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MAMS > Path Exam 2 > Flashcards

Path Exam 2 Flashcards

1
Q

personalized medicine

A

selection of treatment best suited for a particular individual and not an average representation of a population

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2
Q

Analysis of age-standardized death rates shows shows significant success in treatment of ___

A

heart disease

stroke

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3
Q

Death rates for ____ increase despite increased health care spending

A

COPD

diabetes

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4
Q

how are most existing drugs approved?

A

on basis of performance in a population

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5
Q

what is warfarin used for?

A

long-term treatment and prevention of thromboembolic events

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6
Q

what are the 2 genes involved in warfarin metabolism?

A

VKORC1

CYP2C9

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7
Q

Herceptin

A

Monoclonal antibody that targets breast cancers overexpressing HER2/neu gene

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8
Q

how do personalized cancer vaccines work?

A
  • Cell therapy product is created using a technique that fuses the patient’s own tumor cells with immune-stimulating dendritic cells
  • Fusion product is then injected back into the patient causing a specific immune response against the cancer
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9
Q

OncoVax results

A

33% increase in overall survival and a 40% reduction in deaths in colon cancer patients

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10
Q

MyVax

A

investigational treatment that combines a protein derived from the patient’s own tumor with an immunologic carrier protein and is administered with an immunologic adjuvant

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11
Q

DCVax

A

personalized therapeutic cancer vaccine manufactured from the patient’s own DCs that have been modified to teach the immune system to recognize and kill cancer cells bearing the biomarker of patient’s tumor

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12
Q

autologous cell vaccine

A
  • cancer cells are treated with a hapten which binds to molecules on the surface of cells and helps trigger immune responses
  • combined with an adjuvant to enhance effectiveness
  • injected into pt so immune system can better locate and combat cancer cells
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13
Q

BIOVAXID

A

cancer vaccine recognizes and eliminates cancerous lymphoma cells, while sparing normal B cells

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14
Q

how does BIOVAXID work?

A

specific cancer antigen-bearing tumor cells harvested from a patient’s lymph node are fused to antibody-producing mouse cells and the produced large quantities of the protein antigens are then given back to patients with an immune system booster

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15
Q

ChemoFx assay

A

ex vivo assay designed to predict the sensitivity or resistance of a solid tumor to a variety of chemotherapeutic agents

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16
Q

main cancer biomarkers

A

estrogen and progesterone R

HER-2

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17
Q

what is the reason for identifying HER-2 cancers?

A

Identifying breast cancer patients with metastatic disease who may benefit from Herceptin

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18
Q

companion diagnostics

A

Use genetic, proteomic, gene expression or other molecular markers to predict whether a drug will work in someone or not, what dose is optimal and whether there is a risk of adverse effects

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19
Q

Verigene warfarin metabolism nucleic acid test

A

FDA approved test that detects variants of CYP2C9 and VKORC1 genes responsible for sensitivity to warfarin

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20
Q

HLA-B57

A

Marker for the potentially fatal hypersensitivity reactions in some patients taking the HIV-1 reverse inhibitor, abacavir

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21
Q

HLA-B1502

A

Those with this gene have a higher chance of developing adverse drug reactions against carbamazepine

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22
Q

Thiopurine methyltransferase

A

NZ involved metab of azathioprine and 6-mercaptopurin

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23
Q

Patients with low TPMP are at an ___ risk of myelotoxicity if taking azathioprine or 6-mercaptopurin

A

increased

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24
Q

Azathioprine

A

used in renal homotransplantations and for the management of active rheumatoid arthritis

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25
Q

6-Mercaptopurin

A

therapy of acute lymphatic (lymphocytic, lymphoblastic) leukemia

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26
Q

Erbitux and panitumumab

A

Drugs that require testing of patients with colorectal cancer for EGFR receptor before treatment

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27
Q

Imatinib

A

Targeted therapy for leukemia and a test for the bcr/abl translocation determines if a patient benefits from this drug

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28
Q

Ivacaftor is effective in treating patients with the ___ mutation in ___

A

G551D

cystic fibrosis

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29
Q

genetic test for breast cancer

A

BRCA

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30
Q

genetic test of colon cancer

A

MLH1

MSH2

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31
Q

microarray

A

Consists of an arrayed series of microscopic spots of probes on a solid surface which bind to the components of the analyzed sample with high specificity

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32
Q

what are the probes in microarrays?

A

oligonucleotides or fragments of cDNA attached to solid surfaces or beads

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33
Q

how are microarrays created?

A

in situ synthesis

depostion of presynthesized oligonucleotides

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34
Q

Affymetrix arrays

A

oligonucleotide probes are synthesized directly in situ using photolithography techniques adapted from the microelectronics industry

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35
Q

how are microarrays made with ink jet printing?

A
  • Nucleotide monomers are printed onto the chip and coupled using phosphoramidite chemistry
  • Hybridization is detected by using a confocal laser scanning microscope to image the intensity of fluorescently labeled samples
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36
Q

Compared to cDNA arrays, the oligonucleotide arrays offer ________

A

greater specificity and can distinguish single nucleotide polymorphisms (SNPs) and splice variants

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37
Q

4 categories of research with microarrays in humans

A

Normal tissue taxonomy
Disease diagnosis and classification
Disease prognostication
Dissection of biological mechanisms

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38
Q

mammaprint

A

70 gene signature that identifies which early-stage breast cancer patients are at risk of distant recurrence following surgery, independent of estrogen receptor status and any prior treatment

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39
Q

MINDACT

A
  • microarray for node-negative disease may avoid chemotherapy trial
  • aims to determine whether this expression signature can be used for making clinical decisions
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40
Q

Oncotype assay

A
  • RT-PCR assay based on a 21-gene signature derived from 250 candidate genes selected from the published microarray literature
  • used to see if a pt will benefit from chemo
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41
Q

Genome-wide studies of gene expression microarrays

A
  • Differentiation of biological states by differences in gene expression
  • What pathways are affected by different biological states
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42
Q

Locus copy # microarray

A

Disease specific chromosomal loss and amplification

Chromosome instability in cancer

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43
Q

1st generation DNA sequencing

A

“Sequencing by synthesis” → uses DNA polymerase
Adds bases to the 3’ end of a primer bound to a DNA template
Incorporates dNTP bases complementary to the template

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44
Q

limitations of 1st generation DNA sequencing

A

only one sequence per lane can be sequenced and a complex and labor-intensive separation of template sequences is needed

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45
Q

how did fluorescent ddNTPs change DNA sequencing?

A

Allows analysis of all 4 reactions in 1 lane
Fluorescent fragments detected by laser excitation
Possibility for automation

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46
Q

how did fluorescent capillary electrophoresis change DNA sequencing?

A 
Read length is significantly increased 
Adjacent lane spillover is eliminated and lane tracking problems are gone 
Higher sensitivity 
Less reagents and template 
Lower cost, less work 
Highly automated and more consistent
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47
Q

next generation DNA sequencing

A

“Massively parallel”
Cost-effective and rapid
Production of large numbers of low-cost reads makes the NGS platforms useful for many applications, including clinical applications

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48
Q

Chip-Seq

A

sequencing of DNA associated with active chromatin

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49
Q

_% of transcribed RNA are genes

A

1

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50
Q

commensal

A

normal flora or non-sterile body sites

symbiotic colonization

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51
Q

environmental species

A

reservoirs are non human

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52
Q

obligate pathogens

A

capable of causing disease in healthy and immunocompromised hosts

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53
Q

opportunistic pathogens

A

typically rely on some kind of immune impairment, local or systemic, in order to cause infection

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54
Q

iatrogenic suppression

A

immunosuppression/therapuetic regimens that increase risk for infection

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55
Q

ivermectin treats?

A

river blindness caused by the filarial worm, transmitted by flies
lymphatic filariasis caused by worms, transmitted by mosquitoes

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56
Q

artemisinin

A

antimalarial drug

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57
Q

what kind of pathogen is C diff?

A

anaerobic bacterium

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58
Q

possible treatments for C diff

A

fecal microbiota transplants

Monoclonal antibodies block toxin receptors

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59
Q

listeria

A

Can be found in food processing plants

Survives and proliferates at refrigeration temperatures

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60
Q

endemic

A

steady state of disease in a population

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61
Q

examples of endemic diseases

A

malaria
syphilis
TB

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62
Q

outbreak

A

case numbers exceed usual expectation for a defined community, region, or season

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63
Q

epidemic

A

disease spreads rapidly

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64
Q

pandemic

A

global epidemic

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65
Q

examples of epidemics

A

flu
SARS
ebola

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66
Q

examples of pandemics

A

HIV/AIDS

flu

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67
Q

bioterrorism

A

use of infectious agents as weapons

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68
Q

malaria

A

Endemic mosquito borne protozoan disease

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69
Q

what can lead to new strains of pathogens?

A

genetic mutations
adaptation
zoonotic transmission

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70
Q

selective pressure that drive opportunistic infections

A

Immunosuppression

Antimicrobial resistance

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71
Q

plague pathogen

A

Y pestis

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72
Q

CDC category A bioterrorism

A

readily disseminated
pandemic potential
requires public preparedness

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73
Q

CDC category B bioterrorism

A

moderately easy dissemination
morbidity
requires surveillance and diagnostics

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74
Q

CDC category C bioterrorism

A

emerging or engineered

high morbidity and mortality

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75
Q

what allows flu to have persistent genetic mutation

A

segmented RNA genome

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76
Q

antigenic drift

A

minor mutations in outer viral proteins of the flu

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77
Q

antigenic shift

A

major genetic recombinations that can create a risk for epidemics and pandemics

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78
Q

flu reservoirs

A

birds

pigs

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79
Q

what is the reason that we have to change the flu shot every year?

A

antigenic drift

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80
Q

SARS

A

respiratory virus
Enveloped single-stranded RNA unsegmented genome
caused a worldwide outbreak

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81
Q

MERS

A

Enveloped single-stranded RNA unsegmented genome
causes upper resp illness
ongoing

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82
Q

why was the E Coli outbreak in 2011 more virulent?

A

novel genetic exchange between a Shiga toxin producing strain and a different strain that manifests strong adherence to intestinal cell epithelium

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83
Q

antimicrobials

A

Drugs that act against bacteria, viruses, fungi or parasites

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84
Q

2 major adverse consequences of antimicrobials

A

Disruption of normal biologic function

Selection for antimicrobial resistance

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85
Q

what is artemisinin resistance due to?

A

Poor treatment practices
Inadequate patient adherence to regimens
Widespread availability of substandard forms of the drug

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86
Q

Carbapenems

A

broad spectrum beta lactam drugs in the same family as penicillin

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87
Q

prion size

A

<1um

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88
Q

what do prions cause?

A

intracellular propagation of abnormal proteins

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89
Q

virus size

A

<1um

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90
Q

what are viruses?

A

obligate intracellular pathogens

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91
Q

the essential nucleic acid core of a virus is surrounded by a ___

A

capsid

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92
Q

herpesviridae

A

Enveloped viruses with a large complex genome that persist in host cells by establishing latency

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93
Q

how is herpes DNA maintained in the host cell?

A

incorporation into host DNA or as a plasmid-like independent episome, separate from host cell chromosomes by able to interact with DNA

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94
Q

how does herpes cause disease after infecting the host cell?

A

activation of viral replication and release of virus from infected cells causes recurrent symptomatic disease

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95
Q

alpha herpes viruses

A

variable range of tissue tropism including mucocutaneous and neuronal tissue

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96
Q

examples of alpha herpes viruses

A

herpes simplex

varicella zoster

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97
Q

beta herpes viruses

A

longer reproductive cycle and a different if not more restricted tropism

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98
Q

example of beta herpes viruses

A

cytomegalovirus

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99
Q

gamma herpes viruses

A

predominantly lymphotropic, specific to T or B lymphocytes

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100
Q

example of gamma herpes viruses

A

Epstein-Barr

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101
Q

how is HSV transmitted?

A

close contact with lesions

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102
Q

where does HSV establish latency?

A

neuronal ganglia proximal to the site of initial infection

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103
Q

Typical sites of HSV primary and recurrent infection

A

brain
conjunctiva
orofacial and genital mucocutaneous sites

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104
Q

where do shingles outbreak?

A

in a dermatomal pattern in the areas of the skin innervate by infected ganglia

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105
Q

what are the reservoirs for HSV and VSV?

A

only humans

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106
Q

flu transmission

A

respiratory droplets, contact with contaminated surfaces/hands

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107
Q

cytopathic effects

A

changes that can be seen by light microscopy even if the actual virus can’t be seen

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108
Q

what kind of virus is hepatitis B?

A

DNA

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109
Q

what kind of virus is hepatitis C and A?

A

RNA

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110
Q

tropism of hepatitis

A

liver

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111
Q

what kind of cell are bacteria?

A

prokaryotes

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112
Q

bacteria cell wall functions

A

cell integrity
growth
metabolism

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113
Q

gram positive

A

thick peptidoglycan layer

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114
Q

gram negative

A

thin peptidoglycan layer and lipid bilayer

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115
Q

Microbiomes

A

site-defined complex ecosystems of microbes, genes, and products that contribute to our healthy function

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116
Q

Toxigenic C Difficile

A

Anaerobic spore-forming bacterium with toxin-producing and non-toxigenic strains

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117
Q

what kind of cell are fungi?

A

eukaryotes with a cell wall

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118
Q

2 basic kinds of fungi

A

yeast

mould

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119
Q

difference btwn yeast and mould

A

yeasts are single celled

moulds are multicellular

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120
Q

hyphae

A

collections of elongated cells of moulds

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121
Q

how do most fungi reproduce?

A

create environmentally hardy spores that easily disperse

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122
Q

what kind of cell are parasites?

A

Eukaryotes

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123
Q

2 basic kinds of parasites

A

protozoa

helminths

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124
Q

what kind of cell are protozoa

A

single celled eukaryote

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125
Q

helminths

A

Multicellular parasites with complex life cycles

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126
Q

roundworms

A

nematodes
nonsegmented
collagenous tegument

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127
Q

flatworms

A

cestodes
gutless
head and body segments

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128
Q

flukes

A

trematodes

primitive, leaf like worms

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129
Q

Ectoparasites

A

Live on skin or elsewhere outside of the host

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130
Q

are prions prokaryotes or eukaryotes?

A

neither- proteins

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131
Q

are viruses prokaryotes or eukaryotes?

A

neither

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132
Q

how do candida yeast cause infection?

A

part of normal gut flora

changes in flora allow yeast to cause infections

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133
Q

what is the first barrier of defense against pathogens?

A

skin

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134
Q

how is hepatitis A acquired?

A

ingestion of something contaminated, but it is tropic to the liver and causes inflammation of the liver

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135
Q

how is hepatitis B and C acquired?

A

transmitted by blood-borne exposures but also are hepatotropic

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136
Q

how do microbes cause disease?

A

direct cell damage
transformation
cell death

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137
Q

tropism

A

preferential cell or tissue infection

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138
Q

HIV tropism

A

CD4 T cells

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139
Q

where does Epstein Barr establish latency?

A

memory B cell compartment

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140
Q

where does BKV establish latency?

A

renal epithelium

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141
Q

where does CMV establish latency?

A

salivary glands

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142
Q

which herpes viruses insert episomal viral genome into the host nucleus?

A

HSV

VZV

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143
Q

which pathogen incorporates proviral DNA into the host genome?

A

HIV

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144
Q

which viruses control cell apoptosis?

A

HCV
CMV
EBV
HIV

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145
Q

how do microbes avoid clearance by the immune system?

A

immunosuppressive cytokine

alteration of MHC expression

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146
Q

which pathogen stimulates production of immunosuppressive cytokines like interleukin 10?

A

hepatitis C

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147
Q

which pathogens alter host-cell antigen expression to avoid immune recognition?

A

HIV
HSV
CMV

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148
Q

S pyogenes induced immune complexes cause ___

A

renal injury

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149
Q

TB causes

A

granulomatous inflammation and necrosis

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150
Q

endotoxins

A

components of the microbe

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151
Q

exotoxins

A

substances released by the microbe

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152
Q

pathogens that use binary toxins

A

diphtheria

anthrax

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153
Q

what are the symptoms of anthrax a result of?

A

2 Bacillus anthracis exotoxins:
edema factor
lethal factor

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154
Q

how do binary toxins works?

A

the B component binds the host cell R

A component catalyzes cell signaling mechanisms to produce exotoxin

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155
Q

4 basic ways of evading the host immune system

A

staying inaccessible
antigenic variation
evasion of innate defenses
evasion of adaptive defenses

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156
Q

how do pathogens stay inaccessible to host immunity?

A

become enclosed in a protective structure
camouflage
establish latency

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157
Q

how do pathogens use antigenic variation to evade the host immune system?

A

change or shed surface antigens

replication errors

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158
Q

how do pathogens evade innate defenses?

A

bind antibodies
degrade antibodies
avoid phagocytosis
block complement

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159
Q

how do pathogens evade adaptive defenses?

A

prevent MHC expression
express fake MHC
degrade MHCII
infect lymphocytes

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160
Q

suppurative inflammation

A

pathogen encourages an influx of neutrophils to the site of infection → pus or abscess

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161
Q

Granulomatous inflammation

A

organism survives inside macrophages, walled off by surrounding fibrous tissue and other inflammatory cells including multicellular macrophages

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162
Q

examples of cytopathic agents

A

herpes

hepatitis B

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163
Q

examples of cytoproliferative agents

A

HPV

molluscum contagiosum

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164
Q

cytopathic

A

kill cells as they escape to infect another cell

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165
Q

cytoproliferative

A

induce autonomous growth and produce tumors

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166
Q

cytoproliferative pathogens that are potential inducers of neoplasia

A

EBV

HPV

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167
Q

necrotizing pathogens

A

cause rapid and severe tissue destruction via potent toxins and enzymes

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168
Q

examples of pathogens that cause chronic inflammation and scarring

A

hepatitis B and C can cause cirrhosis of the liver

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169
Q

Increased cell turnover associated with chronic inflammation and scarring can lead to ____

A

cellular mutations and increased risk for tumor and malignancy

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170
Q

autosomal chromosomal disorders

A

gain or loss of all or part an autosome

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171
Q

general phenotype of autosomal chromosomal disorders

A 
low birth weight
short stature 
failure to thrive
severe mental retardation 
multiple organ systems affected
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172
Q

single gene disorders

A

Submicroscopic changes to 1 gene, ranging from a single base change to deletion of the whole gene

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173
Q

Pleiotropism

A

a single gene affects a number of phenotypic traits in the same organism

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174
Q

Variable expressivity

A

range of signs and symptoms that can occur in different people with the same genetic condition

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175
Q

Incomplete penetrance

A

If some people with the mutation do not develop features of the disorder, the condition is said to have reduced (or incomplete) penetrance

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176
Q

advanced paternal age is associated with an increased risk of ____

A

autosomal dominant disorders

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177
Q

what kind of transmission is in the autosomal dominant family tree?

A

vertical

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178
Q

_% of offspring are affected in autosomal dominant disorders

A

50%

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179
Q

are more males or females affected in autosomal dominant disorders?

A

= #s

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180
Q

familial hypercholesterolemia

A

elevated levels of cholesterol that induce premature atherosclerosis and increased risk of early myocardial infarction due to a mutant LDL R gene

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181
Q

LDL receptor mutation class 1

A

non LDL R protein made
null allele
uncommon

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182
Q

LDL receptor mutation class 2

A

accumulation in the ER

fairly common

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183
Q

LDL receptor mutation class 3

A

little or no binding of receptor to LDL

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184
Q

LDL receptor mutation class 4

A

poor internalization of LDL+ R

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185
Q

LDL receptor mutation class 5

A

tight LDL R binding

no recycling

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186
Q

where do FH heterozygotes get xanthomas?

A

tendons

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187
Q

where do FH homozygotes get xanthomas?

A

cutaneous

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188
Q

diagnosis of familial hypercholesterolemia

A 
Serum LDL > 200 
Elevated triglycerides
Plasma cholesterol >300 
mg/cc in adults
Xanthomas seen by physical exam
chest pain 
obesity
family history
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189
Q

how do statins works?

A

suppress cholesterol synthesis and allow greater synthesis of LDL R

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190
Q

what kind of disease is Tay Sachs?

A

autosomal recessive

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191
Q

Tay Sachs pathology

A

No detectable hexosaminidase A
No degradation of GM2 ganglioside in the lysosome
Accumulation of GM2 ganglioside in brain cells
Neurologic changes and eventual death

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192
Q

what causes Tay Sachs?

A

Frameshift mutation in hexosaminidase A gene (15q)

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193
Q

what is tested to find out if someone is a Tay Sachs carrier?

A

levels of Hex A activity

<50% activity indicates carrier

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194
Q

Sandhoff’s

A

mutant in hexosaminidase B gene (chromosome 5)

Clinically similar to Tay Sachs

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195
Q

Variant AB

A

mutation in HexA/Hax B activator protein (chromosome 5)

Clinically similar to Tay Sachs

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196
Q

what kind of disease is cystic fibrosis?

A

autosomal recessive

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197
Q

what causes CF?

A

Mutant CFTR gene → Cl channel deficiency

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198
Q

diagnosis of CF

A

symptoms
sibling with CF
sweat test

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199
Q

symptoms of CF

A 
Meconium ileus in infant
Recurrent respiratory infections
Greasy, foul smelling stools due to pancreatic insufficiency and lack of digestive enzymes 
Malnutrition, stunted growth 
Male infertility
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200
Q

how do CF sweat tests works?

A

Sweat absorbed onto filter paper is analyzed for Cl

[Cl] >60mEq/L → positive

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201
Q

CF treatments

A

Antibiotics
Pancreatic enzyme replacement therapy
Lung inhalation therapies
Lung transplantation

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202
Q

what is the current genetic test for CF?

A

CF86

tests for the 86 most common mutations

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203
Q

Founder effects

A

mutant allele appeared in a geographically isolated population and was enriched in subsequent generations

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204
Q

what kind of transmission are X linked dominant disorders?

A

vertical

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205
Q

are there more females or males affected with x linked dominant disorders?

A

females

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206
Q

what kind of disease is hypophosphatemic rickets

A

X linked dominant

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207
Q

what causes hypophosphatemic rickets?

A

Mutation in the PHEX gene on chromosome Xp

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208
Q

hypophosphatemic rickets symptoms

A

defective vitamin D metab causes deranged bone growth, skeletal abnormalities and dental problems

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209
Q

what characterizes hypophosphatemic rickets?

A

Failure to thrive
Short stature
Rickets

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210
Q

age of onset of hypophosphatemic rickets?

A

early infancy

15 months

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211
Q

what kind of disease is hemophilia A?

A

x linked recessive

212
Q

are there more females or males affected with x linked recessive disorders?

A

males

213
Q

what causes hemophilia A?

A

Factor VIIIc gene mutation (x chromosome)

214
Q

severe hemophilia A

A

<1% normal Factor VIIIc levels
Onset of bleeding in newborn period
Bleeding may be spontaneous

215
Q

moderate hemophilia A

A 
1-5% normal Factor VIIIc levels 
Onset during infancy 
Excessive bruising with ambulation
Some arthrosis
Sometimes spontaneous but usually following mild to moderate trauma
216
Q

mild hemophilia A

A

<6% normal Factor VIIIc
Onset during childhood
Bleeding is not spontaneous but follows moderate to severe trauma, dental work or surgery

217
Q

what causes hemophilia B/Christmas disease?

A

Mutation in Factor IX gene decreases blood coagulation

218
Q

what do serum studies of hemophilia detect?

A

Decreased factor VIIIc levels
Prolonged PTT time
Normal → PT, bleeding time, thrombin time, platelet count, Factor VIIvW

219
Q

partial thromboplastin time

A

seconds for plasma to clot in presence of taolin, cephalin, calcium
prolonged in hemophilias

220
Q

prothrombin time

A

seconds for plasma to clot in presence of thromboplastin and calcium
normal in hemophilias

221
Q

Von Willebrand disease

A

Bleeding disorder that is not x-linked

Mutations in the vWF gene later both platelet function and coagulation pathway

222
Q

what kind of disease is Von Willebrand?

A

autosomal dominant and recessive

223
Q

quantitative mutations in vWF

A

change in amount of vWF

224
Q

qualitative mutations in vWF

A

normal amounts of vWF with abnormal function

225
Q

clinical manifestations of vW disease

A

spontaneous bleeding from mucous membranes
excessive bleeding from wounds
menorrhagia
prolonged bleeding time but normal platelet count

226
Q

how is vW disease diagnosed?

A

immunologic tests

ristocetin aggregation test

227
Q

ristocetin aggregation test

A

decreased aggregation of platelets in the presence of the antibiotic ristocetin
diagnoses vW disease

228
Q

multifactorial genetic diseases

A

Caused by multiple factors such as:
Genetic, often multiple genes
Environment
Various genes and environmental interactions

229
Q

threshold model for multifactorial traits

A

Curves indicate distribution of phenotypes

Disease occurs in % of cases that are to the right of the threshold

230
Q

what does the threshold represent in the threshold model for multifactorial traits?

A

measured trait becomes abnormal enough to result in the disease phenotype

231
Q

Characteristics of multifactorial inheritance

A
  • Disorder is familial but with no distinctive pattern of inheritance within a family
  • Risk of expressing the disorder is related to the number of mutant genes inherited
  • Risk to 1st degree relatives is higher than to 2nd degree relatives but both are higher than the risk in general population
  • Recurrence risk is higher when more than 1 family member is affected and when the disease is more severe
232
Q

what is the classic example of multifactorial disease?

A

diabetes

233
Q

type 1 diabetes susceptibility locus is on ____

A

chromosome 6

234
Q

type 1 diabetes is linked with the ____

A

insulin gene allele

235
Q

mtDNA diabetes

A

a subtype of Type II diabetes, caused by mitochondrial DNA mutations (1% of all cases)

236
Q

PPARγ polymorphism

A

people with Pro12 allele are more insulin resistant than those with the Ala 12 allele and 1.25x more at risk for diabetes (connection to fatty acid metabolism)

237
Q

Calpain-10 gene polymorphism

A

increases risk 3-fold (affects -cell function and insulin action in muscle and fat)

238
Q

Impaired glucose tolerance

A

blood glucose levels intermediate between normal and diabetes, following a glucose load predicts those in the general population with a higher risk of developing diabetes

239
Q

what kind of disease is MODY?

A

autosomal dominant

240
Q

what is the primary defect in MODY?

A

beta cell function

241
Q

what causes MODY?

A

mutation in any of 5 transcription factors responsible for regulating the transcription of insulin and other cell genes or in the glycolytic enzyme glucokinase (one copy of any of these mutant genes will cause MODY)

242
Q

MODY1 mutation

A

mutation in hepatocyte nuclear factor → HNF-α

243
Q

MODY2 mutation

A

mutation in glucokinase gene

244
Q

MODY3 mutation

A

mutation in HNF-1α

245
Q

MODY4 mutation

A

mutation in insulin promoter factor (IPF-1)

246
Q

MODY5 mutation

A

mutation in HNF-1β

247
Q

MODY6 mutation

A

mutation in NeuroD/BETA2 gene

248
Q

arteriosclerosis

A

hardening of the arteries

249
Q

Monckeberg’s Medial Calcific Sclerosis

A

Medial calcification of muscular arteries

250
Q

Arteriosclerosis

A

Thickening of walls of small arteries and arterioles → reduction of luminal diameter of the microvasculature

251
Q

what does arteriosclerosis depend on?

A

age

252
Q

what accelerates arteriosclerosis?

A

hypertension

diabetes mellitus

253
Q

2 froms of arteriosclerosis

A

hyaline

hyperplastic

254
Q

Hyaline arteriolosclerosis

A

Amorphous eosinophilic thickening of the wall of arterioles

255
Q

what influences the development of hyaline arteriolosclerosis?

A

old age
hypertension
diabetes mellitus

256
Q

what causes hyaline arteriolosclerosis?

A

leakage of plasma proteins into the blood vessel wall

257
Q

what does hyaline arteriolosclerosis result in?

A

luminal compromise from small size of involved vessels

258
Q

Hyperplastic arteriolosclerosis

A

hypertrophy/hyperplasia of medial smooth muscle in small arteries

259
Q

appearance of hyperplastic arteriolosclerosis

A

“onion skin”

260
Q

where is hyperplastic arteriolosclerosis typically seen?

A

severe hypertension

261
Q

Atherosclerosis

A

Progressive accumulation of lipids, smooth muscle cells, macrophages and connective tissue, within the intima (atherosclerotic plaque) of large and medium size arteries that results in progressive luminal narrowing with impaired organ perfusion

262
Q

atheroma

A

Intimal thickening and lipid accumulation leading to a plaque

263
Q

what does an atheroma consist of?

A

fibrous cap overlying an accumulation of muscle and inflammatory cells with intracellular (foam cells) and extracellular lipid deposits with a necrotic core

264
Q

3 constituents of atheromas

A

cellular
extracellular matrix
lipid

265
Q

cellular components of atheromas

A

smooth muscle cells
macrophages
inflammatory cells

266
Q

extracellular matrix cell components of atheromas

A

collagen
elastin
proteoglycan

267
Q

lipid component of atheromas

A

cholesterol esters

268
Q

what do atheromas cause as they enlarge?

A

vascular ingrowth

269
Q

where is atherosclerosis mainly?

A

abdominal aorta

270
Q

fatty streaks

A

non-raised accumulations of foam cells and extracellular lipid in the intima

271
Q

where are fatty streaks found?

A

Universally present

don’t disturb blood flow

272
Q

what is the favored hypothesis of atherosclerosis pathogenesis?

A

response to injury hypothesis

273
Q

response to injury hypothesis

A

Proposes that atherosclerosis is a chronic inflammatory response to subtle vascular wall injuries occurring over time

274
Q

what causes endothelial injury?

A

shear stress
hyperlipidemia
free radicals (from oxidation of LDL)
hyperhomocysteinemia

275
Q

what do endothelial cell injuries lead to?

A

increased wall permeability

changes in gene expression that enhance leukocyte adherence

276
Q

which genes are upregulated to enhance leukocyte adherence?

A

ICAM-1

VCAM-1

277
Q

lipid insudation

A

Hyperlipidemia and increased endothelial permeability favor the accumulation of lipoproteins (LDL and VLDL) the arterial intima

278
Q

how are foam cells formed?

A

Oxidation of LDL by macrophages and endothelial cells or by free radicals generated by the auto-oxidation of homocysteine creates a compound which is preferentially taken up by the scavenger receptor on macrophages

279
Q

what does oxidized LDL promote and attract?

A

proinflammatory cytokine release
macrophages
monocytes

280
Q

cellular infiltration

A

Inflammatory cells and T and B lymphocytes are recruited into developing plaques

281
Q

what activates cellular infiltration?

A

cytokines such as IL-1 and TNF-alpha

oxidized LDL

282
Q

what induces smooth muscle cell proliferation?

A

PDGF
FGF
TGF-alpha

283
Q

where does neovascularization of a plaque occur?

A

periphery

284
Q

effects of hyperlipidemia

A

endothelial injury/dysfunction
lipid accumulation
oxidized LDL

285
Q

effects of endothelial injury/dysfunction

A

mononuclear cell recruitment
lipid accumulation
oxidized LDL
fibrosis

286
Q

effects of mononuclear cell recruitment

A 
endothelial injury/dysfunction
lipid accumulation
oxidized LDL
myocyte recruitment
fibrosis
287
Q

effects of lipid accumulation

A

endothelial injury/dysfunction

oxidized LDL

288
Q

effects of oxidized LDL

A

endothelial injury/dysfunction
mononuclear cell recruitment
myocyte recruitment
fibrosis

289
Q

effects of myocyte recruitment

A

endothelial injury/dysfunction
mononuclear cell recruitment
fibrosis

290
Q

what disease accounts for the most deaths in the western world?

A

atherosclerosis

291
Q

major complications of atherosclerosis

A

ischemic heart disease
MI
stroke
gangrene of extremities

292
Q

major modifiable risk factors of atherosclerosis

A

hyperlipidemia
hypertension
smoking
diabetes mellitus inflammation

293
Q

major constitutional risk factors of atherosclerosis

A

age
male gender
family history
genetic abnormalities in LDL-R, ApoB, ApoE

294
Q

minor risk factors of atherosclerosis

A 
obesity
stress
factors affecting thrombosis
high CHO intake
homocysteinemia
295
Q

complications of atherosclerosis

A

Acute occlusion → plaque rupture/thrombosis
Thrombosis → sudden arterial occlusion
Chronic narrowing of lumen → chronic ischemia
Aneurysm formation due to weakening of arterial media
Embolism

296
Q

metabolic syndrome risk factors

A

Central obesity
Low serum HDL and increased triglycerides
Increased BP
Insulin resistance or glucose intolerance
Prothrombotic state
Proinflammatory state

297
Q

what causes a prothrombic state?

A

increased fibrinogen or plasminogen activator inhibitor

298
Q

what causes a proinflammatory state?

A

elevated C reactive protein

299
Q

how is metabolic syndrome diagnosed?

A

must have 3 risk factors

300
Q

aneurysm

A

arterial dilation with all 3 normal components in its wall

301
Q

aneurysm shape

A

Saccular, cylindric, or fusiform

302
Q

what is the critical diameter for rupture of an aneurysm?

A

6cm

303
Q

where is the most common atherosclerotic aneurysm?

A

abdominal aorta

304
Q

what does the wall of an atherosclerotic aortic aneurysm contain?

A

atheromatous material
fibroblasts
chronic inflammatory cells

305
Q

complications of atherosclerotic aortic aneurysms

A

rupture

blockage of tributary vessels

306
Q

what is the risk of atherosclerotic aortic aneurysm proportional to?

A

diameter

307
Q

ischemic heart disease

A

Constellation of disorders in which myocardial ischemia is the common pathophysiologic mechanism

308
Q

what does ischemia usually result from?

A

obstruction of coronary artery blood flow by atherosclerosis

309
Q

when does coronary atherosclerosis become symptomatic?

A

luminal cross-sectional area is reduced by more than 75%

310
Q

where do lesions from IHD usually occur?

A

proximal portions of the LAD and LC arteries and the entire length of the RCA

311
Q

4 clinical syndromes of IHD

A

Angina pectoris
Myocardial infarction
Chronic ischemic heart disease and congestive heart failure
Sudden cardiac death

312
Q

pathogenesis of IHD

A

Fixed coronary obstruction
Acute plaque change
Coronary thrombus
vasoconstriction

313
Q

what does acute coronary syndrome include?

A

Unstable angina
Acute MI which
Sudden Cardiac Death

314
Q

angina pectoris

A

symptom complex characterized by recurrent attacks of crushing substernal chest pain

315
Q

3 variants of angina pectoris

A

stable
unstable
prinzmetal (variant)

316
Q

stable/typical angina

A

precipitated by exertion
relieved by rest or nitroglycerin
due do a fixed coronary lesion

317
Q

significant coronary lesion

A

> 50% reduction in diameter
Takes up 75% cross sectional area
Nutritional demand is met at rest
Symptoms develop with exertion

318
Q

critical coronary lesion

A

> 75% reduction in diameter
Takes up 90% cross sectional area
Chronic IHD

319
Q

unstavle/crescendo angina

A

pain which occurs more frequently, with progressively less exertion or at rest
Associated with acute plaque change

320
Q

in what kind of atheroma is rupture most likely?

A

Large core → >40% of atheroma volume with many macrophages

Thin fibrous cap with little smooth muscle

321
Q

prinzmetal/variant angina

A

uncommon, pain occurs at rest

Due to coronary vasospasm either in a normal coronary artery or close to an atherosclerotic plaque

322
Q

what treatment does prinzmetal/variant angina respond to?

A

vasodilator therapy- NO, Ca channel blockers

323
Q

myocardial infarction

A

Ischemic necrosis (coagulation necrosis) in the heart that occurs when myocardial ischemia is prolonged for more than 20 or 40 minutes

324
Q

what is the most common cause of ischemic necrosis

A

occlusive arterial thrombi

325
Q

what causes myocardial ischemia (cell level)

A

anaerobic glycolysis
rise in intracellular Na and fall of K
high intracellular Ca

326
Q

what determines extent of MI?

A 
Location, severity, rate of occlusion 
Size of vascular bed
Duration of ischemic episode 
Metabolic demands
Collateral vessels
327
Q

where are infarcts from LAD?

A

antero/apical LV

anterior 2/3 septum

328
Q

where are infarcts from LCX?

A

lateral LV

329
Q

where are infarcts from RCA?

A

posterior/inferior LV
posterior RV
posterior 2/3 septum

330
Q

evolution of an infarct

A

Necrosis → acute inflammation → chronic inflammation → organization → fibrosis

331
Q

transmural infarct

A

Entire wall

Plaque rupture and thrombosis

332
Q

gross appearance of MI 0-4 hours

A

invisible

333
Q

gross appearance of MI 4-24 hours

A

dark mottling

334
Q

gross appearance of MI 1-3 days

A

increasingly pale center

335
Q

gross appearance of MI 3-7 days

A

sharply outlined with a central pale, yellow region bordered by a hyperemic zone

336
Q

gross appearance of MI 7-10 days

A

maximally yellow and necrotic with a depressed red margin

337
Q

gross appearance of MI 10-14 days

A

margin becomes red-gray

338
Q

gross appearance of MI 2-8 weeks

A

infarcted region progresses to a gray-white scar

339
Q

when is MI scarring complete?

A

after 8 weeks

340
Q

when does an MI appear to have wavy fiber change?

A

1-3 hours

341
Q

when does an MI appear to have coagulation necrosis?

A

4-12 hours

342
Q

when does an MI appear to have nuclear pyknosis?

A

5 hours

343
Q

when does an MI appear to have karyolysis?

A

24-48 hours

344
Q

when does an MI appear to have neutrophilic infiltration?

A

6-8 hours

peaks at 48 hours

345
Q

when does an MI appear to have macrophage infiltration?

A

4 days

346
Q

when does an MI appear to have vessel proliferation?

A

3 days

347
Q

when does an MI appear to have fibroblast proliferation?

A

4 days

348
Q

when does an MI appear to have collagen deposition?

A

9 days

349
Q

when does an MI appear to have granulation tissue peak?

A

2-4 weeks

350
Q

what does tPA do?

A

promotes hemorrhage in the infarct

351
Q

contraction band necrosis

A

Accelerated necrosis of irreversible injured myocytes

352
Q

where does contraction band necrosis occur?

A

margins of infarcts between dead and viable zones

353
Q

hypercontraction

A

Secondary massive influx of calcium from membrane damage

Sarcomeres of Z lines produce eosinophilic bands visible by light microscopy

354
Q

Sequelae

A

a condition that is the consequence of a previous disease or injury

355
Q

what region is most prone to ischemic damage?

A

subendocardial

356
Q

what is subendocardial infarction related to?

A

global reduction in coronary blood flow

357
Q

sudden cardiac death

A

Unexpected death from cardiac causes (lethal arrhythmia) within 1 hour of the onset of symptoms

358
Q

__% of sudden cardiac deaths have IHD

A

80-90

359
Q

Chronic Ischemic Heart Disease

A

typically left ventricular hypertrophy with dilatation and focal white scars corresponding to prior acute infarcts are usually present with severe fixed coronary obstructions

360
Q

Hypertensive heart disease

A

left ventricular hypertrophy in the absence of cardiovascular causes other than hypertension

361
Q

cor pulmonale

A

Right ventricular failure with hypertrophy and dilatation

362
Q

what is cor pulmonale usually secondary to?

A

pulmonary hypertension

363
Q

heart failure

A

A state in which the heart is unable to maintain an output sufficient for metabolic requirements

364
Q

forward heart failure

A

Decreased output
Decreased myocardial contractility and output
Systolic dysfunction

365
Q

backward heart failure

A

Increased EDP
Decreased myocardial compliance
diastolic dysfunction, congestion of veins

366
Q

edema

A

increased fluid in interstitial tissue spaces

367
Q

anasarca

A

severe generalized edema with subcutaneous tissue swelling

368
Q

hyperemia

A

active process secondary to dilation of arterioles → increase blood flow

369
Q

Congestion

A

passive process where blood flows more slowly due to obstruction of the venous system

370
Q

cyanosis

A

Congested areas are blue and purple due to unsaturated venous blood pooling in the vessels

371
Q

acute liver congestion

A

Distention of central vein and sinusoids

Pressure atrophy of centrilobular hepatocytes

372
Q

chronic hepatic congestion

A

Nutmeg liver
centrilobular necrosis with hemorrhage and hemosiderin-laden macrophages
Fibrosis in severe long-standing cases

373
Q

chronic pulmonary congestion

A

Alveolar septal fibrosis

Numerous hemosiderin-laden macrophages within alveolar spaces

374
Q

acute pulmonary congetion

A

Capillary engorgement
Septal edema
Intra-alveolar hemorrhage

375
Q

hemorrhage

A

Blood outside of the blood vessel

376
Q

hematoma

A

hemorrhage which is enclosed within a tissue

377
Q

Petechiae

A

small 1-2 mm hemorrhages which are typically observed on the skin, mucosal membranes, or serosal surfaces such as the peritoneum or pericardium

378
Q

who is likely to develop petechiae?

A

Patients with low platelet counts or dysfunctional platelets can develop these

379
Q

what are petechiae associated with?

A

locally increased intravascular pressure
thrombocytopenia
defective platelet function
clotting factor deficiencies

380
Q

pupura

A

slightly larger hematomas

typically >3mm

381
Q

Ecchymoses

A

large subcutaneous hematomas
1-2 cm
typically observed following traumatic injury
aka a bruise

382
Q

what causes bruise color changes?

A

Enzymatic conversion into hemosiderin

383
Q

hemorrhagic shock

A

Rapid loss of ~20% of the blood volume

384
Q

what can chronic blood loss cause?

A

iron deficiency

anemia

385
Q

2 important functions of normal hemostasis

A

Maintains flow of blood in a fluid state under normal conditions
Cause a rapid and localized hemostatic plug vascular injury occurs

386
Q

normal hemostasis temporal sequence

A

arteriolar vasoconstriction
primary hemostasis
secondary hemostasis
anti-thrombotic events

387
Q

Arteriolar vasoconstriction in hemostasis

A

First event that takes place

Within seconds due to activation of neurogenic mechanisms and production of local mediators

388
Q

primary hemostasis

A

Formed within minutes by the deposition and activation of platelets
Occurs on extracellular matrix proteins which have been exposed at the site of injury

389
Q

secondary hemostasis

A

Platelet plug needs to stabilized and this occurs through activation of coagulation cascade which eventually culminates in local fibrin deposition

390
Q

antithrombotic events in hemostasis

A

Counter regulatory mechanism occur to keep the hemostasis localized to the site of injury by preventing uncontrolled growth and activation

391
Q

antiplatelet effects of the vascular wall

A

secrete prostacyclin and NO which are inhibitors of platelet aggregation

392
Q

anticoagulant effects of endothelial cells

A

membrane associated heparin-like molecules, thrombomodulin, and tissue factor pathway inhibitor

393
Q

fibrinolytic effects of endothelial cells

A

produce tissue type plasminogen activator (tPA) which enhances breakdown of fibrin deposits

394
Q

von Willebrand factors

A

Produced by endothelial cells and this serves as a cofactor for platelet binding to collagen

395
Q

tissue factor

A

Secreted by endothelial cells when they have been stimulated by cytokines
Activates clotting cascade

396
Q

what secretes plasminogen activator inhibitors

A

endothelial cells

397
Q

3 reactions of platelets when exposed to extracellular matrix proteins

A

adhesion
secretion
aggregation

398
Q

what is the bridge btwn platelet R and collagen in the ECM?

A

von willebrand factor

399
Q

what do platelet release during the secretion phase?

A

calcium

ADP

400
Q

role of Ca in coagulation cascade

A

activates cascade

401
Q

role of ADP in coagulation cascade

A

aggregates platelets

402
Q

role of platelet aggregation

A

serves to expand the primary hemostatic plug

403
Q

when is the coagulation cascade irreversible?

A

when the secondary plug is formed

404
Q

coagulation cascade

A

Series of enzymatic steps in which each factor serves to convert inactive pro-enzymes into active enzymes

405
Q

final product of the coagulation casde

A

formation of fibrin

406
Q

how is clotting normally regulated?

A

restricting activation of the cascade to sites of exposed phospholipids (damaged vascular wall)

407
Q

3 types of naturally occurring anticoagulants

A

antithrombins
proteins S and C
tissue factor pathway inhibitor

408
Q

antithrombins

A

Block the activity of thrombin and other coagulation factors

409
Q

what activates antithrombins

A

binding to the heparin-like molecules on endothelial cells or to heparin injected by doctors into patients

410
Q

role of proteins S and C

A

Inactivate specific coagulation factors

411
Q

Tissue factor pathway inhibitor role

A

Binds and inactivates specific coagulation factors

412
Q

thrombin role

A

cleaves fibrinogen to produce fibrin

413
Q

Plasminogen activator inhibitors role

A

decrease fibrinolysis

414
Q

tissue factor role

A

activates the clotting cascade

415
Q

Von Willebrand’s factor role

A

enhances platelet adhesion

416
Q

plasmin

A

molecule that interferes with fibrin polymerization and breaks down fibrin into fibrin split products which can be measured in the plasma as D-dimer

417
Q

plasminogen

A

inactivate circulating precursor of plasmin

418
Q

when is tPA most effective?

A

when attached to fibrin

419
Q

thrombus

A

formation of an intravascular blood clot in a location where it shouldn’t occur

420
Q

virchow’s triad

A

endothelial injury
abnormal blood flow
hypercoagulability

421
Q

what is the most important determinant of whether a thrombus will form?

A

endothelial cell injury

422
Q

what kind of blood flow predisposes thrombus formation?

A

turbulent

slow

423
Q

how is a hypercoagulable state created?

A

alteration of the complex coagulation cascade

424
Q

primary hypercoaguble states

A

due to genetic alterations → mutations or deficiencies of elements of the pathways

425
Q

Factor V Leiden Mutations

A

Results in factor Va that can’t be cleaved by protein C

426
Q

Prothrombin mutation

A

Results in increased prothrombin transcription

427
Q

secondary hypercoaguable states

A

acquired

428
Q

High risk factors of secondary hypercoaguable states

A 
Prolonged bed rest/immobilization 
MI
Atrial fibrillation 
Tissue damage
Cancer 
Prosthetic cardiac valves
Disseminated intravascular coagulation 
Heparin induced thrombocytopenia 
Antiphospholipid antibody syndrome
429
Q

low risk factors of secondary hypercoaguable states

A 
Cardiomyopathy 
Nephrotic syndrome 
Hyperestrogenic states → pregnancy
Oral contraceptive use 
Sickle cell anemia
Smoking
430
Q

arterial thrombi common locations

A

Coronary arteries
Cerebral arteries
Femoral arteries
Superimposed on atherosclerotic plaque

431
Q

where do arterial thrombi typically arise?

A

site of endothelial cell injury such as an atherosclerotic plaque

432
Q

what direction do arterial thrombi form?

A

retrograde

433
Q

lines of Zahn

A

light colored layers of platelets and fibrin alternating with darker areas of blood cells

434
Q

where are lines of Zahn?

A

arterial thrombi

435
Q

mural thrombi

A

large thrombi tightly adhered to the underlying blood vessel wall

436
Q

where are venous thrombi formed?

A

areas of blood stasis

437
Q

what direction do venous thrombi form?

A

same direction as blood flow

438
Q

how are post mortem clots differentiated from venous thrombi?

A

composition:
Soft rubbery white portion → chicken fat
Dark portion → currant jelly
Lack of vascular wall adherence

439
Q

clinical consequences of superficial thrombi

A 
localized pain and swelling
varicose veins
eczema
ulcer
rarely embolize
440
Q

Trousseau’s syndrome

A

Migratory thrombophlebitis

pancreatic cancer

441
Q

4 states of a thrombus

A

propagation
embolization
dissolution
organization and recanalization

442
Q

embolization

A

thrombus travels to other sites in the vasculature and causes acute occlusion

443
Q

goal of anticoagulant therapy

A

prevents the thrombus from forming

444
Q

goal of fibrinolytic therapy

A

attempts to dissolve an already formed thrombus

445
Q

Organization and recanalization

A

Fibrosis of the thrombus can occur in the process of organization and formation of new vascular channels may recanalize the vessel in the area of the thrombus

446
Q

Disseminated intravascular coagulation

A

Widespread formation of numerous fibrin thrombi throughout the micro-vasculature

447
Q

causes of DIC

A

obstetric complications
advanced malignancy
systemic inflammation such as sepsis

448
Q

Embolus

A

detached intravascular solid, liquid or gaseous mass carried by the blood to a site distant from its point of origin

449
Q

what are the majority of emboli?

A

thrombi which have dissolved

450
Q

what can large pulmonary emboli cause?

A

saddle embolus

sudden death

451
Q

what causes fat embolism?

A

Fractures of long bones or soft tissue trauma and burns → fat globules enter the bloodstream and embolize

452
Q

what symptoms characterizes fat emoblism?

A

pulmonary insufficiency
neurologic symptoms
anemia
thrombocytopenia

453
Q

how big does an air embolus need to be to occlude the vasculature?

A

> 100ml

454
Q

amniotic fluid embolus

A

Amniotic fluid or fetal tissue may enter the maternal circulation following a tear in the fetal membranes or rupture of the uterine veins

455
Q

infarct

A

area of ischemic necrosis secondary to occlusion of the vasculature

456
Q

what is ischemic necrosis secondary to?

A

loss of blood flow

457
Q

what characterizes infarctions?

A

coagulative necrosis

458
Q

coagulative necrosis

A

retains the normal appearance of the tissue but there is loss of nuclei and decreased cytoplasmic staining

459
Q

where do red infarcts usually occur?

A

areas of overlapping vascular supplies

460
Q

where do white/anemic infarcts usually occur?

A

end of an arteriole in a solid organ

461
Q

infectious endocarditis

A

Embolization of bacterial valvular vegetation

462
Q

Shock

A

Clinical state where there is systemic hypoperfusion

463
Q

how to determine if someone is in shock

A

measure bp

464
Q

cardiogenic shock

A

myocardial failure results in poor ability to maintain blood pressure

465
Q

hypovolemic shock

A

loss of blood or other fluids also results in dangerously decreased blood pressure

466
Q

septic shock

A

due to overwheling bacterial infections

467
Q

macule

A

fat

468
Q

papule

A

elevated <5mm

469
Q

nodule

A

elevated >5mm

470
Q

vesicle

A

fluid filled <5mm

471
Q

bulla

A

fluid filled >5mm

472
Q

acanthosis

A

diffuse epidermal hyperplasia

473
Q

hyperkaeratosis

A

hyperplasia of stratum corneum

474
Q

letinginous

A

linear melanocyte proliferation along the epidermal basal layer

475
Q

spongiosis

A

intercellular edema of the epidermis

476
Q

eczema appearance

A

Red, elevated lesions that are often oozing and crusty

small <5mm

477
Q

clinical subtypes of eczema

A 
allergic contact
atopic
drug related
light
primary irritant
478
Q

pathogenesis of eczema

A

After initial irritant, some of the patient’s inherent proteins get modified
Processed by langerhans cells in the epidermis and the self proteins are transported to the regional lymph nodes
Processing of antigens in the lymph nodes creates an immunologic memory
On re-exposure a cascade of events initiates the development of eczematous lesions

479
Q

what mediated eczema

A

sensitized T cells

480
Q

contact dermatitis

A

patterned erythema and scale stems from a nickel-induced contact dermatitis

481
Q

microscopic appearance of contact dermatitis

A

fluid accumulation (spongiosis) between epidermal cells that can progress to small vesicles if intercellular connections are stretched until broken

482
Q

psoriasis

A

Common chronic inflammatory dermatitis

483
Q

pathogenesis of psoriasis

A

Sensitized populations of T cells move to the dermis

Secrete cytokines and growth factors that induce keratinocyte hyperproliferation → lesions

484
Q

typical psoriasis lesion

A

well demarcated pink/salmon colored plaque covered by loosely adherent silver white scale

485
Q

impetigo

A

superficial skin infection

486
Q

what usually causes impetigo

A

staphylococcus aureus

487
Q

Verruca vulgaris

A

Lesion seen in children and adolescents

Caused by HPV

488
Q

how does verruca vulgaris work?

A

Interferes with cell cycle regulation → epithelial cell proliferations

489
Q

how is verruca vulgaris trnsmitted?

A

direct contact

490
Q

Pemphigus vulgaris

A

Most common blistering skin disorder

491
Q

Pemphigus vulgaris lesions

A

superficial flaccid vesicles and bullae that rupture easily

Leaves deep and extensive erosions covered with serum crust

492
Q

what causes pemphigus vulgaris?

A

antibody-mediated (type II) hypersensitivity

493
Q

Seborrheic keratosis

A

Common benign epidermal tumor

494
Q

appearance of Seborrheic keratosis

A

dark brown coin like plaques

495
Q

Seborrheic keratosis usually is found in which patients?

A

middle aged and older patients in the trunk

496
Q

Actinic keratosis

A

Squamous cell carcinoma can be preceded by a series of dysplastic changes as a result of chronic exposure to sunlight

497
Q

actinic keratosis lesion

A

Many lesions regress, but some become malignant

498
Q

actinic keratosis microscopic appearance

A

lower portions of epidermis show cytologic atypia

499
Q

Squamous cell carcinoma

A

Common tumor occuring on sun exposed areas of older patients

500
Q

Squamous cell carcinoma appearance

A

red scaling plaques

501
Q

Basal cell carcinoma involves dysregulation of ___

A

sonic hedgehog pathway

502
Q

basal cell carcinoma presntation

A

Present as pearly papules

With dilated blood vessels on surface

503
Q

rodent ulcer

A

basal cell carcinoma ulcerates and invades adjacent skin, bone, other structures

504
Q

Dysplastic nevi

A

nevi that demonstrate atypical features that can transform into melanoma

505
Q

Malignant melanoma

A

deadly disease that often develops in sun exposed skin

506
Q

malignant melanoma mutations

A

Germline mutation in CDKN2A gene
Somatic mutations of the proto-oncogene BRAF or NRAS
Loss of function of the tumor suppressor PTEN gene

507
Q

2 patterns of growth of malignant melanomas

A

radial

vertical

508
Q

ABC’s of melanoma

A 
A → asymmetry 
B → border 
Irregular
C → color changes
D → diameter changes
E → evolution
509
Q

osteoporosis

A

Acquired condition characterized by reduced bone mass → bone fragility and susceptibility to fractures

510
Q

Postmenopausal osteoporosis

A

Trabecular bone loss is often severe → compression fractures and collapse of vertebral bodies

511
Q

Senile osteoporosis

A

Cortical bone loss is prominent

Predisposes to fractures in weight bearing bones

512
Q

most common bone tumor

A

osteosarcoma

513
Q

Osteoma

A

benign bone tumor that appears during teenage years

514
Q

Osteoarthritis

A

Most common disorder affecting joints in older adults

Degeneration of joint cartilage

515
Q

pathogenesis of osteoarthritis

A

alteration in articular cartilage due to wear and tear and mechanical stress

516
Q

Rheumatoid arthritis

A

Autoimmune disease involving complex interactions of genetic risk factors, environment, and the immune system

517
Q

what causes the pathologic changes in RA?

A

cytokine mediated inflammation from CD4 T cells

518
Q

rheumatoid factor

A

antibodies to citrullinated fibrinogen, type II collagen, α-enolase, and vimentin are the most important and may form immune complexes that deposit in the joints

519
Q

what are Tenosynovial giant cell tumor associated with?

A

acquired translocation

520
Q

lipomas

A

benign tumors of fat

521
Q

Liposarcomas

A

malignant neoplasms with adipocyte differentiation

522
Q

Fibromatosis

A

Tumor with an infiltrative pattern of growth
Prone to recur locally
Don’t metastasize

523
Q

Fibrosarcoma

A

Malignant tumors of the fibroblasts

524
Q

what is the pattern of growth of fibrosarcomas?

A

herringbone pattern of growth

525
Q

Rhabdomyosarcoma

A

Malignant tumors of skeletal muscle

MAMS (8 decks)

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