide= different size, decrease ferritin increase TIBC, decrease serum iron and % saturation, 

increase free erythrocyte poroporforin (FEP) :  heme = Fe + proto, free proto 

320

Q image thumb

RBC should be size of lymphocyte purple, here small, -> microcytic hypochromic , iron def anemia

321

older male iron def anemia tx?

rule out colonic carcinoma before tx just with iron supplement

322

Pt with anemia, dysphagia, beefy red tongue

plummer-vinson syndrome

iron def anemia with esophageal web( mucosal protrussion that can obstruct bolus)  and atrophic glossitis -> 

323

anemia of chronic anemia caused  by?

chronic inflammatory diseases( endocardtitis, autoimmune and cancers

produce acute phase reactant from liver: HEpcidin -> sequesters iron -> microcytic anemia

324

Hepcidin does what

present in anemia of chronic disease

sequesters iron and limits iron transfer from macrophages to erythroid precursors -> suppresing erythropoietin (EPO)

normally used by body when infection is present to limit their uptake of iron

325

labs for anemia of chronic disease

H ferritin, L TIBC

L serum Fe, L % sat

H FEP(free erythrocyte protoporpherin) 

 

HEME= Fe+proto

326

progression of anemia of chronic disease

normocytic anemia then microcytic anemia as iron level decreases, 

327

tx anemia of chronic disease

tx underlying causes

exogenous EPO erythropoetin since hepcidin ( whatsequesters iron) also supresses EPO

328

sideroblastic anemia is

leads to

HEME= Fe + proto

defect in protoporphorin synthesis -> L heme -> L hemoglobin -> microcytic anemia

329

protoporphorin syntheisis reactions

rate limiting factors?

1st stp

Succinyl Coa --ALAS+B6--> ALA usin B6 as cofactor (Rate lf: ALAS)

ALA -- ALAdehydogenase--> propholbilinogen

propholbilinogen------> protoporphorin bound to iron -- Ferrochelatase 

(in mitochondria)--> HEME

 

330

enzyme that attached protoporphyrin to iron

where?

ferrochelatase

in mitochondria

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331

where is the iron located

Q image thumb

ringed sideroblast. sideroblastic anemia

In mitochodria

defective production protoporphyrin syntheis

Fe enters erythroblast and into mitochondria that surround the nucleus. but no way of Fe exiting so they collect inside mitchondria

332

sideroblastic anemia types and most common

Congenital: most common is ALAS defect ( rate limiting step) succnyl COA -> ALA

or

Acquired: alcoholism (mitochondrial poison), Lead poisoning ( denatures enzymes ALAD (L prophobilinigen)  and Ferrochelatase ( proto + Fe -> HEME), Vit B6 def :  co enzyme for ALAS to make proto

333

pt with isoniazid develop what type of anemia? why?

it leads to vit b6 def that leads to sideroblastic anemia, a cofactor to ALAS to make proto

334

sideroblastic anemia labs

 

H ferritin, L TIBC

H serum Fe, H % sat

def of proto so extra Fe builds up mitochondria, causes free radicals -> cell dies -> Fe leaks out and bone marrow macrophages of  take it up and some may leak into blood

similar labs to hemochromatosis ( H Fe)

335

thalassemia is 

decreased of globin chain of Hb lead to Microcytic anemia

inherited mutation

* carriers are protected against Plasmodium Falciparum malaria

alpha or beta depending on chains affected

336

types of Hb and which chain most important

 

HbF (alpha2 gamma 2)

HbA (alpha 2 and beta 2)

HbA2 ( alpha 2 omega 2)

alpha most important chain consistent in all

337

alpha thalassemia how many alleles, robem , and what chrmosomes

normal 4 alleles on chromosome 16

problem with gene deletion

1 deltetion = aymptomatic

2 deletions = mild anemia with H RBCs (possible to knock out 2 of same side "cis" if one from each  side "trans") CIS worst with increased risk of severe thalassemia in offspring most seen in Asian

3 genes deleted = severe anemia only one gene. in uteru HgF alpha 2 gamma 2 is enough to avoid problems, when born HgA amd HgA2 start forming with only Beta 2Beta 2 aka HgH which dmg RBCs seen in electrophoresis

4 genes deleted in uteru tetromer of gamma dmg RBC = Hydrops fetalis, Hb Barts

338

Beta Thalassemia

how many genes

what chromosome

what problem

2 genes

on chromosome 11 

problem is mutation, not deletion ( alpha)

 

339

beta Thalassemia Mior vs MAjor

minor : Beta 0 / beta +:; asy,ptomatic with H RBC, microcytic hypochromic RBC : with target cell ( RBC with bleeb) low hb " deflates the rbc", Labs: increased HbA2

major: beta0/beta0: most severe, no problem in fetus because alpha2gamma2,  takes a few months to develop, dime alpha2 tetromer -> dmg RBC-> ineffective erthropoisiesis, spleen destroys, severe anemia -> massive erythroid hyperplasia, need transfusions, with too many in can lead to hemochromatosis, H Fe, microcytic hypochromic target cells and nucleated RBCs ( from liveer and spleen no Hba(alpha2 beta 2) only HbA2( alpha2 delta 2)

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340

chipmunk facies

Q image thumb

massive erythroid hyperplasia

r/t beta thallasemia major where no beta globin is formed fo tetromer of alpa(HgA) dmg RBC causing massive erythropoeitin release from kif=dney leading to abnormal hematopoiesis in bone suh as skull and facial 

pts have extarmedullary hematopoiesis where liver and spleen prod RBC -> hepatosplenomegally. 

risk of aplastic crisis with parvovirus B19 : infects erythroid precurssor shutting them down normally last a few week and wont cause trouble to normal ppl but these pt need every single cell

341

macrocytic anemia causes

folate / vit b12 def -> megaloblastic anemia 

one less division occurs leading to bigger cells

need dna precursor for devision: folate vit b12 : needed for dna synthe precursors

342

effects of folate/vit b12 def

megaloblastic anemia 

hepersegmented neutrophils: greater than 5 lobes: normal 3-5

megaloblastic changes in rapid dividing cell, like epithelial

343

Q image thumb

more than 5 lobes neutorphil normal 3-5

likely megalobalstic anemia, low b12 folate= less dna precursors= less divisions

also some large RBCs

344

macrocytic anemia causes

alcoholism 

liver dis

drugs like 5-FU

345

Folate absorbed in

obtained from

defi causes

jejunum

from greens / fruits

poor diet ( etoh) increased demand ( pregnancy, ca, hemolytic anemia), Folate antagonist (methotrexate)

346

methotrexate 

inhibits what casuing what

dihydrofolate reductase resulting folate def

347

folated def clinical and labs findings

labs : macrocytic RBCs, hypersegmented neut, L serum folate, H serum Homocysteine, normalmethylmalinoc acid( not B12) 

glossitis, epithelial cell not dividing

 

348

vit b12 v folate related anemia

folate related would have normal methylmalonic acid levels or measure b12 levels

folated there is no reserve so develops in moths

b12 liver loaded with b12 so it would take years for anemia

349

B12 how it is absorbed

animal proteins bound

sallivary gland amylase would liberate b12 and also secrete R-binder to bind to b12 -> small bowel by proteases -> bind intrinsic factor from Parietal cells from stomach -> absorbed in illeum

350

most common causes of B12 def

Pernicous anemia

autoimmune dest of parietal cells = no parietal cells stomach (have proton pump, pink histological, pernicious anemia

351

b12 def causes

dietary low  protein takes years very rare except vegans

most common pernicous anemia dest of parietal

pancreatic insuf= prod enzymes to cleave b12-Rbinder(from salivary glands)

dmg to ileum rt Crohns

or Diphyllibothrium latum(fish tape worm)

352

   b12 def  labs and clinical

macrocytic anemia and hypersegmented neut

glosssits

Subacute combined degen of spinal cord : H methylmalonic acid  build in spinal cord caused dmg

L serum b12

H homocystein

H methylmalonic acid 

353

different types of normocytic anemia

peripheral destruction

or

underproduction

look and reticulocytes ( young rbcs larger with blueish cytoplasm) 

A image thumb
354

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reticulocyte young rbcs with bluesih cytoplasm ( residual RNA)

normal count 1-2% (turn over of rbcs)

with anemia reticulocytes is false increased because it is a percentage

 

355

how to correct reticulocyte count

it is a percentage but with normocytic it would be false increased beacese decreased RBc

98+2= 2%

anemia: 48+2 =4%

so if result shows 4% multiply by Hematocrit/45 =2%

with normocytic anemia ask i f cells not prod or destroyed

if corrected reticulocyte is more 3% bone marrow is normal and it is being destroyed

 

356

in hemolysis reticulocyte count is

greater than % because no problem with bone marrow, RBC destroyed extr or intravascularlly

357

reticular endothelial system does what

macrophages of spleen liver and lymph node

break down hemoglobin

globin -> aa

heme-> iron and prtoporphirin

protopophyrin -> unconjugated bilirubin - binds albumin -> liver for conjugation(water soluble) -> bile

358

extravascular vascular hemolysis where

clinical labs

spleen liver lymph

anemia w/ spleenomegally(hypertrophy)

jaundice: liver cannot keep up with unconjugaed prod

increase risk of bilirubin gallstones

marrow hyperplasia 

359

Haptoglobin levels decreased when

intravascular hemolysis

trying to save heme

360

intravscular hemolysis clinical and labs

hemoglobinemia: hgb in blood

hemoglobinuria: urine

Hemosiderinuria: taken up by renal tubules: days after turn over of tubules cell they will be found in urine

decrease haptoglobin: safe some not alot

361

hemosiderinuria is>

renal tubular cells pcik up some of the hemoglobin that is filtered into the urine and break it down into iron, which accumulates as hemosiderin, tubular cell are eventuallu  shed resulting in hemosiderinurua

brown urine

362

Q image thumb

 Hereditary spherocytosis is

inherited defect of rbc cytoskeleton tethering proteins to membrane allowing blebbing and spleen removes them with time the RBC turn ROUND lossing biconcave form, range in size due to removal of part of membrane, smallest are the smallest, leading to H RDW ( multiple sizes). less able to manuver with time in spleen leads to anemia

involves spectrin ankyrin or band 3.1

363

disease with increase MCHC

mean corpuscular Hg concentration

increased with hereditary spherocytosis

rbc turn round due to cytoskleton/membrane disorder and spleen keeps derucing membrane lead to a more concentration inside RBCs, and round

364

round rbcs with loss of central pallor, H RDW, H MCHC, spleenomegally/jaundice

dx?

Heeditary  spherocytosis

365

histological changes when spleen consumes RBCs is?

hypertrophy

366

anemic pt suceptible to what with what infection

aplastic crisis

with Parvovirus B19 infection of erythroid precursors due to limited reserve in bone marrow

367

hereditary spherocytosis

diagnostic test

tx

blood smear will show what after splenectomy?

osmotic fragility test: more suceptible to hypotonic solution burst easily compared to normal rbcs

tx: splenectomy: no problem with having spherocytes, the problem is the spleen handling them leading to destruction of rbcs

spleen normally removes RBCs with fragment of nuclear material, but with spleenectomy it will show up

368

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Howel-Jolly body

nuclear fragments in RBCs

 show in blood smear if spleenectomy

369

sickle cell anemia whats the problem?

AR mutaion in beta chain of Hb

normal Gutamic acid replaced with Valine

protects malaria !)% of population

when deoxygenated ( hypoxemia, dehydration, acidosis) polymerizes needle tlike structures -> sickle shape 

370

what happens to HbS when deoxygenated

polymerizes into sickle cell 

it is reversible

371

Q image thumb

polymerizes into sickle cell when deoxygenated

it is reversible

372

sickel cell pt dont present with symptoms till?

6months after birth

HbF protects them HbS from sickling

 

373

sickle cell tx?
liklely to sufferr from what type of hemolysis?

clinical 

hydroxyuerad -> incrases prod of HbF which protects from sickling

both intra and extra vascualar hemolysis

extra: anemia, jaundice with unconj hyperbili, Hrisk bili stones

intravascular: decreased haptoglobin, target cells on smear 

clinical can show MAssice erythroif hyperplasia: expansion into skull/ facial bone, extramedullary hematopoiesis with hepatomegallu, risk aplastic crisi with parvovirus B19

374

major problem with sickle cell

irriversible sickling -> infarction of tissues -> DActylitis swollen hands and feet due to vasoocclusion of bones common in infants

375

Q image thumb

major problem with sickle cell

 irriversible sickling -> infarction of tissues -> DActylitis swollen hands and feet due to vasoocclusion of bones common in infants

376

autosplenectomy is

shruken fibrotic spleen from infarction of sickle cell vaso occlusion

increased risk infection with encapsulated organism (loss of major AB production)

increased risk of Salmonella p osteomyelitis

Howel-Jolly bodies ( RBC with nucleat material

377

pt presents with pneumonia and develops acute chest syndrome

vasooclusion in pulomanyry circulation due to sickle cell

can present with lung infiltrates

378

sickle cell trait is?

exception?

pt with only one copy of HbS so less than 50% is HbS so in wont sickle

EXCPET in renal medulla extreme hypoxia and hypertonicity resulting infarcition -> hematuria -> decrease ability to concentrate urine

379

sickle cell

dx

labs

metabisulfite: any degree of Hbs, both sickle cell diseas and sickle trait

in disease: 90% HbS, 8% HbF, 2% HbA2 but no HbA

Trait: 55% HbA, 42% HbS ...

380

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Hb C AR mutation in beta

normal glutamic aci

C: lysinne

HbC has LYSINE

Crystal in blood smear

 

 

381

paroxysmal nocturnal hemoglobinuria

PNH

test 

major death by

RBCs live next to complements deadly: to protect themselve used DAF ( decaacelerating factor) and MIRL connected to rBCs by anchor protein GPI

no GPI means cells are suceptible to compliment mediated damage

also WBC, Pt, RBCs 

when we sleep breathing shallow -> retain CO2 -> resp acidosis-> activate compliments-> some night pt get lysis of RBCs -> dark urine

aquired defect in myeloid stem cells result in absent GPI

TesT: introduce sucrose activates complements or by acidifying, also lack of CD55 since it also uses GPI it would be missing if +

death major by: thrombosis since platellets are also affected and would release content -> thrombosis

382

paroxysmal nocturnal hemoglobinuria

10% develop AML, already a mutation so more likely

most common death by thrmbosis

383

G6PD def problem

different types

RBCs use glutothione to protect from oxydative stress

H202 + Glutothione -> GS-SG -NADPH-> GSH

G6PD-> NADPH

if no G6PD it wont be able to protect RBCs

X linked recessive with REDUCE half live

types:

African variant mildly reduce halflife. RBC wont live to 120 days, more like 90 

Mediterrenian variant, markedly reduced half life wont live more than 30 days

 

384

what causes oxidative stressed and how does it affects?

how to confirm

infections

drugs: primaquine, Sulfa, dapsone

fava beans

cause hb to precipitate as Heinz bodies, removed by splenic macrophages resulting in bite cells or removing entire

confirm  by enzematic studies but AFTER episode of hemolytic episode

A image thumb
385

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Bite cell

Oxidative cell cause hb to precipitate as Heinz bodies, removed by splenic macrophages resulting in bite cells 

causes

infections

drugs: primaquine, Sulfa, dapsone

fava beans

 

386

IgG mediated disease is

associated with

Tx

IgG binds RBC-> splenic macrophages-> leading to spherocytes, happens in warm part of body

SLE, CLL, drugs ( methyldopa)

Tx: stop drug, steroids, IVIG(will eat these instead), splenectomy

387

IgM mediated disease 

Associated with

test

IGm binds RBCs in colder part finger and toes, intravascular necrosis

Mycoplasma Pneumonia and Infectious Mononucleosis can result in IgM mediated RBC destroy

Direct Coomb test: do i have RBC bound, anti IgG added to pt's RBCs

Indirect: RBC added to pt serum and test with anti IgG

388

Microangiopathic anemia

causes

histology

leads to Fe def with chronic hemolysis

microthrombi  (TPP -HUS, DIC, HELLP) prosthetic heart valve, aortic stenosis, 

form Schistocytes 

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389

Malarria

infection RBC with Plasmodium by female Anopheles mosquito

RBC rupture as part of cycle

P Faciparum, daily fever

P vivax or ovale, every other day 

spleen consume infected result mild extar vascular hemolysis w/ spleenomegally

390

anemia due to underproduction

low correctd Reticulocyte count

renal failures: decreased EPO by peritubular interstitial cells

dmg to precurssors 

parvovirus: infects progenitor: anemia in succeptible like sickle, infection is self limitting

aplastic anemia, dmg to hematopoetic cell-> pancytopenia(all cells), drug, viral, autoimmune, empty fatty marrow, ceasse drug, transfusion, EPO 

Myelophthisic process: metastatic cancer

391

Hematopoetic stem cells is CD ??

CD34+

392

neutropenia causes

L circulating neut

drug toxicity: chemo with alkylating agents, dmg to stem cells

severe infections (G- sepsis) increased movement into tissues

393

GM-CSF or G-CSF used for

boost granulocyte prod, with  chemo akylating agents pts

granulocyte monocyte stimulatinf fact and granulocyte stimulating factor

394

Lymphopenia

causes?

immunodeficiency ei: DiGeorge Synd, fail develop 3/4th pouch, thymu, t cells do develop right

high cortisol : Cusing synd..-> apoptosis of lymphocytes

autoimmune: SLE AB against RBCs, WBCs, or Platellets

whole body radiation: most sensitve cell to radiation is lymphocytes

395

most sensitive cell to radiation is>?

lymphocytes

396

neutrophilic leukocytosis occurs with

increase in wbc neut

bacterial inf

tissue necrosis 

high cortisol state disrupt the adheison of marginated neutrophils, with steroids meds also 

397

left shift ineutrophils indicates

what characterizes them

increased release of immature forms 

characterized by decresed Fc receptors ( CD16) : helps recognize immunoglobulin for phagocytosis, so lease usefull than mature 

 

398

eosiniphilia

in?

driven by

H eosiniphils 

Ax Rx type 1

Parasitic 

+++Hodkin Lymphoma: subset of pt, -> increased IL-5 prod

driven byby an increased IL-5

399

Hodgkin lymphoma incresed WBC ____ driven by??

eosinophils, IL-5

400

basophilia associated with

H basophils

CML

401

lymphocytic leukocytosis

r.t

EXCEPTION

Virals infections: CD8+ cells

Bordetella Pertussis : BACTERIA : BUT EXCEPTION, secretes Lumphocytosis Promoting factor- blocks circulationg lymphocytes from leaving blood to enter lymph node-> cannot learn new antigens...

402

Infectious Mononucleosis

EBV infections, less common CMV

results in lymphocytic leukocytosis reactive CD8 T 

tramsmitted by saliva

EBV infects oropharynx: sore throat, Liver: hepitits, B cells 

CD8 response due to virus prod MHC I -> generalized lymphadenopathy ( hyperplasia of paracortex)

spleenomegally. red pulp (RBC) white pulp (WBC) (B and T cell) Periarterial ly,phatic sheat hyperplasia

H WBC with atypical lymphocytes

Test: Monospot detects IgM heterophile antibodies, turns positive within 1 week, if negative it can be CMV, definitive dx EBVviral capsid antigen

complications: splenic rupture, Rash if rx PCN, dormancy of virus

403

EBV infection what happens to lymph nodes and where

spleen and where

Para cortex hyperplasia that produces T cells 

cortex: b cells

para cortex: T cells

M

 

Periarterial ly,phatic sheat PALS  hyperplasia of the white pulp`

A image thumb
404

Q image thumb

atypical lymphocyte

Nucleus bigger than RBCs normally same size

abundant blue cytoplasm. nomal doesnt have

almost looks like a monocyte: infectious mononucleousis ( before it was thought they were monocytes)  but actually it is REACTIVE T cells CD8

405

pts with classical mononucleosis s/s but negative Monospot test

it can CMV

that test for EBV

406

complications of mono nucleosis 

increased resk for splenic rupture: capsule of spleen can rupture, avoid all contact sport for 1 year after resolution

rash with PCN

dormant within Bcell: increased risk for re infection, risk for future Lymphoma

407

 acute leukemia

hallmark

#?

H meyloblast and H lymphoblast, doesnt develop further

1-2% normal  blast numbers

20%< in bone marrow

they crowed out normal cells : RBC anemia, platellet thrombocytopenia, neutropenia, BUT WBC elevated

408

Q image thumb

blast of acute leukemia

larger than RBCs

not much cytoplasm : immature

nucleolus: punch out are

409

ALL vs AML

markers?

hematopoeitic stem cell divides into two

1: Myeloblast: AML, MPO+ (myloperoxidase) -> crystal aggregates -> Auer Rods

2: lymphoblsat: acummmulation of lymphoblast= ALL, positive TDT +

410

ALL 

whats unique and what it is?

most common in?

subclass

accumulation of lymphoblast

+ TdT ( DNA polymeraase) : 

in children r/t Down's after age of 5 years old

B-ALL most common

or 

T- ALL

both have Tdt but surfers markers unique

411

B-ALL 

characteristic

prognosis

translocation?

Tdt like ALL

plus express CD10, 19, 20

great response to chemo but requires prophylaxis to scrotum and CSF: cannot cross these barriers so require injected directly in them

t(12:21) good prognosis mor common in kids

t (9:22) poor prognosis: more common in adults, Ph+ ALL ( philadelphia chromosome)

412

T-ALL

markers 

mneumonic

Tdt+ 

CD2-CD8 BUT NOT CD10

T thymic mass

in 

T teen ager

presents as a mediastinal thymic mass in a teenager

Acute lymphoblastic lymphoma( instead of leukemia since not cells floating)

413

Q image thumb

larger than RBCs, punched out nuclolus, auer rod

AML 

characterized by

MPO: myeloperoxidase or may be seen aslo as Auer rods

most seen in adults 50 yrs

t(15:17): acute promeylocytic leukemia, RAR (retioit acid receptor) disrupted, promeylocytes accumulate, risk for DIC (can activate coag cascade), tx: ATRA, binds RAR -> nuetrophils

414

t(15:17)

problem

risk

tx

: acute promeylocytic leukemia, RAR (retioit acid receptor) disrupted, promeylocytes accumulate, risk for DIC (can activate coag cascade), tx: ATRA, binds RAR -> nuetrophils

415

AML subclassified?

based on cytogenic abnormalities, liniage of myoloblst, and surface mrkers

APL : acute promelocytic leuk

acute monocytic leukemia

acute megakaryoblastic leuk

416

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acute monocytic leukemia

prolif of monoblast

lack MPO

characteristic: infiltrate the gums

417

acute megakaryoblstic leukemoa

prolif of megakaryoblast

lack MPO: dont do o2 dependent killing

r/t DOWN;s synd before age 5: 

418

Downs Syndrome related to leukemia?

more likely to develop acute megakaryoblastic leukemia BEFORE age 5

after 5 ALL

419

MEylodysplactic syndromes

cytopenia with hepatocellualr bone maroow

increased blast but less than 20%

more 20% = acute leukemia

420

CML

neoplastic prolif of CIRCULATING lymphocytes

H WBC

insidious onset( asympt) 

older adults

421

CLL

CD?

labs

smear?

if into lymph nodes what can cause?

complication

chronic lymphocytic leukemia

prolif of naive B cels  CD5(normally on T cell) CD20 

incraeased lymphocytes

smudge cells

causes generalized lymphadenopathy -> small lymphocytic lymphoma (mass)

hypogammaglobulinemia: dont prod Ig -> most common cause death infections

Ig made are bad -> autoimmune

 

 

422

Q image thumb

increased # of lymphocytes

smudge cell, splattered cell in corner

423

hairy cell leukemia

stain

clinical

mnemonic?

clinical 

neoplastic prolif of mature B cell

hairy cytoplasmic processes

+ for TRAP tartrate reisistamt acid phosphotase stain

splenomegaly RED PULP> normally white pulp where white cell , get dry tap with bone marrow aspiration, no lymphoadenopathy

Trap in red pulp, TRAP in bone marrow,  so cant go to lymphnodes

 

 

424

hairy cell leukemia tx

excellent response to 2-CDA

adenosine deaminase inhibitor, adenosine accumulate to toxic levels -> death

425

ATLL

associated with ??

clinical

acute t cell leukemia/lymphoma

neo prolif of CD4

r/t HTLV-1 japan and caribbean

Rash, gen LAD with HSM, llytic bone lesion with hypocalcemia 

426

pt present with lytic bone lesion, hypercalcemia and Rash

ATLL

dont think multiple myeloma before ruling out ATLL

A image thumb
427

Mycosis Fungoides

meoplast prolif of mature CD4: like to go to skin -> cereating a rash, plaques or nodules -> biopsy:  neoplatic t cells in epidermis: Pautier microabcess

if spred to blodd Sezary syndrome 

 

428

Q image thumb

Sezary cells, lymphocytes with cerebriform muclei

Mycosis Fungoides

429

whtats a meyloproliferative sybdrime

complicatiuon

neoplastic prolif of mature cell of meyloid lineage

H WBC 

all myeloid cells increased nut classified for dominant meytloid cell produce

complication hyperuricimeia and gout : polycythemia vera ( RBC nuclues is removed activates purine degradation pathway -> uric acid -> hyperuricimia and gout)

marrow fibrosis

transform to acute leukemia

430

 

CML

translocation

tx

clinical

neo prolif of mature myeloid cells especially granulocytes

Basophils : basophilia related

t(9:22) BCR-ABL fusion with increase tyrosine kinase activity

tx Imatinib, block tyrosine kinse activity

clinical: chronic ( enlarge spleen, accelerated phase ( elarging more), worse is transoformation to acute leukemia ( AML 2/3 ALL 1/3)

431

Q image thumb

CML

incrreased in granulocytes particular Basophils

 

432

if CML pt develop transformation mutation where is it 

hematopoetic cell or myeloblast 2/3 AML /lymphoblast 1/3 ALL

433

pt presents with H basophils

ddx?

CML vs Leukemoid reaction ( infection

CML granulocytes are LAP Leukocyt alkaline phosphotase for inflammation: negative

H basophils: L shift

exhibit t(9:;22)

434

Polycythemia vera

driven by

s/s

tx:

driven by: JAK2 Kinase mutation

s/s H viscosity: blurry vison headaches, thrombosis (Budchiarri synd), flushed face, itch after bathing ( extra mast cell, release of histamine)

Tx: 1st line phlebotomy, 2nd linehydroxyurea

435

pt presents with itching after bathing, flushed face blurry vison and headache

 

polycythemia vera

driven by: JAK2 Kinase mutation

s/s H viscosity: blurry vison headaches, thrombosis (Budchiarri synd), flushed face, itch after bathing ( extra mast cell, release of histamine)

436

polycythemia vera vs reactive polycythemia

reactive:

lung disease, L SaO2: increases EPO

ectopic tumor of EPO -> renal cell carcinoma with normal SaO2

PV: normal SaO2, L EPO

437

Essential thrombocythemia

driven by

s/s

JAK 2 kinase mutaiton

bleeding or thrmobosis: funtion or not

rarely progresses to marrow fibrosis or acute leukemia

no risk goat/ huperuricemia ( platellet buds off megakaryocytes so no need to remove DNA)

438

Q image thumb

essential thrombocythemia many platellets or iron def anemia alot of pt

 

439

Myelofibrosis

driven by

produces

clinial

neo prolif of mature meyloid: Megakaryocytes

JAK@ kinase mutation

prod PDGF -> marrow fibrosis

spleenomegally extramedullary hematopoiesis, bone marrow cannot make anymore

leukoerthoblastic smear: immature cells in blood

increased risk infection, thrombosis, bleeding, spleeen cannot make enough as bone marrow

440

Q image thumb

tear drop cell 

r/t myelofibrosis: heamatopoeisi move to spleen but some still develop in fibrotic marrow and need to squeeze into tear drop to go into blood

441

lymphadenopathy

acute vs chronic

acute infection painful, hyperplasia, RA, eraly HIV: expansion of follicles (CD4+ cells),  viral infection: expansion of Paracortex /( where T cells prod, ie mononucleosis), sinus histiocytes: draining a region of cancer

chronic inflammation : metastatic carcinoma or lymphoma

 

442

areas and whats in it

Q image thumb

RA, eraly HIV: expansion of follicles (CD4+ cells), 

viral infection: expansion of Paracortex /( where T cells prod, ie mononucleosis),

sinus histiocytes: draining a region of cancer

A image thumb
443

types of lymphoma

nonhodking vs hogkin

 

444

3 types of small cell lymphomas and where tehy from››››

Q image thumb

Follicular lymphoma

mantle cell lymphoma

margical cell lymphoma

445

what is it?

marker?

translocation?

when it presents

s/s

Tx

Q image thumb

Follicular lymphoma, contains dozens of follicles

small b cell ( CD20 ) neo follicular like nodules

adulthood painless LAD

T 14:18 .  14=Ig heavy chain H production, 18 BCL2. when translocation increases prod of BCL2 ( stabilizes mitochond membrane no Cytochrome C leak -> block apoptosis

Tx for symptomatic: low dose CTX or rituximab (anti cd20 AB)

can progress to diffuse B cell lymphoma, enlarging lymph node

446

t 14:18

??

Follicular lymphoma

T 14:18 .  14=Ig heavy chain H production, 18 BCL2. when translocation increases prod of BCL2 ( stabilizes mitochond membrane no Cytochrome C leak -> block apoptosis

447

Follicular hyperplasia vs lymphoma

 

Q image thumb

lymphoma: disruption of normla LN architecture

lack of tingible body macrophages in GC, 

expression of BCL2 in follicles

monoclonality:  normal 3:1 kappa to lamda

A image thumb
448

neoplastic prolif expanding region adjacent to follicle

what

 when

s/s

Translocation?

Mantle Cell lymphoma

neo small B cells CD2+ that expand mantle zone

late adult, painless

t11:14 11 cyclin D1 ( causes cells G1-> S phase), 14 Ig heavy chain

449

t 11;14

t11:14 11 cyclin D1 ( causes cells G1-> S phase), 14 Ig heavy chain

450

MArginal Zone lymphoma

what 

when

associated with

MArginal Zone lymphoma

just outside mantle(covering follicle)

neo B cells CD2+ 

associated with chronic inflam states: Hashimoto's thyroiditis, Sjogrens synd ( unilateral enlargements parotid), Hpylori gastritis (o mucosal sites) MALToma regresses with tx of infection

451

 

what 

when

s/s

different forms

translocation

Q image thumb

Burkitt lymphoma

neo of intermediate size b CD20

extranodal mass in child or young adult , african form involves jaw, sporadic in abd

t 8;14 most common c-myc, 8 c-myc to 14 Ig heavy, c-myc nuclear regulator oncogene that promotes cell growth

HIGHLY rapid growth

STARRY SKY APP

452

DLBCL

DLBCL

diffuse large b cell lymphoma

most common form  NHL

very aggresisve

adult enlarge lymphnode

453

Hodgkin L vs NHL

NHL entire mass is malignat

Hod: rare neoplastic cell (Reed-sternberg) ->  secrete cytokine draw other inflammatory cells that create mass

454

what 

s/s

leads to

Q image thumb

Reed-Sternberg cells

Hodking lymp: rare neoplastic cell (Reed-sternberg) ->  secrete cytokine draw other inflammatory cells that create mass

CD15+ and CD 30+

large B cell with multilobed nuclei and prominent nucleoli ( owl-eyed nuclei surrounded by 100s of reactive cells 

cytokines can result in B symtomps ( fever chills night sweats) attracts reactive lymphocytes, plasma cells, macrophages and eosinophils, 

may lead to fibrosis

 

455

Hodkin lymphoma subtypes

prognosis?

depend on reactive inflammatory cells

Nodular sclerosis( 70% of cases): enlarge neck lymph or mediostinal, young female adult most, biopsy: 

Lymphocyte-rich: best prog

Mixed cellularity: abundant eosiniphils (Reedsternber secretes IL-5 call eosinophils)

Lymphocyte-depleted worst prog, elderly, HIV

456

young female adult, enlarge neck lymph or mediastinal biopsy:

Q image thumb

Nodular sclerosis( 70% of cases): enlarge neck lymph or mediostinal, young female adult most,

biopsy: broad pink bands of fibrosis nodular sclreosis subtype

457

UA -> Bence jones proteins

driven by

s/s

test

risk

Q image thumb

multiple myeloma

prolif of plsma cells in bone marrow

driven by IL6

bone pain with H Ca:  plasma cells activate RANK receptor on osteoclast -> lytic punched out lesions -> H Ca, risk fractrure

plasma cell -> Ig -> H serum protein  (serum protei electropheresis) M spike IgG/IgA

risk to loose antigenic diversity (monoclonal) -> infections

Rouloeaux formation of RBCs: due to H protein in blood alters RBCs charge and group together

risk for amyloidosis: free light chain  ( overprod of it) -> urine Bence Jones proteins -> deposit in kidney -> Myeloma kidney

A image thumb
458

pt with H serum protein

SPEP M spike

no lytic lesion, norm Ca, AL amyloid -, Bence-jones protenuria -

 

M spike can be Multiple myeloma

Dx: monoclonal gammopathy of undetermined significance MGUS

459

Waldenstrom macroglobulinemia

what

s/s

tx

B cell lymphoma with monoclonal IgM prod : IgM is BIG thats why MACRO

+ M spike IgM

cisual neurological deficits

bleeding

tx plasmapheresis: removes IgM

460

what

characte

subtypes

Q image thumb

dendritic cell in skin from bone marrow monocytes, present antigen to naive T cells

neo = Langerharns cell histiocytes

characteristic Birbeck teninis racket granules

CD1a+ and S100+

Letterer-Siwe disease: name = malignant 2 names children less than 2, skin rash, rapid fatal

Eosinophilic granuloma: benign, pathologic fracture, skin not involved, 

Hand Schulle Christian disease: 3 names malignant scalp rah, lytic skull DI, child 3<

 

461

If disease has peoples name it is

2 names

3 names

malignant

<2

3<

462

Vasculitis

etiology

s/s

etiology unknown

s/s: fever, myalgia, fatigue nonspecific) symptoms of organ ischemia endotheilial dmg exp subendo collagen expose -> thombosis

or 

with healing of wall-> fibrosis -> s/s organ ischimia

463

common in

where

Labs

biopsy

tx

risk

Q image thumb

Temporal Giant cell arteritis

older adult 50

branches of carotid: temporal headache, opthalmic visual dist, jaw caudication, flu like s/s with joint muscle plain

lab ESR greater than 100

bio:  inflammed giant cells with intimal fibroiss, Granulomatous vasculitis, segmental ( only one piece will show thats why biopsy has to be large and section in multiple pieces and examin each. Negative biospsy does not exclude disease

photo intima separated from media by big area of fibrosis causing reduction in lumen -> ischimia s/s

tx: corticosteroids even w/o confirmation 

risk blindness ( is not reversible)

464

Takayasu arteritis vs Temporal Giant cell arteritis

Takayasu arteritis still a granulomatous vasculitis BUT adult ( Young Asian Female) less than 50

more likely aortic branch points-> visual and neuro s/s

weak/ absent pulses " pulseless disease

tx still same cortico

 

465

medium-vessel vasculitis

involve?

muscular arteries that supply organs: renal artery

466

Polyartiritis Nodosa

s/s expcept where

r/t

stages

multiple arteries

necrotizing vasculitis

Lungs spared, alll other organs can

s/s renal:HTN, mesenteric:abd pain...

r/t HBsAg

stage: early:transmural inflammation (fibrinoid necrosis), after healing : massive fibrosis (Nodosa) "string of pearls appearance"

467

fibrinoid necrosis

when

malignnat HTN and vasculitis

468

Q image thumb

String of pearls 

lesion of varying stage

early lesions ( fibrinoid necrosis) can cause aneurism -  fibrosis - aneurism-...

469

tx

if not tx?

Q image thumb

fibrinoid necrosis 

corticoid or cyclophosphomide

can be fatal 

470

3 yo asian children with fever conjunctivits, erythmatous rash of palms and soles, enlarged cervical lymph nodes

who

s/s

complication???

tx?

Q image thumb

ASian children less 4yo

fever

conjunctivits,

erythmatous rash of palms and soles,

enlarged cervical lymph nodes

Coronary artery involbed: thrombosis with MI -> aneurysm with rupture

ASA (even contraind for children with virus RIce synd) (prevent pt aggregation) and IVIG, disease is self limited

(asian kid driving kawasaki hands/feet used so are red, HR goes up so it can affect heart -> ASA and IVIG)

 

471

pt presents with ulceration gangrene and autoamputaion of fingers and toes

what

also present?

r/t

tx

Buerger Disease

necrotizing vasculitis involve digits

ulceration gangrene and autoamputaion of fingers and toes

Raynaud phenomena present: vaso spasm -> discoloration 

white -> Blue ->red

r/t smoking 

tx: stop smoking

472

middle age male with sinusitis / nasopharyngeal ulceration

hemoptysis

hematuria

labs?

biopsy shows?

tx? 

Q image thumb

Wegener Granulomatosis

weCener  "C"

necro vasculitis involve nasopharynx, lung and kidneys hemoptysis withbilateral nodular lung infilttrates

rapid progress glomerulonephritis:hematuria

have c-anca: (anti  neut cytoplasm AB) pt serum added to test neutrophil to see if attacks it, correlate with disase activity

biopsy: large area of necro Left, wall has giant cell granuoma

tx: cyclophosphimide

473

microscopic polyangiitis 

labs

tx

microscopic polyangiitis 

necro vascu multiple organ: lung and kidney

no nasopharyngeal or granulomas unlike WG

Labs: P anca, ( c-anda on WG)

tx: cortico and cyclophosphamide

474

Churg- Strauss Syndrome

involves

labs

necro granuloma vasculitis with eosinophils

lung and heart: 

p- anca +

475

p-anca posistive diseases

differences

microscopic polyngiatis: no granulomas, no asthama, no eosinophilia

Churg-strauss synd : + granulomas, asthma, peripheral eosiniphilia

476

children with palpable purpura on buttocks and legs, abd pain, hematuria, hx of upper resp infection

what

when

tx

HSP

Henoch-Schonlein Purpura

vasculitis due to IgA complex deposition

Most common vasculitis in children

children with palpable purpura on buttocks and legs: palpable cuz inflammation

, abd pain: GI pain and bleed

hematuria: Iga nephropathy : deposition

 hx of upper resp infection : IgA prod increased 

tx steroids

477

primary HTN 

etiology risk

unknown etiology

95% of cases

age, H aa, L asian, obesity, stress, lack of activity, high salt( increases blood volumen and peripheral resistance: both syst and diast)

478

Secondary artery disease

 

causes and to what pts

renal artery stenosis: L flow to renal artery: decrease flow to glomerulus: juxtoglomerural appratus secretes renin: converts angiontesinogen into angitensin 1: to lung where ACE converts to ANgio 2 -> 2 ting to raise BP: contstrict artirioles and promotes adrenal aldosterone relesase: to distal convulated tubules and retains Na

if one kidney : unilateral atrophy: 

causes: atherosclerosis (old males),

Fibromuscular dysplasia (young females) developmental defect of vessel wall 

479

benign HTN

mild/mod htn

clinical silent dmg vessels and organs over time

480

Malignat HTN 

present with

greater 200/120

arise from: benign or de novo

acute renal fail, headache, papilledema

its a medical ER 

481

arteriosclerosis

patterns

Atherosclerosis: thickening of the intima, in medium and large size vessel

Arterioloscleros: small

Monckeberg medial sclerosis: medial sclerosis

482

what 

contents

undergoes what

must common involves what

risk factors

causes?

complications

Q image thumb

Atherosclerosis

intimal plaque that obstrcuts flow, necrotic lipid core (cholesterol ) with  fibromuscular 

can undergo dystrophic calcification

photo: cholesterol cleft covered by fibromuscular cap

large and medium art: abd Aorta, coronary, popliteal, internal carotid

risks: HTN, H cholest, smoking, DM, nonmodifiable: age male,, post menopausal female (estrogen is protective)  genetics

causes stenosis: peripheral vascular disease, angina, ischimic bowel disease, need at least 70% stenosis for sympt

complication: 1 rupture can induce coag cascade -> thrombus -> infarction

or can cause embolism , aneurysm due to weakening of vessel not getting enough o2

483

symptoms of stenosis dont occur till

70% obstruction

484

Q image thumb

atherosclerotic embulus 

hallmark cholesterol clefts

485

arteriolosclerosis types 

arteriolosclerosis

1. hyaline arteriolosclerosis : protein leak into vessel causing thickening: pink heayline on micro

2. hyperplastic arteriolosclerosis: hyperplasia of smooth muscle, onion skin appearance

 

486

arises from **

results

Q image thumb

hyaline arteriolosclerosis : protein leak into vessel causing thickening: pink heayline on micro

arises from : benign HTN (forces protein into vessel) DM ( causes non enzymatic glycosilation causing wall leak and protein in)

result: reduced vessel caliber end organ ischemia: arteriolonephrosclerosis-> chronic renal fail ( reason why DM and HTN end up with kidney problems) -> shrunken kidney 

487

Q image thumb

result: reduced vessel caliber end organ ischemia: arteriolonephrosclerosis-> chronic renal fail ( reason why DM and HTN end up with kidney problems) -> shrunken kidney 

488

caused by

classic finding in 

necrosis associated

Q image thumb

hyperplastic arteriolosclerosis:

hyperplasia of smooth muscle, onion skin appearance

by MALIGNANT htn: SM tries to contain the BP -> narrowing end organ ischemia 

fibrinoid necrosis

classic finding: acute renal fail: flea bitten appearance 

 

489

Q image thumb

monckeberg medial calcific sclerosis

calcification of media, non obstructive, not clinical significant

in mamograms your are looking for calcification for signs of cancer

490

what does it requires?

progression of patho??

s/s

death by

Q image thumb

aortic dissection

intimal tear with dissection of blood through media of aortic wall

need alot of stress: like proximal 10 cm of aorta from heart plus pre existing weakness of media ( by HTN : causes hyaline arteriolosis of vasa vasorum causing decrease flow) or ( CT defects ( Marfan synd)

sharp tearing pain radiates to back

death by periocardial tamponade, next hemorrage or ischemia of organs liek kidney

491

common in

need

what can cause

complications

Q image thumb

thorasic aneurism

need weakness in wall: thoracic: tertiary syphilis: treebark appearance: vasa vasurum affected

complic: dilatation of aortic valve root: pulls on root and valve causing insuficiency, or can compress structres in mediast, or increase risk for thrombosis

492

pt presents male, smoker 60 plus HTN

what

where it occurs

what causes it

incidence

s/s

complica

Q image thumb

Abd Aortic Aneu

** below renal arteries but above aortic bifurcation

caused by atherosclerosis: thickening decreases o2 transfer

incidence in male, smoker 60 plus HTN

pulsatile abd mass growth with time

rupture greater than 5 CM

493

what

progression?

if pressed?

Q image thumb

hemangi oma(benign tumor)

tumor comprised of blood vessels

present at birth but regress through childhood dont remove 

skin and liver

pressure blenches

494

Angiosarcoma

sites?

angio sarcoma( malignant prolif endothelial

highly agrgressive

skin breat liver

liver r/t to PVC( pipe vessel), also arsenic and thorotrast

495

r/t

clnical

if pressed?

seen on and tx

Q image thumb

KApposi sarcoma

low grade malignant prolif of endothelial

HHV-8 of endotheilia cells

purple patched plaque or nodise on skin and viceral organs: prolif of endothelial vessel: not full vessel so if pressed WONT blench

older eastrn eurpe males: sx remove

AIDS: HHV8 infect of endothelia cells: tx antiretroviral agents: 

transplant recipients: decrease immuno suppresion

496

stable angina

causes

hallmark

s/s, how long

EKG

tx

atherosclerosis: decreased flow when 70% stenosis

Reversible injury to myocytes: hallmark swelling

CP less than 20 min, radiates L arn or jaw, diaphoresis, SOB

ST segment depression: coronary art begin in epicardium->Myo-> endo.  Endocardium would be affected most ( subendocardial ischemia)

tx rest and nitroglycerin ( vasodilation of art and veins decreasing the preload) 

497

cp at rest

when

cause

type of injury

EKG

tx:

Q image thumb

unstable angina

at rest

caused by rupture of stherosclerotic plaque with thombosis and imcomplete occlusion of coronary art

reversible injury to myosite: swelling

EKG ST seg dep

tx: nitro -> dialtion -> decreases preload

498

Prinzmetal angina

by

injury type

ekg

tx

coronary artery vasospasm episodic and unrelated to exertion 

reversible injury

skg: ST elevation due to transmural ischemia: all layers epi/myo/endo supplied cutted

tx: nitro: decrease preload, CCB: to control spasms

499

Myocardial Infarction

by

involves

s/s

tx

what section and vessel of heart must likely involved

phases ekg

 

Q image thumb

rupture of atherosclerotic plaque and COMPLETE blockage of coronary a. -> necrosis of cardiac myoscytes

coronary art

s/s: sevee crushing CP MORE 20 min, dyspnea: heart not pumping:pulmonary congestion edema

tx not releived by NG

must common LV (L anterior descending: infarct of anterior wall of LV and anterior portion of intraventricular septum) 2nd most common R coronary art  ( infarct of posterior wall of LV and posterior section of intraventricular septum), third circumflex ( infarct of lateral wall of LV), RV and both atria gen spared

phase: initial: subendo necrosis less 50% thickness ekg depression, more advance transmural necrosis ekg st elevation

A image thumb
500

MI vessels and areas they affect

and anterior portion of intraventricular septum) 2nd most common R coronary art  ( infarct of posterior wall of LV and posterior section of intraventricular septum), third circumflex ( infarct of lateral wall of LV), RV and both atria gen spared

A image thumb
501

MI labs

pt presents 5 days after infarct how to prove 2nd one happended

rises, peaks and normal return

membrane dmg causes leak for enzymes:

Best Troponin I most sensitive and specific: rises 2-4 hours after infarct, peaks 24 hr, normal by 7-10 days

CKMB: rises 4-6 hours, peaks 24 hours, returns 72 hours

CKMB can be used to proven recurrent infarct within the 7 day window of Troponin I

502

MI tx

Rx 

and interventional (complications)

ASA/ heparin: eliminate more thrombosis

o2: reduce ischemia

nitrates: dilation of vein decrease preload

BBlocker: slow HR, decrease risk for arrythmia a complication

ace inhibitor: prevent convertion of AT2: casuing vasodilation of arterioles ( decreasing afterload) and dcreasing Na reabsorp and volumen 

Fibrinolysis or angioplasty:

1. Contraction band necrosis ( when reperfusion Ca into cell causing banding of muscles in cell)

2. reperfusion injury form o2, 

503

caused by

Q image thumb

Fibrinolysis or angioplasty after MI:

1. Contraction band necrosis ( when reperfusion Ca into cell causing banding of muscles in cell) 

no nucleus in myocyte = necrosis

504

infaction timeline

1 day: coag necrosis(no nucleus), inflammation -arrhythmia due to dmg of conductive system

1 week: > 1-3 daysNeut( can cause pericarditis form inflammation, pain with riction rub) -> 4-7 days: macro( eat debri, wall weakest can cause rupture-> tamponade), ->granulation (tissue with red border: new vessel)

1 month: -> scar( white, weaker than myocard, risk for aneurysm, thrombus , Dressler synd (AB formed against periacardial tissue due to exposure during inflammation-> autoimmune pericarditits 6-8wks) 

KNOW CHART

A image thumb
505

papillary muscle supplied by

risk

R coronary art: 

can cause rupture of papillary muscle during the macrophages stage while they are eating the debris 4-7 days after MI

506

Dressler synd

Dressler synd (AB formed against periacardial tissue due to exposure during inflammation-> autoimmune pericarditits 6-8wks) 

507

what

time

whats happening microscopically

Q image thumb

dark discoloration around

4-6 hours

subendocardial infarction since its not all the way. 

coad necrosis 

508

what is it

whats happening

time

Q image thumb

myocyte

no nucleus= coag necrosis= 4-24 hours

 

509

510

Q image thumb

after coag necrosis

neutrophil come in day 1-3 can cause fibrinois pericarditis due to leak of inflamamtion-> fibrin on surface of heart only happens if it is transmural MI

511

Q image thumb

Fibrinous pericarditis

1-3 days after mi when neut come in can leak inflammation

ONLY WITH transmural MI NOt  with sub endocardial infarc

512

time

Q image thumb

rupture

macrophages 4-7 days can weaken the wall

513

what

vessel

time

Q image thumb

rutprue of papillary muscle

due to macrophages 4-7 days after

supplied by R coronary a

514

time

microscopic would show

Q image thumb

scar within myocardium

micro: dense collagen ( type 1 ) can lead to aneyrysm, thombosis

515

caused by

complication

Q image thumb

due to scar tissue can develeop . aneurism-> ballon dialation can form mural thombus

516

sudden cardiac death

by

s/s

etiology

unexpected death 

w/o s/s or within 1 hour

fatal ventricular arrhythmia

pre existing severe atheroslcerosis, mitral valve prolapse, cocaine ( vasospasms

517

Chronic Ischemic Heart Disease

by

porgresses

poor myocadial function

due to ischemic damage w/ or . w/o infarction

progres to CHF

518

Left CHF

causes

consequences

tx

ischemia

HTN

Dilated cardiomyopathy: 4 chamber dilatation of heart

MI

Restrictive cardiomyopathy: 

consequences: pulmonary congestion: edema dyspnea, crackles, small capillaries may burst -> hemorrhage -> marked by hemosiderin -laden macrophages " heart failure cells". decreased foward perfusion : activates renin-angiotensin system ( decrease renal perfusion), can cause R sided heart failure

tx:  ACE inhibitor

519

what

from

Q image thumb

L HF : pulmonary capillaries may burst -> hemorrhage -> marked by hemosiderin -laden macrophages " heart failure cells"

520

R HF 

causes

s/s

most common cause if L HF

also L to R shunt, COPD (cor pulmonale)  

s/s: JVD, painful hepatospleenomegally -> cardiac cirrhosis, dependent pitting edema

521

Q image thumb

nutmeg liver dure to congested liver failure

522

Cardiac congenital defects 

arise during

%

what types 

weeks 3-8 in embrogenesis

1% live births

 

523

most common congenital heart defect?

associated w/

causes

Ventricular septum defect

fetal alcohol syndrome

lead to L to right shunt

causes to pHTN -> with time causing R to L shunt causing BLUE blood cyanosis

 

524

reversal of shunt

causes

tx

late cyanosis ( Eisenmenger syndrome) with R ventricle hypertrophy, polycythemia, and clubbing

large sx closure

525

Atrial septal defect

most common types

what disease is r/t to one this

heart sound

com

Most common Ostium secundum

ostium primum r/t Downs synd

L ti R shunt : S2 on ascultation (delay closure of aortic and oulmonic close

526

 

patent ductus arteriosum

r/t

where s/s

tx

fail to close : blood from aorta to pulm -> (eisenmenger syndrome) reversible shunt -> blue blood -> cyaonosis in lower ext

r/t CONGENITAL RUBELLA

tx: endomethacin -> decreases PGE causing PDA closure

527

clinical

Q image thumb

tetralogy of fallot

"BOOT CHAPED HEART"

 1. stenosis of the pulm outflow tract

2. vsd

3. aorta overriding VSD

4. R vent hypertrophy

early cyanosis depend on stenosis., cyanosis with exercisse to reverse it aquat down increase afterload sending more blood to pulm 

r to L shunt

A image thumb
528

transposition of great vessels

tx

r/t

s/s

aort aof R

pulm trunk out of L

two separate circuit that dont mixed

tx: maintain PDA ( given PGE " Keeps opened the pda")

r/t maternal DM

s/s early cyanosis

A image thumb
529

truncus arteriosus

s./s

 single large vessel from both ventricles

Trunus fails to divide 

early cyanosis due to mixing

530

Tricuspid atresia

r/t

s/s

tricuspid valve orifice fails to develop

R ventricle becomes hypoplastic due to no blood going through

r/t ASD

s/s ealry cyanosis due to shunt 

531

types

 

Q image thumb

Coartation of aorta

narrowing of aorta 

infantile: r/t PDA, distal to aortic arch but proximal to PDA, causing walry cyanosis going to LOWER ext cyanosis, r/t TURNER SYND (

adult form: not r/t PDA, distal to aortic arch,  HTN of upper ext and HYPO TN of lower ext, r/t bicupid aortic valve , " notching of the ribs by engorge arteries trying to bypass

 

532

Q image thumb

coartation of aorta

adult form: not r/t PDA, distal to aortic arch,  HTN of upper ext and HYPO TN of lower ext, r/t bicupid aortic valve , " notching of the ribs by engorge arteries trying to bypass

533

  Acute Rheumatic fever

r/t

how long after

what happens

R/T pharyngitis due to group A B-hemolytic strep

2-3 wks after strept throat

molecular mimicry bacterial M prot resembles human tissues

534

Dx of A Beta-hemolytic strep infection

Jones criteria

ASO or anto DNase B titer

minor criteria fever and elevated ESR

major criteria

J : joint wrist knees ankles

O: heart problems, endo myo and pericarditis ( main problem)

N : nodules on skin 

E :  erythema marginatum erythemous borders

S : Sydenham chorea ( rapid involuntary muscle movements)

 

535

regurgitationwhat

where is most common

leads to?

Q image thumb

pancarditits : all layers inflammed

endocarditis: tiny vegetations ( round pink on mitral valve #1, aortic #2) -> regurgitation

 

536

what

cell in it

hallmark

#1 cause of death

Q image thumb

Aschoff bodies involving myocardium surrounded by myocytes

its a focus of chronic inflammation and giant cells and fibrinoid material with group of cells called 

Anitschkow cells

cells with slednder nuceli HALLMARK 

# 1 COD of acute rheumatic fever is the myocardititis ( Aschoff bodies with contained Anitschkow cell)

537

chronic Rheumatic disease

if pt doesnt die from # 1 COD of acute rheumatic fever is the myocardititis ( Aschoff bodies with contained Anitschkow cell)

with chronic it increases the risk for valvular disease : Scarring from many acute attacks: stenosis : Mitral valve ( thickening of chordae tendineae and cusps) and maybe aortic if more ( fusion of commisures

538

Q image thumb

with chronic it increases the risk for valvular disease : Scarring from many acute attacks: stenosis : Mitral valve ( thickening of chordae tendineae and cusps) and maybe aortic if more ( fusion of commisures

scarring fusses the edges of the commisures aka fish mouth appearacne of vavle

 

539

due to

presents in

more common

Q image thumb

aortic stenosis

fibrosis and calcification from wear and tear disorder more common 60 plus

bicuspid aortic valve more common ( normally tricuspid but bicuspid have to do work of 3 increases the risks and earlier) each of the cusp should be smooth but they look fibrotic, harder to push blood through

 

540

stenois form

rheumatic disease vs wear and tear

Rheumatic: stenosis from mitral and aortic (mitral alwyas first),  Fusion of aortic valve commissures 

Wear and Tear: if aortic only, 

 

A image thumb
541

valvular stenosis

 clinical

complications

tx

prolongued asymptomatic stage

ventricle compensates and blows open the harden valve : systolic ejection clicl followed by crescendo-decrescendo murmur

Concentric left ventricular hypertrophy, angina, syncope, microangiopathic hemolytic anemia

tx : after the onset of the complication

542

most common cause of  aortic regurgitation

clinical

isolated aortic root dilatation

some times can be related to damage to valve itself like Infective endocarditits, 

clinical: early blowing diastolic murmur, bounding pulses, pulsation nail bed, head bobbing (HYPERDYNAMIC CIRCULATION) widening of PULSE pressure

543

pt presents with bounding pulse, pulsating nail bed, head bobbing, 

aortic regurgitation

clinical: early blowing diastolic murmur, bounding pulses, pulsation nail bed, head bobbing (HYPERDYNAMIC CIRCULATION) widening of PULSE pressure

544

aortic regurgitaiton

clinical

tx

LV dilation: Eccentric hypterrophy ( one side only) 

tx: valve repla

545

rt

clinical

complicaiton

tx

Q image thumb

Mitral balve prolapse

balloning of mitral into LA during systole

due to myxoid degeneration of valve making

 R/T MArfan and EDS

clinical: Mid systolic click followed by regurgitation: asymptomatic

comp: IE, arryhythmia ,sever regurgitatiom 

tx: replace

546

mitral stenosis when

clinical

complications

due to chronic rheumatic valve d -> creates stenoiss

acute rheumatic d- > creates regurgitation

opening snap fllowed by diastolic rumble

comP : overload of LA and dilatation -> pulm congestion, pulm HTN atrial fibrillation : due to dilation

547

chronic rheumatic valve d ->

acute rheumatic d- >

chronic rheumatic valve d -> creates stenoiss

acute rheumatic d- > creates regurgitation

548

Q image thumb

mural thrombus due to blood stasis ie: w/ LA overload due to stenosis

549

most common caise of endocariditis

results in

pathogenesis

most common endocard in IV drug abusers

S viridans low virulence organsm : so can only affect previously dmg valve: rheumatic fever/prolapse

result in small vegetation that DO NOT destroy valve

dmg valve -> thombotic vegettation ( pt and fibrin) -> trapps bacteria during transiet bacterimia

----------------------------------------------------------------------

S aureus

high virulaence , infects normal valve -> large vegetations that destoy the valve -> normally Tricuspid

550

most common endocarditis in IV dcrug abuse

S aureus

high virulaence , infects normal valve

551

Most common cause of endocarditis of prosthetuc valves

prosth - S epidermis

 

552

endocarditits with underlying colorectal carcinoma

caused by

S bovis

553

pt with S Bovis endocarditis check for

colorectal carcinoma

554

endocarditis with negative blood culture by?

HACEK organisms

H emophilus

A ctinobacillus

C ardiobacterium

E ikenella

K ingella

555

endocarditis clinical

labs

 

 

Fever,

Murmur ( flow altered) 

those vegetation can dislodge and cause embolixationof septic vegetatiosn cause lesion such as:

JAneway lesion: erythmatous nontender lesion on palms and soles

Osler nodes ( tender lesion on fingers or toes ( Ouch Osle painful)

nailbed hemmorrages

Anemia of chronic disease: Microcytic anemia: L Hg, L MCV, H Hepcidin ( traps iron) -> Ferritin H, Transferritin L

TEE detect lesion on valves

556

nonbacterial thrombotic endocarditis by?

sterile vegetation by hypercoag state or  underlying adenorcarcinoma

ussually on mitral line

557

Libman Sacks Endocarditis

sterile vegetations r/t SLE, on both sides of Mitral Valve -> regurgitation

558

leads to 

complications

cause?

tx?

Q image thumb

dilateted cardiomyopathy

all 4 chamber dilated: systolic dysfunction -> biventricular CHf

mitral and tricupid regurgitation ( from stretching)

cause: genetic mutation ( autosomal domi), myocarditis ( cox sackie virus ), alcohol abuse, drugs ( cocaine, doxyrubicin) , pregnacy

tx: transplant

559

clinical

biopsy result?

Q image thumb

hypertrophic Cardiomyopathy

massice hypertrophy of LV: genetic mutationin sarcomere protein autosomal dominant-> decreade output due to so much muscle, sudden death due to vent arrhtythmia ( athletes die) , syncope w/ exercise

bio: Myofiber hypertophy with disarray , normally myocytes should be organize parallel

 

560

what

by

s/s

restrictive Cardiomyopathy

decreased compliance of ventricular endomyocardium

by: amylidosis, sarcardosis, hemochromatosis, endocardial fibroelastosis ( children ), Loeffer syndrome eosinophilic infiltration

s/s : CHF, low voltage EKG, diminished QRS amplitudes

561

Myxoma

benign mesenchymal prolif with gelatinous appearance

histo: abundant grund subs

most common primary cardiac tumor in adults

LA as a peduculated mass that may obstruct mitral valve

562

Rhabdomyoma

 most common in>

r/t?

benign hamartoma of cardiac muscle

most common primary cardiac tumor in children

r/T : tuberous scleroisis

ventricle

 

563

metastasis to heart from

where in heart

breast, lung carcinoma, melanoma, lymphoma

pericardium -> pericardial effusion

564

rhinitis

cause

s/s

inflamation of nasal mucosa

adenovirus: 

sneezing congestion runny nose ( common cold) 

565

allergic rhinitis

cause

histo

r/t

type HSR eg pollen

inflammatory infiltrate w/ eosiniphils

r/t: asthma and eczema

566

chhildren with nasal polyps

what

causes

THINK ABOUT?

protrusion of edematous inflamed nasal mucosa

2ry to bouts of rhinitits 

CYSTIC FIBROSIS AND ASA-intolelrant asthhma ( adults taking asa causing spasms)

567

adolescent mamle present wit growt in nasal mucosa and profuse epistaxis

angiofibroma

benign tumor of nasal mucosa composed of large blood vessels and fibrous tissue

adolescent male

profue epistaxis

 

568

Chinese adult with enlarged lymph node  

r/t

demographics

biopsy show pleomorphic keratin possite epithelial

nasopharyngeal carcinoma (can spread to cervical lymph node quick)

malignant epithelium

r/t EBV

seen in African children and Chinese adults

pleomorphic keratin possite epithelial in a background of lymphocytes -> carcinoma

569

by

seen in 

s/s

complication

Q image thumb

Acute epiglititis

H influenza type B in both immunized and nonimmized children

high fever, sore throat, droolin, dysphagia, muffled voice, inspitory striddor 

risk acute airway obstruction: medical emerrgency

570

pt presents with hoarse barkeing cough and inspitroy . stridor

by

Laryngotracheobronchitis ( CROUP)

upper airway inflam

by parainfluenza virus

571

due to

s/s

tx

Q image thumb

vocal crod noduels

due to excesive use ( bilateral) wear and tear

 

s/s hoarness

rest

572

Laryngeal papilloma

by

adults vs children

s/s

Laryngeal papilloma 

benign papillary tumor of vocal cord

due to HPV 6 and 11

single in adult and multiple in children

hoarness

573

Laryngeal carcinoma

risk factors

s/s

Laryngeal carcinoma

SCC from epi of vocal cord

risk factor: etoh and tobacco, but also from low risk laryngeal papilloma (HPV 6 11) 

hoarsenes cpugh stridor

574

pneumonia

increased risk . with

clinical

infection of lung paranchyma 

H risk with dmg to mucociliary escalator eg viral pneumonia, 

clinical: fever, cough green sputum/rusty sputum, PLEURITIC CHEST PAIN (expantion), decreased breath soun and dullness percussion, H WBC

575

diagnosis pneumonia 

CXR:  Lobular pneumo, Bronchopneu ( patchy) both baterial

Interstitial pneumo ( increased un lung marking) viral

sputum cult

blood cult

576

type

micro

histo

phases, which stem cell?

Q image thumb

lobar pneumonia

usually bacterial :

S pneumonie community acquired old adults

Klensiells pneu ( malnourished , DM, alcoholics, enteric flora aspiration ) has a thick mucoid capsile -> gelatinous sputum, complicated by abcess

air sac filled with neut 

phases: congestion vessels -> red hepatization ( rbcs into air space -> grey hepatization ( RBCs die) -> resolution ( heal type 2 pneumocyte is the stem cell)

577

type

micro

histo

Q image thumb

broncho pneuumonia

scatterd patchy consolidation around bronchioles 

by bacteria

-staph A, mostt common of 2ry pneumonia ( bact superimposed on viral upper resp inf ( kills escalator, complicated by abcess or empyema

-Haemophilus influenza: 2ry and suuperimposed on COPD -> exhacerbation of COPD

Pseudomonas Aeruginosa: in cystic fibrosis

Moraxella catarrhalis: community acq and superimposd on COPD

LEgionella pneumophilia: communuit acqu, superimp copd, immuno compromised, transmitted water source,  an intracellular organism bes t visualized by silver stain

histo: patchy of inflammation

578

LEgionella pneumophilia:

know all

LEgionella pneumophilia: communuit acqu, superimp copd, immuno compromised, transmitted water source,  an intracellular organism bes t visualized by silver stain

579

type

s/s

histo

micro?

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interstitial pneumonia ( atypical : atypical s/s, bugs

diffuse intestitial infiltrates

minimal sputum, cough low fever)

histo air sac empty but alot of inflammatory cells

 Mycoplasma pneu: most common atypical, yoyung adults (military or college stud) complications -> hemolytic anemia ( IgM against I antigen on RBCs causes cold hemolytic anemia. not visible in gram stain due to lack of cell wall

-Chlamydia pneumonia: 2nd most common of atypical in young adult

RSV resp syncytial virus: most common atypical in infants

-Cytomegalovirus: atypcial pneu with posttranplant immunosuppresive therapy    

- influenca, atypical pne in elderly, immunocomp, increases risk for superimpo S Aureus or H influe bacterial ( ca ncause of death) 

-Coxiella burnetii: farmers and veterinarian(cattle placentas) , high fever (interstitial norm low) , 

580

- influenca Virus interstitial pneu

- influenca, atypical pne in elderly, immunocomp, increases risk for superimpo S Aureus or H influe bacterial

581

Aspiration Pneu

risk

micro

results

 

pt at rsik of aspiration alcoholiucs, comatose

micro: anaerobic bacteria in oropharynx eg; bacteroides, fusobacterium and Peptoccus

results in R lower lobe abcess, easier to go to R than left branch

582

micro

types

clinical

biopsy

stain

 

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tuberculosis

inhalation of aerolized Mycobacterium tuber

1ry: when arise with initial exposure -> focal caseating necrosisin lower lobe and hilar lymph nodes, foci undergo fibrosis and calcification ( Ghon complex:" A picture white spot), s/s asymptomatic but ppd postiive

2ry : Gohn complex reactivated: r/t AIDS and with aging, occurs at apex of lung, forms cavitary foci of caseous necrosis-> miliary pulm TB or tuberculous bronchopneum

clinical : fever nigh sweats: cough with hemoptosis, weight loss, 

biosy: caseating granulomas ( fungus and TB

Stain AFB reveal red acid fast bacilli (C : red bacilli)

 

583

TB spread to?

any tissue but most common

Meningitis  with granulomas(base of brain)

Cervical lymph node

Kidney ( sterile pyuria) 

Pott disease lumbar vertebrae

584

COPD

spirometry changes?

airway obst: L FVC, LL FEV1(1sec): decreased FEV1:FVC ratio, H TLC ( trapping)

585

pt presents with productive cough lasting 3 months in a 3 year. cups of mucus

r/t

histo

clinical expected

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Chronic bronchitis

r/t smoking: lung increase amount of mucus by hypertrophy of mucinus glands ( Reid index more than 50% norm less than 40, of thickness of bronchial wall) 

histo Upper right : resp epi, circular spaces are mucinous glands 

clinical : prod cough, Cyanosis ( H PaCO2, L PaO2 ), increased risk infection ( generally tube blocked = causing infection distal to it) increased risk for Cor Pulmonale ( arterioles constricts to shunt blood to other areas to increase exchange)

586

Emphysema

cause

suceptible for

destruction of alveolar air sacs-> loss of recoil and collapse of small airway-> trapping

obstruction is physiological: due to loss of elastic loss-> causes obstruction when wall collapse

imbalance of proteases and antiproteases: inflammation due to normal macrophages activity can induce proteases but anti proteases to protect the lungs ( A1AT).  balance is disrupted

causes: H inflamation like in, smoking ( H proteases activity), A1AT deficiency 

587

types of emphysema

centricacinar emphysema: smokin most common cause of emphysema, more severe in upper lobe

panacinar emphysima: r/t to A1AT  more severe of lower lobe, Liover cirrhosis may also be present ( protein misfolded and accumulates in liver causing DMG)

588

biopsy reveals 

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hepatocytes, center one with dark center = A1AT msfolded in ER ad to cirrhosis, It is an antiprotease so the lack of it in lunngs results in emphysema

biopsy reveals pink PAS positive globules in hepatocytes

589

A1AT def allele?

mutations?

clinical

PiM is nomal allele

mutation

is PiZ: misfolded protein accumulates in ER of hepatocytes -> cirrhosis

PiMZ heterozygotes: asympt with decreased lvls of A1AT -> significant risk for emphysema w/ smoking

PiZZ homozygtes : panacinar emphysema plus cirrhosis

dyspnea minimal sputum, prolongued expiration with pursed lips (pink puffer to keep airway open and prevent collapse) , wt loss, barrel chest ( chest wall wins tug of war due to loss of elastic RESets FRC) , ( fibrosis  (increased FRC as elastic increased) 

590

ASthma

presents 

pathogenesis

 

a COPD 

reversible airway bronchoconstriction, ( type 1 HSR) 

chilhood r/t to az rhinitis, eczema, 

patho: gneticaly suceptible, allergen induce Th2 phenotype in CD4 -> secrete IL4 ( plasma cell -> IgE) ,5,( calls eosiniphils) 10( inhibit Th1 and indice Th2 )

 

591

reexposure to allergen in astham causes?

patho: gneticaly suceptible, allergen induce Th2 phenotype in CD4 -> secrete IL4 ( plasma cell -> IgE) ,5,( calls eosiniphils) 10( inhibit Th1 and indice Th2 )

reexposure causes 1. mast cell activation -> dumps histamine granules ( histamine induce vasodilation ( arterioles ) and increased vascular perm ( post cap venule. 2. phase by prod of leukotrienes C4 D4 E4 -> vasoconstriction, increased perm, broncho constriction

late phase: inflammation eg major basic protein perpetuates bronchoconst 

592

592

asthma clinical features 

 

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dyspnea and wheexing prod cough, CRUSCHMAN SPIRALS ( spirals within mucsus) and Carcot Leyden crystals ( photo: crystals of eosiniphils major basic proteins) withing the mucus 

severe attack -> status asthmaticus -> death

593

 Non Allergic cause of asthma

 

ASA intolerant asthama: get broncho spasm and nasal polyps 

exercise

viral

occupational exposures

594

what

cause

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bronchiectasis a . cOPD

permanent dilation of bronchioles and bronchi ( pipe bigger than face if u blow u cant feel it)-> air trap

due to necrotizing inflammation to airways -> cystic fibrosis ( block infection), Kartagener synd ( defective in DYNEIN ARM of ciia for movement), ( s/s sinusistis, infertility, ( por motility), situs inversus ( position of major organs is reversed e g heart of L  , tumor or foreign body, necrotizung infection, allergic bronchopulm aspergullosis ( Asthmatic and cystic fibrosis)

photo : on edge of lung severa dilatation

595

Kartagener synd

( defective in DYNEIN ARM of ciia for movement), ( s/s sinusistis, infertility, ( por motility), situs inversus ( position of major organs is reversed e g heart of L  

596

pt with cough dyspnea foul smelling sputum

possible

complication

bronchiectasis

hypoxemia

 cor pulmonale

secondary amylidosis ( over prod of SAA turns into AA causing 2ry maylidosis) 

597

what

histo

etiology 

drugs r/t

tx

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idiopathic pulmonary fibrosis

histo: empty = air sac, in between alot of fibrosis

cyclical lung injury related

pneumocyte release TGFB ( like macrophages IL10 and TGFB) -> fibrosis

secondary causes like: Bleomycin and Amiodarone, radiation therapy. rule this out 1st

lung transplant

598

 

pneumoconiosis

 

pneumoconioses 

fibrosis due to occup[ational exp: chronic exp to small particles thatt are fibrogenic ( large particles are filtered out.

mediated by macrophages -> starts inducing fibrosis

 

 

599

Coal workers pneumonociosis

 : black lung r/t Caplan synd ( RA), mild exp doesnt do anything ( Anthracosis

600

Only pneumoconiosis than increases risk for TB

 

Silicosis

Silica in sandblastes, miners:

silica impairs formation of phagolysosoe by macrophages -> increases risk TB

Fibrotic nodules in upper lobes

601

pt works for nasa 

berylliosis

seen in miners and aerospace industry workers

noncaseasting granulomas lungs and hilar lymph nodes and systemic organs

increased risk for lung cancer

602

what 

can cause

histo 

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Asbestosis

 asbestos fibers in constructuion workers, plumbers, and shipyard worker

asbestos: causes fibrosis of  lun or pleura, cancer of lung and pleura ( Mesothelioma ) MORE LIKELY FOR LUNG CA THAN MESOTHELIOMA

rods containg iron

603

what

seen in

etiology

histo defining cell

Q image thumb

Sarcoidosis

noncaseating granulomas in multiple organs, most common lung and hilar lymph nodes

common in AA females

likey due to CD4 t cell response to antigen

histo defining of a granulomacell is a epithialoid histiocyte ( noncaseating = all cells are alive no necrosis)

send image: in granuloma can see ASTEROID BODY  

604

Sarcoidosis

involves

most common lung and hilar lymph nodes

uvea

skin

salivary and lacrimaglands ( mimics Sjogren syndrome but will see non caseasting granulomas

 

605

pt presents with cant chew cracker, dirt in eye , increased dental caries

Sarcoidosis

salivary and lacrimaglands affected but most common lung and hilar lymph nodes ( mimics Sjogren syndrome but will see non caseasting granulomas

606

Sarcoidosis

clincal

tx

dyspnea/ coug

H ACE : 

hypercalcemia : noncaseating granulomas can activate vit D( by increase in 1 alpha hydroxylase activity which converts Vitamin D to active form)

tx steroids, can resolve spontanou w/o tx

607

Hypersensitivity Pneumonitis

clinical

leads to 

granulomatous rx ( eosiniphil) to inhaled organic antigens ( pigeon breeders lung)fever cough dyspnea after hours of exp, resolves w/ removal

chronic leads to interstitail fibrosis

608

Pulmonary HTN 

characterized by

histo

leads to

Q image thumb

more than 25, norm is 10

Atherosclerosis of pulm trunk, smooth hypertophy of art, intimal fibrosis, PLEXIFORM LESIONS W/ SEVERE LONG STANDING. 

histo: plexiform lesion: groups  of tuft of cappilaries group together that occur with sever longstanding htn 

-> RV hypertrophy and cor pulmonale

609

pt presents with excerptional dyspnea

dx

can be pulm htn -> rv hypertrophy -> RHF

610

Primary pulm HTN

 

seen in YOUNG ADULT FEMALE

etiology unknown

Familia r/t INACTIVATION MUTATION OF BMPR2 : causes proliferation of vascular smooth muscle -> pulm htn

611

2ry pulmonary HTN

due to

1. hypoxemia ( in COPD AND interstitial lung disese) lung tries to shunt that area and move to other with more o2 but ends up being entire lung ,

2.  from increased volumen in pulm circuit ( CHF) ,

3. Recurrent pulm EMBOLISM

612

  pulm HTN causes 

BMPR@ inactivation -> prolif of  vasc smooth muscle -> plexiform lesion -> atherosclerosis 

613

what 

cause

Histo

clinical 

cxr?

Q image thumb

ARDS

dmg  to alveolar capillary interface ->  protein leak into air sac  -> HISTO formation of hyaline membranes in alveoli ( air sca lined by pink hyaline membrane) -> thickens diffusing barrier -> hypoxemia and cyanosis, also  hyaline is sticky and would cause collapse

CXE diffuse white of lungs

614

ARDS 

etiology

tx

etio: sepsis, infect, shock, trauma, asp, pancreatitis, DIC, Ax Rx, drugs 

activation of neutrophils -> proteases mediated FR damage type I and II pneumocytes:  

tx: ventilation w/ PEEP  positive endexp pressure ( due to collapse from hyaline membrane covering sac), maybe complicated by interstitial fibrosis ( since pneumocyte II the stem cell died there is no regeneration but repair) 

615

newborn presents with cyanosis, use of accessory muscles, hypoxemia
due to 

clinical

cxr

associated w/

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Neonatal Resp dist Synd

due: inadequate surfctant levels : prod by type 2 pneumocyte ( stem cell and prod surf), prevent collapse 

clinical: increased resp effort after birth -> tachypnea use of accessory muscle, hypoxemia cyanosis,

diffuse granularity of lung on xray

R/t prematurre ( surfact starts at 28 wks adequate lvls at 34 wks) screen with L:S ratio ( lecethin/ sphengomyelin) lecithin is component of surfactant so it should increased toward 34 wks ( ratio greater than 2)  

 C-section deliver ( stress from natural delivery causes steroid pod: increase prod of surfact) but csection is easier no stress to newborn

Maternal DM: high blood sugar, babys pancreas prod exccess insulin: inhibitor of surfactant pro

616

whats the major component of surfactant

Phosphatidylcholine = Lecithin, increases as surfactant is produced, sphingomyelin remain constant 

617

neonatal resp distress synd

complications

hypoxemia increases risk for persistence of patent ductus art ( closes when good oxygenation of blood) and necrotizing enterocolitis ( decreased o2 to gut)

supplemental o2 increases risk for free radical injury ( injury retina (blindness) , immature lung ( 2 years to mature ) get hit with free radical it will injure it -> bronchopulmonary dysplasia)

618

most coomon cause of cancer mortality?

presents at

risks

lung cancer

60 yo

risk: smoking( polycyclic aromatic hydrocarbons( arsenic : increase risk squamous cell carcinoma of lung) r/t pack years , radon(generated from decay of uranium in soil -> colorless ordorless gas, also urainium miners) , abestos ( more likely to develop lung cancer than mesiothelioma

619

 pt with nonspecific s/s of lung , CXR solitary nodule "coin lesion" (2-5cm) whats the next step? 

check with prior cxr and check if stable = benign. if new or growing possible biopsy for cancer dx

620