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MAMS > Path Exam 3 > Flashcards

Path Exam 3 Flashcards

1
Q

Autosomal recessive polycystic kidney disease

A

Enlarged kidneys composed of saccular or cylindrical cysts

Replace renal parenchyma

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2
Q

when does Autosomal recessive polycystic kidney disease present

A

Usually presents in prenatal period, can present in childhood

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3
Q

other effects of Autosomal recessive polycystic kidney disease

A

Can prevent lung development → stillborn, or die shortly after birth
Cysts and bile duct proliferation are seen in the liver

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4
Q

effects of juvenile onset of Autosomal recessive polycystic kidney disease

A

hepatic fibrosis and disease is dominated by liver manifestations

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5
Q

Autosomal dominant polycystic kidney disease

A

Genetic disease with high penetrance
Kidneys greatly enlarged with numerous cysts
Pressure atrophy effects from cysts tubules and vessels

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6
Q

what do most cases of Autosomal dominant polycystic kidney disease result from?

A

gene defects on chromosome 16

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7
Q

when does Autosomal dominant polycystic kidney disease present?

A

mid- adulthood but may manifest in perinatal period or in old age

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8
Q

treatment for Autosomal dominant polycystic kidney disease

A

transplant

dialysis

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9
Q

what can chronic dialysis cause?

A

atrophy of kidney

many small cysts

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10
Q

what can cause acquired cysts?

A

long term dialysis patients

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11
Q

simple cysts

A

Single or multiple cysts, translucent, filled with clear fluid and lined by single layer of simple epithelial cells

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12
Q

when can simple cysts become problematic?

A

large cysts may rupture, hemorrhage

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13
Q

Glomerulonephritis

A

Inflammatory disease of the glomeruli that can show different patterns of glomerular injury

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14
Q

Glomerulonephritis symptoms

A

asymptomatic hematuria or proteinuria
nephrotic syndrome
nephritic syndrome
acute renal failure

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15
Q

nephrotic syndrome

A

marked proteinuria that is indicative of significant dysfunction of glomerular ultrafiltration

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16
Q

nephritic syndrome

A

presence of red blood cell casts in the urine that is indicative of severe glomerular injury

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17
Q

diffuse

A

most or all glomeruli are affected by disease

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18
Q

focal

A

only some glomeruli are affected by disease

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19
Q

segmental

A

only part of the glomeruli is affected by disease

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20
Q

global

A

entire glomeruli is affected by disease

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21
Q

normal glomerulus

A

Highly specialized filter in which the blood in the capillaries are filtered through epithelium, BM, and endothelium

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22
Q

type 1 mesangial cells

A

contractile

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23
Q

type 2 mesangial cells

A

phagocytic

secretory

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24
Q

features of endothelial cells of glomeruli

A

fenestrated with 70-100 nm pores
Anionic charges restrict negatively charged molecules
Size filter restricts proteins that are around the size of albumin

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25
Q

what composes the glomerualar BM?

A

collagen type IV, laminin, polyanionic proteoglycans, fibronectin, glycoproteins

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26
Q

role of glomerualar BM

A

size charge and filter

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27
Q

Visceral epithelial cell

A

podocyte with complex interdigitating processes

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28
Q

Bowman’s space

A

space for pre-urine ultrafiltrate from capillary loops

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29
Q

Parietal epithelium

A

epithelial cells lining Bowman’s space

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30
Q

3 mechanisms of immune injury within the glomerulus

A

Immune complexes formed within the glomerulus → anti-glomerular BM antibodies

Immune complexes formed outside the glomerulus and trapped by the glomerulus

Activation of immune response not involving antigen-antibody formation

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31
Q

Mesangial cell hypercellularity clinical correlation

A

hematuria

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32
Q

Mesangial matrix increase clinical correlation

A

decreased GFR

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33
Q

Epithelial cell foot process effacement clinical correlation

A

proteinuria

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34
Q

Crescent formation clinical correlation

A

acute renal failure

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35
Q

Pyelonephritis

A

Inflammation of the renal parenchyma, calyces and renal pelvis as a result of infection

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36
Q

acute pyelonephritis

A

Ascending bacterial infection from the bladder

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37
Q

Hematogenous seeding

A

Infection elsewhere in body that travels to kidney

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38
Q

what can hematogenous seeding lead to?

A

obstructed kidney

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39
Q

who is more prone to acute pyelonephritis

A

diabetics

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40
Q

___ papillae are convex and resist reflux urine

A

Renal

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41
Q

___ papillae are concave and allow easier access

A

compound

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42
Q

chronic pyelonephritis

A

Chronic tubulointerstitial disease with gross, irregular, and often asymmetric scarring and deformation of the calyces

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43
Q

gross appearance of chronic pyelonephritis

A

Dilated calyces

Opaque urethral membranes

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44
Q

features of end stage renal failure

A 
Tubules dilated with hyaline casts → “thyroidization” of kidney
Chronic inflammatory cells
Thickening of vessels 
Fibrosis 
Global sclerosis
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45
Q

global sclerosis

A

all scared, non functional glomeruli

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46
Q

what can scar tissue in the kidney lead to?

A

loss of renal cortex

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47
Q

calculi

A

renal stones

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48
Q

intrinsic obstructive lesions

A

calculi
strictures
tumors
blood clots

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49
Q

extrinsic obstructive lesions

A

pregnancy
endometriosis
tumor

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50
Q

Sclerosing retroperitonitis

A

Produces ill-defined fibrous masses with pronounced chronic inflammatory response

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51
Q

treatment for kidney stones

A

sound waves

can pass on their own

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52
Q

most common patients with bladder outflow obstruction

A

elderly males due to prostatic hypertrophy or disease

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53
Q

80% of all malignant tumors are ___

A

renal cell carcinoma

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54
Q

renal cell carcinoma is ___% of all cancers

A

1-3

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55
Q

when do cases of renal cell carcinoma peak?

A

6th and 7th decade

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56
Q

hypernephroma

A

renal cell carcinoma

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57
Q

adenocarcinoma of kidney

A

renal cell carcinoma

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58
Q

renal cell carcinoma etiology

A

increased in smokers

chromosome abnormalities in 3,8, 11

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59
Q

renal cell carcinoma sites

A

more common in upper pole

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60
Q

gross appearance of renal cell carcinoma

A

spherical
hemorrhagic or cystic
usually large size 3-15cm

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61
Q

where do renal cell carcinoma tend to invade?

A

renal vein

can stretch to atria

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62
Q

microscopic appearance of renal cell carcinoma

A

commonly composed of large clear or granular cells

Areas of hemorrhage and necrosis are common

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63
Q

Small basophilic cells with papillary patterns tend to have ___

A

chromosomal trisomies

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64
Q

large chromophobic cells tend to have ____

A

chromosome deletions

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65
Q

sacromatoid pattern cells tend to have ___

A

multiple cytogenic abnormalities

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66
Q

which cells in renal cell carcinoma have a poorer prognosis?

A

sarcomatoid pattern cells

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67
Q

complications of renal cell carcinoma

A

metastasis, commonly to lungs and bone

Paraneoplastic syndromes from secretion of active compounds

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68
Q

secretion of erythropoietin from renal cell carcinoma causes ___

A

polycythemia

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69
Q

secretion of parathormone from renal cell carcinoma causes ___

A

hypercalcemia

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70
Q

secretion of renin from renal cell carcinoma causes ___

A

hypertension

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71
Q

secretion of ACTH from renal cell carcinoma causes ___

A

cushing’s syndrome

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72
Q

signs and symptoms of renal cell carcinoma

A 
painless hematuria
flank pain or mass
malaise
weakness
weight loss
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73
Q

how to clinically diagnosis renal cell carcinoma

A

X-ray
CAT
MRI
surgical exploration

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74
Q

how to lab diagnosis renal cell carcinoma

A

histologic examination

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75
Q

renal cell carcinoma treatment

A

nephrectomy

chemotherapy

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76
Q

Transitional cell carcinoma usually arises in ___

A

the bladder

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77
Q

Transitional cell carcinoma is _% of all cancers

A

2-3

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78
Q

Transitional cell carcinoma risk factors

A

Occupational exposure to naphol and some phenols
Tryptophan
Cigarette smoking
Treatment with cyclophosphamide

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79
Q

gross appearance of transitional cell carcinoma

A

Flat pattern with plaque like thickenings

Fingerlike papillary projections

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80
Q

microscopic appearance of transitional cell carcinoma low grade/grade 1

A

resemble normal transitional cell epithelium

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81
Q

microscopic appearance of transitional cell carcinoma high grade/grade 3

A

anaplastic

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82
Q

when is transitional cell carcinoma considered invaded?

A

penetration of BM

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83
Q

pre-neoplastic changes in transitional cell carcinoma

A

Hyperplastic
dysplasia
carcinoma-in-situ are commonly seen in uninvolved areas of bladder mucosa

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84
Q

carcinoma in situ

A

anaplastic, malignant cells with mitoses confined completely to the mucosa

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85
Q

____ is a precursor lesion of invasice TCC

A

carcinoma in situ

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86
Q

Hyperplasia of the transitional epithelium

A

increase in number of cell layers >7

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87
Q

Dysplasia of transitional epithelium

A

Cytological atypia and mitotic activity within transitional epithelium
Changes with or without hyperplasia
Cells lose polarity

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88
Q

clinical course of TCC

A

painless hematuria

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89
Q

what is Wilms tumor associated with

A

abnormality on chromosome 11

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90
Q

what does wilms tumor look like?

A

primitive kidney

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91
Q

prostate

A

retroperitoneal organ that encircles the neck of the bladder and urethra

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92
Q

2 layers of prostate

A

basal layer of low columnar epithelium

Columnar, mucus secreting epithelium

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93
Q

if ____ is missing in the prostate, indicates cancer

A

basal layer of epithelium

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94
Q

where do most prostate cancers occur?

A

peripheral zone

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95
Q

where does BPH occur in the prostate?

A

central zone

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96
Q

what is the most common cancer in the US?

A

Prostatic adenocarcinoma

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97
Q

who is most at risk for Prostatic adenocarcinoma?

A

age >60

African Americans

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98
Q

gross appearance of Prostatic adenocarcinoma

A

gritty and firm, poorly demarcated
Can infiltrate adjacent structures
Occurs in peripheral areas and posterior lobe of prostate
Usually yellowish or white-grey

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99
Q

histology of prostatic adenocarcinoma

A

glandular pattern with small disorganized gland architecture
Single cell layer of epithelium, no basal layer
Papillary or cribriform pattern

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100
Q

gleason score

A

Grade (1-5) + grade (1-5) = Score (2-10)

primary pattern and secondary pattern

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101
Q

what is staging of prostatic adenocarcinoma based on?

A

degrees of access of tumor to different body parts

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102
Q

stage I-II of prostatic adenocarcinoma

A

confined to prostate

Curable

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103
Q

stage IV of prostatic adenocarcinoma

A

pelvic node or other metastatic lesions

80% here when symptoms occur

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104
Q

symptoms of stage IV of prostatic adenocarcinoma

A

Pain
hematuria
dysuria,
frequency or urinary flow problems

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105
Q

where does prostatic adenocarcinoma metastasize

A

bone

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106
Q

prostatic adenocarcinoma treatment

A

surgery
castration
radiation
hormonal treatment

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107
Q

Prostatic intraepithelial neoplasia

A

Precursor to malignancy of the prostate

Prostatic glands with intact basal layer, increased # and stratification of cells lining glands

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108
Q

when does Prostatic intraepithelial neoplasia incidence increase?

A

age 40

10 years before increase in cancer

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109
Q

G1 Phase

A 
Cell grows in size 
Monitors availability of growth factors, nutrients, amino acids, whether or not there is room to grow
Makes ultimate “go, no go” decision 
Restriction; point of no return 
6-12 hours
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110
Q

S phase

A

Replication of all genomic DNA
Accurate but not perfect
Proofreading and error correction mechanisms exist
6-12 hours

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111
Q

G2 phase

A

Cell continues to grow in size
Cell synthesizes all of proteins necessary for mitosis
2-4 hours

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112
Q

M Phase

A

Mitosis
Replicated chromosomes are equally segregated into 2 daughter cells
Stressful to cell
Only lasts 15-45 minutes

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113
Q

loss of ____ is a hallmark of all human cancers

A

G1/S regulation

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114
Q

pro-growth factors

A

RTKs
MAPK
PI3K

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115
Q

anti-proliferative factors

A

p52
Rb
PTEN
p16

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116
Q

RTKs are bound by ___

A

growth factors

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117
Q

RTK cascades lead to transcription of genes important for growth such as:

A

myc

cyclin D

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118
Q

Elevated Cyclin D proteins binds and activates ___

A

Cdk4/6 kinases

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119
Q

Active cyclin D:Cdk4/6 complexes phosphorylate Rb protein, which sequesters ____

A

E2F transcription factors

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120
Q

E2F drive expression of?

A

genes necessary for S phase

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121
Q

oncogenes

A

genes that when activated/overexpressed promote cancer

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122
Q

tumor suppressors

A

genes whose functional loss promotes cancer

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123
Q

what is Rb

A

E2F inhibitor

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124
Q

what is p53

A

transcription factor

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125
Q

what is PTEN

A

PI3K inhibitor

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126
Q

what is p16

A

Cdk inhibitor

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127
Q

mutation

A

change in the nucleotide sequence of an organism

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128
Q

most common BRAF mutation

A

single nucleotide change from T to A at 1799

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129
Q

endogenous factors that contribute to cancer

A

ROS

DNA replication mistakes

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130
Q

__% of cancer driving mutations arise from normal mutation rates

A

66

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131
Q

__ DNA repair genes in humans

A

150

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132
Q

BRCA mutation

A

predisposes women to breast and ovarian cancers

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133
Q

what is aneuploidy a consequence of?

A

abnormal mitosis

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134
Q

aneuploid

A

possessing an abnormal number/structure of chromosomes

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135
Q

aneuploidy can ___ oncogenes

A

amplify

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136
Q

aneuploidy can __ tumor suppressor genes

A

deplete

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137
Q

multi hit hypothesis

A

Multiple genetic changes are required for tumorigenesis
activation of an oncogene
loss of a tumor suppressor
replicative immortality

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138
Q

how many genetic changes for tumorigenesis to start?

A

4-6

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139
Q

why are oncogene specific inhibitors failing in trials?

A

developed resistance

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140
Q

Metastasis

A

spread of cancer cells from 1 organ to another via the bloodstream

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141
Q

how do tumors achieve immortality

A

expression of telomerase

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142
Q

what happens when solid tumors cause inflammation?

A

immune cells release ROS and cytokines

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143
Q

how do tumors avoid apoptosis?

A

overexpressing anti-apoptotic proteins

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144
Q

why do cancer cells have increased rates of glycolysis?

A

need to synthesize building blocks for rapid growth

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145
Q

goal of targeted therapeutics and personalized medicine in cancer

A

identify the relevant driving mutations in individual patients

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146
Q

neoplasia

A

The process of uncoordinated cell growth exceeding the limits established for normal tissues due to loss of responsiveness to normal growth conditions

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147
Q

tumor

A

Swelling that can be produced by edema, hemorrhage, or neoplasm

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148
Q

hyperplasia

A

An increase in the # of cells comprising a tissue or organ

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149
Q

hypertrophy

A

Increase in size of individual cells making up a particular tissue or organ

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150
Q

metaplasia

A

Reversible change from one adult cell type to another adult type

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151
Q

are metaplastic changes precancerous?

A

no but can lead to cancerous transformation

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152
Q

dysplasia

A

Loss of normal orientation of one epithelial cell to the other
Accompanied by alterations in cell size and shape, nuclear size and shape, mitotic activity and staining characteristics

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153
Q

where is dysplasia usually occur?

A

lining epithelia

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154
Q

are dysplasia changes precancerous?

A

yes

assoc with anaplasi

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155
Q

anaplasia

A

lack differentiation

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156
Q

what marks anaplastic changes?

A 
Pleomorphism
Nuclear pleomorphism
Increased nuclear:cytoplasm ratio
abundant/abnormal DNA content
Aneuploidy
Presence of prominent nucleoli
Increased mitotic activity
Tumors giant cell formation
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157
Q

how are tumor giant cell forms?

A

Result of nucleus dividing but cytoplasm not dividing

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158
Q

differentiation

A

Extent to which parenchymal cells of a particular growth resemble the normal cells in the tissue or organ from which the growth arose both morphologically and functionally

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159
Q

well differentiated tumors

A

cells that closely resemble normal cells of parent organ/tissue

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160
Q

poorly differentiated tumors

A

more primitive appearance

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161
Q

what is the degree of differentiation of glandular neoplasms dependent on?

A

Degree of differentiation is determined by ability of tumor cells to form well-defined glands or to occur in solid sheets with minimal gland formation

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162
Q

what is the degree of differentiation of squamous epithelial tumors dependent on?

A

Degree of differentiation depends on extent of keratinization

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163
Q

2 basic divisions of neoplasms

A

benign

malignant

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164
Q

benign neoplasms

A

Abnormal growth of cells that cytologically closely resembles the normal cells of the tissue from which the tumor arises

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165
Q

what suffix denotes benign neoplasms?

A

oma

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166
Q

Benign tumor of fibroblasts

A

fibroma

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167
Q

Benign tumor of smooth muscle cells

A

leiomyoma

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168
Q

Benign tumor of chondrocytes

A

chondroma

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169
Q

Benign tumors of gland forming cells

A

adenomas

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170
Q

where do benign tumors of gland forming cells form tubular structures?

A

colon
kidney
thyroid

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171
Q

where do benign tumors of gland forming cells form solid sheet?

A

adrenal cortex

liver

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172
Q

cysadenoma

A

large ovarian cysts

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173
Q

Benign tumors of squamous epithelium

A

epitheliomas or papillomas

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174
Q

verruca

A

wart

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175
Q

polyp

A

tumor that projects above a mucosal surface

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176
Q

where are glandular polyps?

A

colon

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177
Q

where are squamous polyps?

A

vocal cord

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178
Q

teratomas

A

tumors that arise from germ cells

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179
Q

hamartoma

A

results from disorganized collection of normal tissue

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180
Q

Benign tumor of meninges

A

meningioma

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181
Q

Benign tumor of ependymal cells in 3rd ventricle

A

ependymoma

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182
Q

2 fundamental properties define a tumor as malignant

A

Invasion and destruction of adjacent tissues

Spread to distant sites → metastasis

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183
Q

Malignant tumors of mesenchymal tissue

A

sarcomas

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184
Q

Malignant tumors of fibroblasts

A

fibrosarcoma

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185
Q

Malignant tumor of chondrocytes

A

chondrosarcoma

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186
Q

Malignant tumor of smooth muscle

A

leiomyosarcoma

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187
Q

Malignant tumors of epithelial cells

A

carcinomas

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188
Q

Malignant tumors of squamous epithelial cells

A

squamous cell carcinomas or epidermoid carcinomas

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189
Q

Malignant tumors of glandular epithelial cells

A

adenocarcinomas

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190
Q

Malignant tumors of transitional epithelial cells

A

transitional cell carcinomas

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191
Q

grade 1 tumor

A

well differentiated
closely resemble parent cell of origin
less aggressive behavior

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192
Q

grade 3 tumor

A

poorly differentiated
departs from normal
aggressive behavior

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193
Q

what does the stage of a tumor tell you?

A

stage

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194
Q

what does tumor staging take into account?

A

Local growth → size, contiguous invasion
Lymph node metastasis
Distant metastasis

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195
Q

T of TNM cancer staging system

A

primary size of tumor

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196
Q

N of TNM cancer staging system

A

of node metastases

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197
Q

M of TNM cancer staging system

A

presence and extent of distant metastases

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198
Q

__ staging for colon adenocarcinoma

A

Duke

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199
Q

___ classification of melanomas of skin

A

Breslow and Clark

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200
Q

__ staging for ovarian carcinoma

A

FIGO

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201
Q

___ classification for lymphoid malignancies

A

Ann Arbor

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202
Q

most frequency cause of death due to cancer

A

colorectal carcinoma

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203
Q

pre invasive neoplasm of colorectal cancer

A

adenoma or polyp

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204
Q

when does risk for colorectal cancer start?

A

age 50

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205
Q

cumulative life risk for colorectal cancer

A

5%

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206
Q

60-80% of colorectal cancers are the ___ pathway

A

classical, APC

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207
Q

how does the classical pathway of colorectal originate?

A

bi-allelic mutation of the APC gene in a stem cell of the colonic mucosal crypt

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208
Q

classical pathway colorectal cancer mutation

A

crypt cell produces truncated version of APC protein

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209
Q

what critical function is lost because of the classical pathway of colorectal cancer?

A

function of sequestering beta catenin

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210
Q

what is the earliest stage of classical colorectal cancer?

A

one or a small # of effected crypts

adenoma

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211
Q

formation of small dysplastic polyp leads to formation of ___

A

tubular adenoma

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212
Q

what is upregulated in tubular adenomas of colorectal cancer?

A

COX2 enzyme activity that inhibits apoptosis

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213
Q

Mutations of ___ are acquired in polyps that increase in size

A

oncogene Kras

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214
Q

adenomatous phenotype

A

adenomas show low-grade dysplasia

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215
Q

High grade dysplasia is present when there is _____

A

increased nuclear atypia and extreme gland architectural abnormality

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216
Q

APC pathway is associated with __ mutation

A

p53

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217
Q

PIK3CA mutation is present in _% of CRC

A

15-25

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218
Q

what is the marker for COX2 mutation in CRC?

A

PIK3CA mutation

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219
Q

Specific region on ___ is deleted in ~75% of colon cancers and in 50% of advanced adenomas

A

chromosome 18q

encompasses a suppressor gene

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220
Q

what characterizes the endpoint of the classical CRC pathway?

A

MSS

chromosomal instability

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221
Q

where is classical CRC found?

A

distal colon

rectum

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222
Q

appearance of classical CRC

A

flat, plaque-like, ulcerated or polypoid

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223
Q

histological appearance of classical CRC

A

moderately differentiated

grade 2-3/4

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224
Q

___ pathway accounts for 20-30% of colorectal adenocarcinomas

A

serrated polyp

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225
Q

appearance of serrated poylp CRC

A

series of polyps that have glands or crypts with a characteristic saw tooth/serrated outline

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226
Q

how does serrated polyp CRC originate?

A

crypt stem cell that develops an activating mutation of an oncogene in the RAS-RAF-MAPK intracellular signaling pathway

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227
Q

senescence

A

crypts enlarged to accommodate colonocytes that have normal nuclei but increased cytoplasmic volume and reduced tendency to slough into the lumen

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228
Q

BRAF mutation CRC

A

marked serration of crypts
Cytoplasm of cell is filled with small mucin vacuoles
Microvesicular serrated polyp

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229
Q

Microvesicular serrated polyp appearance

A

Predominance of microvesicular cells

Serration extending deeply but not to crypt base

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230
Q

KRAS mutation CRC

A

less prominent serration
Marked by tufting of surface
Increased number of goblet cells
Goblet cell serrated polyp

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231
Q

where do hyperplastic polyps occur

A

distal colon

rectum

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232
Q

what is upregulated in hyperplastic polyps?

A

cell cycle inhibitors → p16, p14

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233
Q

what can happen to BRAF mutated hyperplastic polyps?

A

develop disordered growth → atypical variant called sessile serrated adenoma (SSA)

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234
Q

dysplastic serrated polyp

A

sessile serrated adenoma with cytological dysplasia

This can develop into cancer

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235
Q

Endpoint carcinomas of BRAF mutation are ___ located and show ____

A

proximally

microsatellite instability

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236
Q

what drives BRAF mutation

A

epigenetic process of CpG methylation

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237
Q

what leads to microsatellite instability?

A

mismatch repair gene hMLH1 becomes inactivated due to bi-allelic methylation of its promoter region

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238
Q

what is the equivalent of p53 mutation of APC pathway in the serrated pathway?

A

development of microsatellite instability

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239
Q

location of serrated polyp BRAFmut CRC

A

proximally

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240
Q

mean age of serrated polyp CRC

A

later than APC

76

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241
Q

histologic appearance of serrated pathway CRC

A

Serrated glands/undifferentiated
Mucin
Lymphocytic response

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242
Q

which has more CpG island methylation BRAF or KRASmut?

A

KRAS

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243
Q

which occurs more proximally BRAF or KRASmut?

A

BRAFmut

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244
Q

environmental pathology

A

disorders that occur because of exposure to harmful chemical and physical agents in the immediate environment

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245
Q

toxicology

A

study of harmful agents and their distribution, effects, and mechanisms of action

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246
Q

xenobiotics

A

environmental chemical agents

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247
Q

how are xenobiotics metabolized?

A

cytochrome P450 enzymes

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248
Q

particulates

A

Combustion particles and mineral dusts derived from major compounds in the earth → coal, silica and iron

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249
Q

when are particulates harmful?

A

<10um diameter

too small to be trapped by the nasal hairs or mucociliary lung epithelium

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250
Q

what happens after particulates are phagocytosed?

A

Release inflammatory mediators that may cause lung damage

Can lead to heart rate irregularities

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251
Q

main outdoor air pollutants

A 
particulates
sulfur dioxide
CO
ground level ozone
nitrogen dioxide
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252
Q

symptoms of mild CO poisoning

A

dizziness
confusion
headache

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253
Q

symptoms of severe CO poisoning

A

depression of CNS
heart damage
death

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254
Q

what generates ground level ozone

A

photochemical reaction between NOs with UV light

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255
Q

adverse effects of ground level ozone

A

Forms free radicals → inflammation, damage lung epithelium

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256
Q

what can smog cause?

A

inflammation

lung damage

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257
Q

formaldehyde sources

A

foam insulation
glues
wood

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258
Q

formaldehyde toxic effect

A

asthma
eye/nose/throat irritation
contact dermatitis
nasopharyngeal cancer

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259
Q

asbestos source

A

insulation

floor and ceiling tiles

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260
Q

asbestos toxic effect

A

mesothelioma
lung fibrosis
lung cancer

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261
Q

radon source

A

soil

uranium mines

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262
Q

radon toxic effect

A

lung cancer

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263
Q

lead source

A

water
lead paints
leaded gas

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264
Q

lead toxic effect

A 
hematologic
skeletal 
neurologic
GI
renal 
more in children than adults
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265
Q

lead mechanism of toxicity

A

binds to sulfhydryl groups in proteins and blocks Ca metabolism

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266
Q

mercury source

A

contaminated fish

dental amalgums

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267
Q

mercury toxic effect

A

tremors
confusion
mental retardation
death

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268
Q

mercury mechanism of toxicity

A

binds to sulfhydryl groups in proteins

esp in CNS and kidney

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269
Q

arsenic source

A

soil
water
wood preservers
herbicides

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270
Q

arsenic toxic effect

A 
acute GI
CVS and CNS damage
hyperpigmentation
hyperkeratosis
lung, bladder, skin cancers
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271
Q

arsenic mechanism of toxicity

A

trivalent arsenic replaces phosphates in ATP which inhibits mito ox phos

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272
Q

cadmium source

A

nickel cadmium batteries get into water, soil, food

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273
Q

cadmium toxic effect

A

obstructive lung disease
kidney damage
lung cancer

274
Q

cadmium mechanism of toxicity

A

increased ROS?

275
Q

lead effects on bone

A

lead lines

poor remodeling of cartilage and bone trabeculae

276
Q

burtonian line

A

characteristic blue line at the junction of the gums and teeth due to deposition of sulfate in lead poisoning

277
Q

volatile organic compounds

A

choloform
carbon tetrachloride
benzene
1,3 butadiene

278
Q

where do you find carbon tetrachloride?

A

degreasing agents → dry cleaning, paint remover

279
Q

where do you find benzene and 1,3 butadiene?

A

Used in manufacturing of plastics, lubricants, rubbers, and dyes

280
Q

how do volatile organic compounds enter the body?

A

lungs

281
Q

symptoms of volatile organic compounds

A

headache

dizziness

282
Q

chronic exposure to volatile organic compounds causes?

A

impaired liver and kidney function

283
Q

organochlorines

A

polychlorinated biphenyls
dioxin
DDT

284
Q

organochlorines source

A

old capacitors and transformers
incompletely incinerated waste
pesticides

285
Q

organochlorines toxic effect

A

chloracne
rashes
liver damage
endocrine disorder

286
Q

organochlorines mechanism

A

probable carcinogens bind to aryl hydrocarbon R on cells and cause transcriptional changes

287
Q

vinyl chloride source

A

manufacturing of polyvinylchloride products

288
Q

vinyl chloride toxic effect

A

liver angiosarcoma

289
Q

vinyl chloride toxic mechanism

A

processing of metabolites in liver

290
Q

phthalate esters source

A

flexible plastics

291
Q

phthalate esters toxic effect

A

reproductive toxin in animals

292
Q

BPA source

A

bottles

coating of cans

293
Q

BPA mechanism and effect

A

estrogen mimic

proliferative effect

294
Q

chloracne

A

acne-like eruption of cysts, hyperpigmentation, hyperkeratosis

295
Q

what causes 90% of lung cancers?

A

cigarette smoking

296
Q

Life expectancy for smokers is __ years lower

A

10

297
Q

how does nicotine work?

A

Binds to nicotinic ACh R in the brain → release of catecholamines from sympathetic neurons → increased HR, BP, CO

298
Q

Polycyclic hydrocarbons

A

toxic compound in cigarettes
Bind to aryl/aromatic hydrocarbon R
carcinogen

299
Q

nitrosamines

A

toxic compound in cigarettes

Associated with increased risk of gastric cancer

300
Q

why are smokers at increased risk for MI?

A

Toxins injure endothelial cells → atherosclerosis

301
Q

why are smokers at increased risk for chronic bronchitis?

A

Tar, formaldehyde, NOs → irritants → inflammation with mucus production → chronic bronchitis

302
Q

why are smokers at increased risk for emphysema?

A

inflammatory mediators in the lung recruit neutrophils that produce elastase → destroys elastin in alveolar walls
Leads to enlarged air spaces
insufficient gas exchange and impaired respiratory function → irreversible lung disease called emphysema

303
Q

Chronic bronchitis and emphysema → ?

A

COPD

304
Q

ADH decreases __

A

NAD

305
Q

what does ADH form?

A

toxic acetaldehyde

306
Q

why is acetaldehyde toxic?

A

Carcinogen that acts by interfering with DNA replication and repair
Contributes to incoordination, memory impairment, sleepiness, facial flushing, nausea, rapid HR

307
Q

what does ALDH form?

A

converts acetaldehyde into acetic acid

308
Q

what cofactor does ALDH use?

A

NAD

309
Q

what do variants of ADH and ALDH enzymes cause?

A

acetaldehyde level and tolerance to alcohol

310
Q

effects of fast ADH and/or slow ALDH

A

higher levels of acetaldehyde
Lower tolerance to alcohol
Protects against alcoholism

311
Q

BAC of 200 mg/dL → ?

A

drowsiness

312
Q

BAC >300 mg/dL → ?

A

stupor with greatly diminished responsiveness

313
Q

acute alcoholism

A

1 time high alcohol consumption

314
Q

effects of acute alcoholism

A 
Affects CNS 
Depression of neuronal centers
Reversible liver and stomach damage can occur 
Fat accumulation in hepatocytes
Gastritis, ulceration
315
Q

chronic alcoholism

A

repeated long-term high alcohol consumption

316
Q

liver effects of chronic alcoholism

A

Liver shows fatty change and alcoholic hepatitis (inflammation of liver)
Progresses to fibrosis and cirrhosis → irreversible replacement of hepatocytes by scar tissue
Impairs blood flow through liver → portal hypertension with large swollen veins in GI
These varices can rupture → internal bleeding with life threatening complications

317
Q

fetal alcohol syndrome

A

From consumption of alcohol during pregnancy, especially in the 1st trimester

318
Q

fetal alcohol syndrome symptoms

A

Microcephaly
Facial abnormalities
Growth retardation
Reduced mental functioning

319
Q

fetal alcohol syndrome incidence

A

3/1000 children in US

320
Q

leading cause of death for those <44

A

Unintentional injuries

321
Q

mechanical injury

A

whenever a force of sufficient magnitude is applied to the body

322
Q

most significant sites of mechanical injury

A

Soft tissues
bones
head

323
Q

abrasion

A

scraping or rubbing

removes superficial layer of skin

324
Q

contusion

A

bruise from a blunt object

extravasation of blood into tissue

325
Q

laceration

A

tear or disruptive stretching from a blunt object

intact bridging blood vessels

326
Q

incised wound

A

from a sharp object

severed bridging blood vessels

327
Q

puncture wound

A

pierced tissue from penetration of a long and narrow sharp object

328
Q

when is a puncture wound perforating?

A

if exit wound if formed

329
Q

what determines clinical significance of thermal burns?

A

Depth of burn
% of body surface involved
Presence of internal injuries from inhalation of hot and toxic fumes
Promptness and efficacy of therapy

330
Q

superficial burn

A

Limited to epidermis
Appears red and dry
Painful

331
Q

partial thickness burn

A

Destroys the epidermis and part of the dermis
Read and moist with blisters
Painful

332
Q

full thickness burn

A

Destroys epidermis and dermis
Anesthetic → not painful because nerve endings in skin are destroyed
Not capable of regeneration
Pose high risk of infection

333
Q

hyperthermia

A

Consequence of prolonged exposure to high ambient temperature

334
Q

heat cramps

A

occur as a result of loss of electrolytes via sweating

335
Q

heat exhaustion

A

most common, manifestation as prostration (extreme physical weakness) and a brief period of collapse

336
Q

what causes heat exhaustion

A

hypovolemia caused by dehydration

337
Q

heat stroke

A

cessation of sweating due to failure of thermoregulatory mechanisms with prolonged core temperature >40 C

338
Q

why is heat stroke the most serious hyperthermia?

A

Leads to peripheral vasodilation

Can lead to reduced blood flow to the brain and heart → confusion, coma, death

339
Q

hypothermia

A

Consequence of prolonged exposure to low ambient temperature

340
Q

mild hypothermia

A

32-35 C core temp
Hyperventilation
lethargy
vigorous shivering to generate heat

341
Q

moderate hypothermia

A

28-32 C core temp
Hypoventilation
confusion
loss of coordination

342
Q

severe hypthermia

A

<28 C core temp
Unconsciousness
slow or no breathing
low or no pulse

343
Q

effects of local hypothermia

A 
frostbite
trench foot (gangrene)
344
Q

how does frostbite occur?

A

Suppression of vital metabolism
Crystallization of intra and extracellular water
Increased permeability of vessels
Ischemia, hypoxia, infarction

345
Q

Wet skin lowers resistance to the conductance of the current ___

A

100x

346
Q

what determines severity of electrical injury?

A

type and intensity of current
path of current
resistance of tissue
duration of exposure

347
Q

types of electrical injury

A

Burns at entry and exit sites and internal organs
ventricular fibrillation or cardiac and respiratory center failure
paralysis of medullary centers and extensive burns from high voltage current

348
Q

what can AC current cause?

A

tetanic muscle spasms, prolonged clutching of current source → asphyxia from spasm of chest wall muscle

349
Q

particulate radiation

A

Arises from nuclear decay and comprises alpha and beta particles and neutrons

350
Q

ionizing forms of radiation

A

X-rays and gamma rays, and alpha, beta and neutron particles

351
Q

what does ionizing radiation induce formation of?

A

free radicals by molecules with which they collide

352
Q

ionizing radiation is ___

A

mutagenic

353
Q

how does ionizing radiation cause mutation?

A

directly by free radical formation in DNA and indirectly by inducing other free radicals (ROS)
If DNA is not repaired → mutations lead to cell death or contribute to carcinogenesis

354
Q

cells with highest sensitivity to ionizing radiation

A

rapidly dividing cells → lymphoid cells, hematopoietic cells, germ cells, and GI epithelium

355
Q

rapidly dividing cells die when exposed to __SV

A

<25

356
Q

cells with moderate sensitivity to ionizing radiation

A

Skin
blood vessels
squamous epithelium
growing bone and cartilage

357
Q

cells with lowest sensitivity to ionizing radiation

A 
kidney
muscle
brain
endocrine organs
adult bone and cartilage
358
Q

injuries from ionizing radiation

A

Vascular damage
inflammation
Fibrosis
Radiopneumonitis in the lungs

359
Q

Radiopneumonitis

A

Alveolar spaces are filled with CT

360
Q

most energetic and harmful UV

A

UVC

361
Q

ozone layer absorbs which UV?

A

UVC

362
Q

UVB causes?

A

Causes dimerization of pyrimidines in DNA → transcriptional errors → cancer

363
Q

UVS causes ____ damage

A

non neoplastic

364
Q

sun burn symptoms

A

Erythema → reddening of skin
Pigmentation → tanning
Depletion of Langerhans cells
All these changes are reversible

365
Q

long term exposure to UVA causes?

A

irreversible degeneration of skin elastin and collagen → wrinkles, leathery skin
increased risk of cataracts

366
Q

what can high electromagnetic field radiation cause?

A

burns and possibly cancer

367
Q

what gives off electromagnetic field radiation

A

radiowaves

microwaves

368
Q

anemia

A

reduction in oxygen carrying capacity of blood

369
Q

what is the most common form of nutritional deficiency?

A

anemia

370
Q

total body iron in women

A

2g

371
Q

total body iron in men

A

6g

372
Q

__% of iron is in Hb

A

80

373
Q

storage pool of iron

A

ferritin, hemosiderin

374
Q

transport of iron

A

transferrin

375
Q

what regulates iron balance?

A

absorption of dietary iron

376
Q

Most iron required to maintain erythron is salvaged from ___

A

the turnover of senescent RBCs

377
Q

Daily loss of iron

A

1-2 mg/day through shedding of mucosal and skin cells

378
Q

primary iron absorption site

A

duodenum

379
Q

causes of iron deficiency anemia

A

low intake
malabsorption
increased demand
chronic blood loss

380
Q

Sprue

A

inflammation of duodenum, loss of villi

381
Q

most common cause of iron deficiency anemia in western world

A

chronic blood loss from ulcers, tumors, dysfunctional uterine bleeding

382
Q

Megaloblastic anemia

A

Condition where RBC are larger than normal with a hypercellular bone marrow

383
Q

what can cause Megaloblastic anemia

A

dietary deficiency of vitamin B12 or folic acid

pernicious anemia

384
Q

Pernicious Anemia

A

A megaloblastic anemia associated with atrophic gastritis

Complete achlorhydria and malabsorption of vitamin B12 due to a deficiency of intrinsic factor

385
Q

source of B12 in diet

A

animal products

386
Q

how is B12 absorbed in salivary gland?

A

R binders

387
Q

what 2 rxns require B12?

A

Methyltransferase in conversion of homocysteine → methionine
Isomerization of methylmalonyl coenzyme A to succinyl coenzyme A

388
Q

Atrophic gastritis

A

Chronic inflammation of mucosa associated with atrophy of glands and intestinal metaplasia

389
Q

most common autoantibodies in pernicious anemia

A

90% → antiparietal cell antibodies
75% → anti-IF antibodies
50% → antibodies to thyroid tissue

390
Q

risk factors for PA

A

Northern Europeans
More common in males
50-80 years old

391
Q

Atrophic glossitis

A

shiny, glazed, depapillated tongue

392
Q

GI tract symptoms of PA

A

Epithelial atrophy
Atrophic glossitis
Atrophic gastritis

393
Q

what is seen in the bone marrow of PA pts

A 
hypercellular
erythroid hyperplasia, megaloblasts
nuclear/cytoplasmic dyssynchrony
giant metamyelocytes
Larger cells, neutrophils with more lobes
394
Q

what is seen in the peripheral smear of PA pts

A

macroovalocytes
hypersegmented polys
giant platelets

395
Q

neurologic symptoms of PA

A

symmetric numbness and tingling of extremities
impaired vibratory and position sense
spastic ataxia
Degeneration of posterior and lateral columns of the spinal cord

396
Q

lab tests for PA

A

serum B12

schilling test

397
Q

serum B12 test

A

measured by radioisotope dilution assay

<100 confirms PA

398
Q

schilling test

A

measures absorption of labeled vitamin B12

repeat test with IF to confirm PA

399
Q

PA therapy

A

Lifelong therapy with B12
Initial dose of 1000 ug
1000 ug weekly, then every month for life
~10-15% of administered dose is retained

400
Q

why is folate important?

A

Folic acid acts an intermediate in the transfer of 1C units to various components involved in synthesis of purines, methionine → homocysteine, deoxythymidylate monophosphate (DNA)

401
Q

folate deficiency impairs ___ and leads to___

A

DNA synthesis

megaloblastosis

402
Q

where do we get folate?

A

diet, no stores

Green vegetables, fruits, liver

403
Q

where is folate absorbed?

A

prox jejunum

404
Q

3 major causes of folate deficiency

A

Decreased intake, inadequate diet, malabsorption
Increased requirement
Impaired use

405
Q

what causes Decreased intake, inadequate diet, malabsorption folate def?

A

Chronic alcoholism, elderly, poor, sprue, lymphoma, drugs

406
Q

what causes increased req of folate?

A

Pregnancy, infancy, malignancy

407
Q

what causes impaired use of folate?

A

Folic acid antagonists inhibit dihydrofolate reductase in the recovery of tetrahydrofolate

408
Q

what does hemolytic anemia include?

A

altered shape of the red cells as in hereditary spherocytosis
immune hemolytic anemia as may occur in Rh incompatibility
mechanical trauma to the red blood cells

409
Q

aplastic anemia

A

Defect of the stem cell of the bone marrow

410
Q

what causes Polycythemia Rubra Vera

A

mutation of JAK2

411
Q

babesiosis

A

Endemic to cape cod

Inclusions within RBC

412
Q

2 main components of lymph node cortex

A

central germinal center surrounded by mantle zone

413
Q

central germinal center of. lymph node

A

Composed of follicular cells
Represent various stages of B cell maturation
Follicular dendritic reticulum cells form the scaffolding for the germinal center and are antigen presenting cells for B cells

414
Q

mantle zone of lymph node

A

composed of small round to slightly irregular lymphoid cells and represents an early stage of B cell activation

415
Q

paracortex of lymph node

A

area between the secondary follicles

composed primarily of small lymphocytes with admixed larger transformed lymphoid cells called immunoblasts

416
Q

sinuses of lymph nodes

A

Vascular-like channels extending throughout the node lined by histiocytes
Act as filters to cleanse the lymph via the phagocytic activity of the lining histiocytes

417
Q

medullary cords of lymph nodes

A

inner medulla of the lymph node is composed of predominantly plasma cells and extensions of the vascular sinusoids that contain histiocytes

418
Q

where is the B cell area of the lymph node

A

secondary follicles

419
Q

B cell associated antigens

A

CD19
CD20
CD10

420
Q

where is the T cell area of the lymph node

A

paracortex

421
Q

T cell associated antigens

A 
CD2
CD3
CD4
CD5
CD7
CD8
422
Q

non neoplastic lymph node disorders

A

Neutrophilia with reactive changes → increase neutrophils

Infection

423
Q

Neoplastic transformation of lymphoid cells results in ___

A

malignant lymphomas

424
Q

non hodgkin’s lymphoma

A

malignant lymphomas represent clonal expansions of discrete stages of differentiation of the cell as it progresses from a small round regular B cell to a plasma cell

425
Q

A malignancy of the small round regular lymphocytes (circulating lymphocyte) gives rise to

A

malignant lymphoma, small lymphocytic type/chronic lymphocytic leukemia

426
Q

A malignancy of germinal center cells (small and large cleaved, small and large non-cleaved) gives rise to

A

group of lymphomas collectively or known as follicular center cell lymphomas which may grow in a follicular (nodular) or diffuse growth pattern

427
Q

A malignancy of germinal center small non-cleaved cells →

A

Burkitt’s lymphoma

428
Q

A malignancy of plasma cells →

A

multiple myeloma, plasmacytoma

429
Q

Luke Collins B cell lymphomas

A 
small lymphocytic
follicular center cell- small and large cleaved
small non cleaved (Burkitt's)
large non cleaved
immunoblastic sarcoma
430
Q

Luke Collins T cell lymphomas

A

small lymphocyte
mycoses fungoides/sezary
immunoblastic sarcoma

431
Q

are more lymphomas T or B cell type?

A

B cell (80%)

432
Q

how to determine lineage of malignant lymphoma

A

Immunophenotypic studies

Determination of lineage via detection of specific surface antigens

433
Q

what is the most common lymphoma

A

follicular lymphoma

tries to mimic B cell follicles

434
Q

__ is neg in a normal lymph node but is pos in a lymphoma

A

Bcl-2

435
Q

WHO classification

A

Sorts lymphoid neoplasms into 5 categories

436
Q

Hodgkin lymphoma is a neoplasm of ___

A

Reed Sternberg cells

437
Q

Hodgkin lymphoma

A

Lymphoid malignancy composed of distinctive large bi-nucleated cells called Reed-Sternberg (RS) cells associated with a characteristic mixed inflammatory background

438
Q

classical RS cell histology

A

large, binucleated
Prominent eosinophilic centrally located nucleoli surrounded by a halo
Abundant eosinophilic/amphophilic cytoplasm

439
Q

RS variant histology

A

mononuclear and multinucleated forms of RS cells
Lacunar cells
Popcorn cells
Malignant cell, but usually <5% of the population

440
Q

Proportion of RS and RS variants present determines ___

A

the subclassification of Hodgkin’s lymphoma

441
Q

Rye classifications

A

lymphocyte predominance
nodular sclerosis
mixed cellularity
lymphocyte depletion

442
Q

Going from LP to LD there is an __ relationship between the proportion of lymphocytes present and the number of RS cells

A

inverse

443
Q

4 major cell types in marrow

A

Erythroid → RBC
Myeloid → white blood cells
Megakaryocytes → platelets
Lymphocytes → B cells, T cells, plasma cells

444
Q

leukemia

A

presence of circulating abnormal cells in blood

445
Q

acute leukemia

A

circulating blasts of either myeloid origin (acute myelogenous leukemia) or lymphoid origin (acute lymphoblastic leukemia)

446
Q

chronic leukemia

A

circulating mature cells of myeloid origin (chronic myelogenous leukemia) or lymphoid origin (chronic lymphocytic leukemia)

447
Q

Acute Myelogenous Leukemia

A

Replacement of normal marrow elements by blasts

>30% of the marrow cellularity

448
Q

Myeloblasts in AML have:

A

large eccentrically placed nuclei
delicate nuclear chromatin
2-4 nucleoli and abundant cytoplasm which may or may not contain granules
myeloperoxidase positive

449
Q

what surface antigens ID myeloid blasts in AML?

A

CD13

CD33

450
Q

Auer rods

A

abnormal granules

diagnostic of AML

451
Q

normal age range for AML

A

15-39

452
Q

Clinical presentation of AML

A 
Generally abrupt 
Fatigue
Fever
infection
Easy bruising/bleeding
453
Q

leukopenia

A

decrease in white cells

454
Q

thrombocytopenia

A

decrease in platelets

455
Q

AML prognosis

A

60% of patients achieve remission with chemotherapy but only 15-30% remain free of disease in 5 years

456
Q

Acute Lymphoblastic Leukemia

A

Replacement of marrow by lymphoblasts of B or T cell origin

457
Q

Lymphoblasts in ALL have

A

Predominantly round nuclei
Condensed chromatin
Single nucleoli
Scant agranular cytoplasm

458
Q

most common form of ALL

A

pre-B cell type and primarily occur in childhood

459
Q

how to distinguish btwn B and T cell ALL

A

immunophenotypic studies → flow cytometry

460
Q

Presence and detection of the DNA polymerase → TdT (terminal deoxy-transferase) is very useful in the diagnoses of ___

A

ALL

461
Q

when do cases of ALL peak

A

age 4

462
Q

Infiltration of lymph nodes, spleen and liver is more common in ___

A

ALL than in AML

463
Q

CNS involvement is more common in ALL than in AML

A

ALL than in AML

464
Q

treatment of ALL

A

aggressive chemo cures 2/3 pts

465
Q

Chronic Myelogenous Leukemia

A

Proliferation in the bone marrow of myeloid elements

466
Q

who does CML primarily affect?

A

age 25-60

467
Q

CML is associated with a specific chromosomal translocation

A

Involves the bcr gene on chr 9 and the abl gene on chr 22 → Philadelphia chromosome - PhP1P

468
Q

clinical presentation CML

A

Mild to moderate anemia, fatigue, weight loss

Dragging sensation in LUQ due to enlarged spleen

469
Q

Majority of CML patients undergo ___ with evolution to acute leukemia

A

blast crisis

470
Q

how many CML pts develop AML vs ALL?

A

~70% AML, 30% ALL

471
Q

what drug treats CML?

A

gleevec

472
Q

plasma cell neoplasms

A

Proliferation of a B-cell clone (plasma cells) that secrete a single homogeneous immunoglobulin or its fragments

473
Q

multiple myeloma

A

Characterized by multiple tumorous masses scattered throughout the skeletal system

474
Q

M component

A

Monoclonal immunoglobulin in the blood of multiple myeloma pts
aka monoclonal gammopathy

475
Q

Bence Jones proteins

A

Free light chains of Igs are small enough to be excreted in the urine

476
Q

Plasmacytoma

A

localized plasma cell tumors

477
Q

what organ system is predominantly affected by multiple myeloma?

A

bone

478
Q

multiple myeloma risk factors

A

men, people of African descent and older adults

479
Q

how to diagnose multiple myeloma

A

Bone marrow electrophoresis

480
Q

pathologic fracture

A

Multifocal destructive bone tumor composed of plasma cells → erode bone cortex

481
Q

what bones are most affected in multiple myeloma

A 
Bones in the axial skeleton
vertebra 66%
skull 41%
pelvis 28%
femur 24%
482
Q

microscopic appearance of multiple myeloma

A

bone marrow reveals an increase in plasma cells (mature, immature, binucleated, multinucleated)
comprise greater than 30% of the cellularity

483
Q

lab findings in multiple myeloma

A

Serum Ig > 3 gm/dL
M spike on SPEP
Bence Jones proteinuria may present as an isolated finding
normocytic/normochromic anemia, decreased WBC, decreased platelets
hypercalcemia due to increased bone resorption
rouleaux formation → high Ig causes red cells to stick to each other

484
Q

clinical presentation of multiple myeloma

A 
Confusion, weakness, lethargy due to hypercalcemia
Recurrent infections (Strep, Staph, E. coli) due to suppression of humoral immunity
Renal insufficiency (50% pts) due to the toxic effects of BJ proteins on renal tubular cells
Amyloidosis
485
Q

Myelodysplastic syndromes

A

Disease often affects older patients who present with cytopenias involving varying lineages that are often refractory to treatment

486
Q

Myelodysplastic syndromes eventually progress to __

A

AML

487
Q

Disseminated intravascular coagulation

A

Activation of the coagulation cascade → microthrombus formation in the vasculature

488
Q

causes of DIC

A

Sepsis
Malignancy
Major trauma
Obstetric complications

489
Q

what can DIC cause

A

hemolytic anemia

Can be fatal

490
Q

Von Willebrand’s disease

A

bleeding disorder

Characterized by bleeding from mucous membranes

491
Q

most common from for VWf disease

A

type 1 → autosomal dominant

492
Q

coagulation disorders

A

hemophilias

493
Q

why is factor VIII replacement therapy no longer used?

A

Iatrogenic HIV from replacement from patients with HIV

494
Q

Acute neuronal cell injury and neuronophagia

A

manifestations of acute, lethal injuries

495
Q

Central chromatolysis

A

morphological manifestations of a reparative response to injury

496
Q

Acute (hypoxic-ischemic) neuronal injury → ?

A

cell body shrinks, pyknosis, red neurons

497
Q

red neurons

A

cytoplasms becomes hypereosinophilic

498
Q

Neuronophagia

A

dying neuron is overrun by inflammatory cells

499
Q

what remains after neuronophagia?

A

microglial nodule

500
Q

where is central chromatolysis usually seen?

A

lower motor neurons

501
Q

components of central chromatolysis

A

swelling of cell body, disappearance of Nissl bodies, displacement of nucleus to periphery

502
Q

gliosis

A

proliferation of astrocytes upon brain tissue injury

503
Q

Most common dementing disorder

A

AD

504
Q

AD presentation

A 
Memory failure
Especially short term 
Deficiencies in abstract thinking, problem solving, visual-spatial orientation, mood regulation 
Profound disabilities
Mute
Immobile
505
Q

AD brain morpholgy

A

Diffuse symmetrical cerebral atrophy
Mainly in temporal, frontal, parietal lobes
Thinning of cortical ribbon

Prominent atrophy of medial temporal lobe structures
Mainly in hippocampus

506
Q

microscopic features of AD

A

neurofibrillary tangles
senile plaques
amyloid angiopathy (sometimes)

507
Q

neurofibrillary tangles

A

intracellular inclusions containing abnormally phosphorylated tau protein

508
Q

where are NFTs found

A

neuropil threads

dystrophic neurites

509
Q

senile plaques

A

extracellular deposits of beta amyloid

510
Q

amyloid angiopathy

A

deposits of Aβ in vascular walls of meningeal and parenchymal vessels

511
Q

how to visualize amyloid angiopathy

A

Congo red

512
Q

how is amyloidogenic Aβ generated

A

If APP is not cleaved by a-secretase

513
Q

what does Cleavage by β-secretase and g-secretase cuase

A

Aβ which promotes inflammation that can alter tau phosphorylation and induce neuronal oxidative injury

514
Q

where is APP located

A

chr21

515
Q

familial AD

A

point mutations in APP

develops in 20s/30s

516
Q

what do mutations in presenilins cause?

A

gain of function of g-secretase → generates increased amounts of Aβ

517
Q

sporadic AD is more likely in patients with

A

individuals of a particular allele (e4) of ApoE gene

This isoform promotes Aβ generation and deposition

518
Q

what is the mutation in frontotemporal dementias, not AD

A

Mutations in gene encoding tau (MAPT)

519
Q

clinical presentation of frontotemporal dementias

A

progressive deterioration in language and changes in personality

520
Q

morphology of frontotemporal dementias

A

Atrophy of frontal and temporal lobes

Degree and combo affects presentation

521
Q

subtypes of frontotemporal dementias

A

Pick disease
Corticobasal degeneration
Progressive supranuclear palsy

522
Q

Molecular genetics and pathogenesis of frontotemporal dementias

A

Some families with FTD have mutations in tau-encoding MPTP gene → tau forms with 4 or 3 MAP binding regions (4R or 3R tau)

523
Q

how to tell difference btwn AD and frontotemporal dementias?

A

neuropathological diagnosis

524
Q

what clinically characterizes PD?

A

Rigidity
Bradykinesia
resting tremor

525
Q

what are clinical manifestations of PD due to?

A

decreased dopaminergic input to the striatum because of degeneration of dopaminergic neurons of the substantia nigra

526
Q

Clinical hallmark on gross exam of PD

A

pallor of substantia nigra

527
Q

microscopic appearance of PD

A

Loss of pigmented (dopaminergic) neurons
Gliosis in substantia nigra
Presence of Lewy bodies

528
Q

Lewy bodies

A

intraneuronal inclusions that contain primarily alpha-synuclein (protein associated with synaptic transmission)
assoc with PD

529
Q

Parkinsonism

A 
clinical syndrome characterized by:
Decreased facial expression 
Stooped posture
Slowness of movement 
Rigidity 
“Pill-rolling” tremor
530
Q

what causes the symptoms of parkinsonism

A

damage to nigrostriatal dopaminergic system or blockade of postsynaptic R

531
Q

a-synuclein

A

lipid binding protein associated with synapses

1st gene to be identified as a cause of autosomal dominant PD encodes

532
Q

Mutations in ___ are more common causes of autosomal dominant PD

A

LRRK2

533
Q

parkin

A

E3 ubiquitin ligase

534
Q

Juvenile autosomal recessive PD is caused by a loss of function mutation in the gene encoding __

A

parkin

535
Q

DJ-1

A

protein involved in regulating redox response to stress

involved in autosomal recessive PD

536
Q

PINK-1

A

kinase important for mitochondrial function

kinase important for mitochondrial function

537
Q

what causes HD

A

mutation in gene that codes for huntingtin protein

538
Q

what sequence is important in huntingtin

A

CAG repeat

abnormally long in HD pts

539
Q

when doe HD start

A

middle/late life

540
Q

symptoms of HD

A

Chorea

Cognitive and affective disorders

541
Q

gross exam of HD brain

A

striatal atrophy of caudate nucleus

Frontal atrophy in later stages

542
Q

microscopic exam of HD brain

A

neuronal loss and astrogliosis

543
Q

ALS

A

Neurodegenerative disorder affecting upper and lower motor neurons

544
Q

symptoms of ALS

A

Severe muscle atrophy

Hyperreflexia

545
Q

why does severe muscle atrophy occur in ALS

A

Due to anterior horn loss

546
Q

why does hyperreflexia occur in ALS

A

Due to degeneration of corticospinal tracts

547
Q

fasciculations

A

Involuntary contractions of individual motor units

symptom of ALS

548
Q

__% patients have an autosomal dominant inherited form of ALS

A

10

*starts 10 years earlier than sporadic

549
Q

ALS gross exam

A 
atrophy of anterior motor nerve roots of the spinal cord
Precentral gyrus (motor cortex) may be atrophic
550
Q

ALS microscopic exam

A

loss of anterior horn cells (motor neurons) and astrocytosis in the spinal cord
Loss of motor neurons in brainstem and motor cortex
Degeneration of corticospinal tracts
Skeletal muscle shows denervation atrophy

551
Q

what mutation causes most familial ALS cases?

A

Mutation in SOD1 on chr21

552
Q

SOD1 role

A

removes superoxide radicals

553
Q

clinical presentation of MS

A 
Hyperreflexia
Weakness
Spasticity
Dysarthria
Tremor
Ataxia
Extraocular muscles and vision disturbances 
Spontaneous exacerbations and remissions
554
Q

why does MS have distinct episodes of neurologic deficits separated in time

A

white matter lesions

555
Q

microscopic MS appearance

A

Active plaques of demyelination show ongoing myelin breakdown
Abundant macrophages containing lipid rich debris
Lymphocytes are found around vessels

556
Q

appearance of inactive MS plaque

A

thinning of axons and prominent astrogliosis

Macrophages are mostly gone

557
Q

common location of MS plaques

A

periventricular area

558
Q

symptoms of CTE

A 
Deterioration in attention, concentration, memory 
Disorientation 
Confusion 
Dizziness
Headache 
Later, dementia
559
Q

distinct abnormalties in. what in CTE?

A

phosphorylated tau

560
Q

why is CTE unique?

A

represents progressive tauopathy with obvious environmental etiology

561
Q

Neurofibrillary degeneration in CTE characterized by

A

Preferential involvement of superficial layers of frontal and temporal cortices with patchy distribution and propensity for sulcal depth
Tau-immunoreactive NFTs, neuropil threads, astrocytic tangles
Prominent perivascular involvement

562
Q

cerebral infarct

A

An area of CNS tissue necrosis localized to a particular territory of vascular supply
All cellular elements are rendered non-viable by hypoxia/ischemia

563
Q

stroke

A

clinical term for syndrome of rapidly evolving or sudden-onset, non-epileptic neurologic deficit that lasts for >24 hrs

564
Q

venous infarction

A

tissue ischemia is due to occlusion of a large vein and consequent stasis

565
Q

what is most sensitive to neuronal ischemia

A

protein synthesis

566
Q

when is protein synthesis suppressed?

A

0.40 ml/g/min

567
Q

what happens to glc use when there is neuronal ischemia

A

Glucose utilization transiently increases at a flow rate below 0.35 before sharp decline to 0.25

568
Q

anoxic depolarization

A

rise in extracellular K+ below 0.15 and parallel influx of Ca++ → demise of membrane potential and structural integrity

569
Q

presentation of brain hemorrhage

A 
Sudden headache
Onset of neurologic deficit
Edema
Increased intracranial pressure 
Herniation 
Bloody CSF
570
Q

common causes of brain hemorrhage

A 
Hypertension 
Cerebral amyloid angiopathy
Anticoagulant administration 
Primary or secondary brain neoplasm 
Arteriovenous malformations
Aneurysms 
Recreational drug use
571
Q

Hypertensive intraparenchymal hemorrhage

A

Results from rupture of parenchymal arterioles that have become less compliant and weakened due to replacement of smooth muscle by fibrocollagenous tissue
Usually attributed to arteriosclerosis due to chronic hypertension

572
Q

what characterizes Hypertensive intraparenchymal hemorrhage

A 
Intimal hyperplasia
Elastic tissue reduplication 
Presence of foamy macrophages in arterial wall 
Thickening of media
Adventitial fibrosis
573
Q

where do SAH usualyl occur

A

Commonly develops from rupture of aneurysm in the circle of Willis

574
Q

berry aneurysms

A

most common cause of non traumatic SAH
Certain segments of smooth muscle media prone to develop aneurysms
Associated with hypertension and atherosclerosis

575
Q

concussion

A

no structural damage, brief impairment of consciousness

576
Q

contusion

A

bruise of brain parenchyma

577
Q

skull fracture

A

no consequences or accompanied by brain contusion, CSF leak due to meningeal tear, or epidural hematoma due to vascular tear

578
Q

how does an epidural hemorrhage happen?

A

Results from a skull fracture → tearing of middle meningeal artery

579
Q

what does epidural hemorrhage affect in adults?

A

temporal fossa

580
Q

what does epidural hemorrhage affect in children?

A

posterior fossa

581
Q

clinical presentation of epidural hemorrhage

A

Momentary loss of consciousness
Followed by asymptomatic period
1-48 hours
Followed by symptoms of elevated intracranial pressure
Without surgical intervention → herniation of medial temporal lobe, coma, death

582
Q

acute SDH results from?

A

Rapid acceleration or deceleration → brain inertia, traction/tearing of bridging veins between brain and dura occurs

583
Q

chronic SDH

A

Rupture of bridging veins → cycles of organization and re-bleeding due to formation of densely vascular granulation tissue tend to bleed spontaneously and perpetuate pathologic process

584
Q

most common sites of metastatic tumors

A 
Lung
Breast
Skin → melanoma
Kidney 
GI
585
Q

how do tumors spread to the. brain?

A

Spread to brain is mainly by hematogenus dissemination

586
Q

Meningeal carcinomatosis

A

tumor nodules studding surface of brain, spinal cord, intradural nerve roots

587
Q

what is meningeal carcinomatosis associated with?

A

small cell carcinoma and adenocarcinoma of lung

Carcinoma of breast

588
Q

Primary tumors arise from _____

A

cells that are intrinsic to the CNS

Including calvarium and tumors of neuroepithelial origin and non-neuroepithelial origin

589
Q

where do gliomas occur?

A

throughout CNS

590
Q

what are low grade gliomas more likely to how?

A

phenotypic markers of mature cells

591
Q

microscopic appearance of high grade gliomas

A

mitoses, microvascular proliferation, necrosis

592
Q

WHO grade diffuse astrocytomas

A

II

593
Q

what age is affected by diffuse astrocytomas

A

30-40

594
Q

macroscopic appaerance of diffuse astrocytomas

A

tumors enlarge and distort involved brain structures

Often blur normal anatomic landmarks

595
Q

microscopic appaerance of diffuse astrocytomas

A

moderately cellular tumors composed of well-differentiated astrocytes

596
Q

diffuse astrocytomas are __% of adult primary brain tumors

A

80

597
Q

WHO grade anaplastic astrocytomas

A

III

598
Q

where do anaplastic astrocytomas occur

A

Arise in setting of preexisting low-grade diffuse astrocytoma
Can also present de novo

599
Q

microscopic appearance of anaplastic astrocytomas

A

tumors are more cellular and pleomorphic than grade II tumors
Contain mitoses or vascular proliferation

600
Q

glioblastoma WHO grade

A

IV

601
Q

what age do glioblastomas peak

A

45-70

602
Q

radiologic/macroscopic presentation of gliomas

A

butterfly pattern caused by spread of tumor across the corpus callosum into opposite hemisphere

603
Q

microscopic presentation of gliomas

A

high cellularity, marked pleomorphism, mitoses, microvascular proliferation, pseudopalisading necrosis

604
Q

oligodendroglioma WHO grade

A

II

605
Q

oligodendroglioma peak ages

A

30-60

606
Q

oligodendroglioma

A

Diffusely infiltrating glioma composed of cells morphologically resembling oligodendrocytes
Relatively benign, slowing growing

607
Q

oligodendroglioma presentation

A

Patients may often present with a long history or neurological symptoms
Often chronic seizure

608
Q

Anaplastic Oligodendroglioma WHO grade

A

III

609
Q

Anaplastic Oligodendroglioma microscopic appearance

A

histological appearance of oligodendroglioma with focal or diffuse features of overt malignancy
Increased cellularity
Cytologic atypia
Frequent mitoses
Sometimes microvascular proliferation and necrosis

610
Q

where do ependymoma arise?

A

next to ependymal-lined ventricular system

611
Q

where do ependymomas occur in <20yr

A

near 4th ventricle

612
Q

where do ependymomas occur in adults

A

spinal cord

613
Q

why are ependymomas difficult to remove

A

Difficult to remove because of proximity to vital pontine and medullary nuclei

614
Q

microscopic appearance of ependymoma

A

perivascular pseudorosettes

615
Q

anaplastic ependymoma WHO grade

A

III

616
Q

microscopic appearance of anaplastic ependymoma

A

cellular pleomorphism, necrosis, mitoses, vascular proliferation

617
Q

Gangliocytomas WHO grade

A

I

618
Q

what do gangliocytomas consist of?

A

Consist entirely of mature readily recognized ganglion cells (mature neurons)
Mitoses and necrosis are absent

619
Q

gangliogliomas

A

Mix of mature appearing neurons and glial cells

Glial component can become anaplastic

620
Q

medulloblastoma WHO grade

A

IV

621
Q

where do medulloblastoma arise

A

cerebellum

Usually in vermis

622
Q

what can medulloblastomas cause

A

Ataxia
Headache
Vomiting
Obstruction of 4th ventricle with hydrocephalus

623
Q

medulloblastoma histology

A

small blue cell tumors with mitoses, necrosis, apoptosis

624
Q

meningiomas

A

Benign, slow growing tumors of adults

Usually attached to dura

625
Q

what do meningiomas arise from?

A

meningothelial cells of arachnoid

626
Q

common sites of meningiomas

A 
Parasagittal aspect of brain convexity 
Dura over the lateral convexity 
Wing of sphenoid
Olfactory groove
Sella turcica
Foramen magnum
627
Q

schwannoma WHO grade

A

I

628
Q

what CN do schwannomas arise on?

A

vestibular branch of CN XIII → acoustic neuroma

629
Q

where do schwannomas arise in spinal nerve roots?

A

sensory nerve roots in the lumbosacral region

630
Q

neurofibroma WHO grade

A

I

631
Q

what are neurofibromas composed of?

A

fibroblasts and pericytes mixed with Schwann cells and scattered mast cells

632
Q

Cutaneous neurofibromas

A

nodular lesion in the skin

633
Q

peripheral single nerve neurofibroma

A

solitary neurofibroma

634
Q

peripheral major nerve trunk neurofibroma

A

plexiform neurofibromas

635
Q

Malignant peripheral nerve sheath tumors

A

Highly malignant sarcomas → WHO grade IV

De novo or from transformation of plexiform neurofibromas

636
Q

Neurofibromatosis type 1 symptoms

A

multiple neurofibromas
gliomas of the optic nerve
LIsch nodules
cafe au lait spots

637
Q

lisch nodules

A

pigmented nodules of iris

638
Q

cafe au lait spots

A

cutaneous hyperpigmented macules

639
Q

Neurofibromatosis type 1 frequency

A

1/3000

640
Q

NF1 gene and product

A

tumor suppressor gene

neurofibromin

641
Q

neoplasms associated with neurofibromatosis type 1

A

MPNSTs, rhabdomyosarcomas, pheochromocytomas, carcinoid tumors

642
Q

Neurofibromatosis type 2

A

Develop a range of tumors
Commonly bilateral VIII nerve schwannomas and multiple meningiomas
Gliomas occur in the spinal cord

643
Q

Neurofibromatosis type 2 frequency

A

1/40,000

644
Q

NF2 gene product

A

merlin

645
Q

NF2 associated neoplasms

A

Bilateral schwannomas, neurofibromas, ependymomas, other gliomas, multiple meningiomas

646
Q

meningitis

A

inflammatino of meninges

647
Q

encephalitis

A

inflammation of brain

648
Q

Route of entry of microorganisms into CNS

A

hematogenous spread
Retrograde spread through venous system is possible
Direct implantation can follow traumatic injury or following surgery
Extensions of local infections, such as a tooth
Spread from peripheral nerves

649
Q

Acute pyogenic meningitis cause in elderly

A

Streptococcus pneumoniae, Listeria monocytogenes

650
Q

Acute pyogenic meningitis cause in young adults

A

Neisseria meningitides

651
Q

Acute pyogenic meningitis cause in young adults

A

E. coli, B streptococci

652
Q

classic presentation of acute pyogenic meningitis

A

Stiffness in neck due to irritation of meninges

653
Q

gross exam of acute pyogenic meningitis

A

diffuse swelling of brain with focal collections of pus beneath meninges → clouding and opacification
Pus

654
Q

complications of acute pyogenic meningitis

A

Swelling → compromise of blood flow→ cerebral infarction
Herniation
Compromise of respiratory centers or cranial nerve impingement
Long term → fibrosis of meninges can occur with development of chronic adhesions

655
Q

Aspergillosis

A

2nd most common fungal infection of CNS encountered at autopsy
Cause → inhalation of airborne spores with hematogenous dissemination to the brain

656
Q

Mucormycosis

A

regional brain infection due to spread from nose or sinuses, or from systemic disease with hematogenous dissemination in immunocompromised hosts

657
Q

myocytic infections

A

aspergillosis

mucormycosis

658
Q

what can myocytic infections lead to?

A

invade blood vessels growing directly through the wall

Can lead to thrombosis and subsequent brain infarction and necrosis

659
Q

Toxoplasma gondii

A

intracellular protozoan parasite of domestic cats

660
Q

Acquired toxoplasmosis

A

Acquired through contamination with feces from infected cats
Neurologic impairment can be localized or diffuse
Fatal in immunocompromised patients

661
Q

what characterizes acquired toxoplasmosis

A

necrosis
Encapsulated form of trophozoites → bradyzoites are found near necrosis
Abscess formation

662
Q

symptoms of congeintal toxoplasmosis

A

Infant convulsions
Chorioretinitis
Hydrocephalus

663
Q

pathology of congeintal toxoplasmosis

A

areas of parenchymal necrosis and calcifications

664
Q

symptoms of CNS viral infections

A

Meningoencephalitis with similar features regardless of specific agent
Brain is edematous with petechial hemorrhages and necrosis

665
Q

microscopic symptoms of CNS viral infections

A

perivascular lymphocytic infiltrate

666
Q

RNA viruses

A 
enteroviruses
paramyxoviruses
rubella
rabies
arboviruses
667
Q

Progressive rubella panencephalitis

A

rare and delayed complication of childhood or congenital rubella infection

668
Q

Congenital rubella syndrome

A

low birth weight, cardiac defects, cataract, chorioretinitis, neurologic defects

669
Q

Rabies

A

Acute neurologic disease develops after incubation and prodrome
Virus replicates in muscle and is transported by axons to the CNS

670
Q

how to diagnose rabies

A

Diagnosed by identification of Negri bodies in neuronal cytoplasm

671
Q

arboviruses

A

Cause encephalitis
Usually have animal or mosquito vectors
Example: West Nile, Western equine encephalitis (infants), Eastern equine encephalitis (children and elderly), St. Louis, La Crosse

672
Q

gross pathology of arboviruses

A

generalized edema and focal petechial small hemorrhages in the gray and white matter

673
Q

CNS DNA viruses

A

HSV
varicella-zoster
cytomegalovirus

674
Q

how does HSV-1 work

A

travels by retrograde axonal transport along sensory fibers to the trigeminal ganglion where latency is established

675
Q

how does HSV-2 work

A

established latency in the sacral dorsal root ganglion

Can infect brain of fetus passing through the canal

676
Q

how does varicella zoster affect CNS

A

Virus post infectious encephalitis due to latent infection in dorsal root or trigeminal ganglia
After retrograde axonal transport of virus from periphery

677
Q

cytomegalovirus

A

Typically in fetuses and immunocompromised patients
Most common intrauterine viral infection with residual lesion in survivors of acute neonatal illness
Intranuclear viral inclusions within large cells

678
Q

microscopic path of prion disease

A

spongiform change
Neuronal death
Synaptic loss

679
Q

spongiform change

A

microvascular bubbles within neuropil

680
Q

CJD

A

prion disease
Typically begins with subtle motor signs
Followed by severe cerebellar ataxia and global dementia in under a year
Death within 3 years

681
Q

kuru

A 
prion disease
Found among tribes of Papua New Guinea 
Decreased since cannibalism has declined
Motor signs 
Characteristic amyloid plaques in cerebellar cortex

MAMS (8 decks)

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