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Pathology Sp 16 > Exam 2 Diseases > Flashcards

Exam 2 Diseases Flashcards

1
Q

What is pulmonary edema? where does it start then proceeds to

A

Pulmonary edema: fluid accumulation in lungs

starts in interstitial tissues then proceeds to fill up distal air spaces

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2
Q

Causes of pulmonary edema

A

INC intravascular pressure (CHF)
hypoproteinemia
vascular damage from infections, autoimmune disease

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3
Q

what are the problems with pulmonary edema

A

inhibits normal O2 exchange

predisposes pt to infection

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4
Q

what is the main cause of a pulmonary thromboemboli?

Describe the problems that arise from a small, large, and very large emboli

A

main cause: deep veins of legs or pelvic veins
small emboli: may cause minimal damage
large emboli: causes hemorrhage or infarction
very large emboli lodge at the bifurcation of pulmonary arteries can cause sudden death

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5
Q

what are the predisposing factors to Thrombo emboli

A

chronic illness, prolonged bed rest (immobility), hypercoagulable state (factor V leidin) and deep vein thromboses (DVTS)

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6
Q

what are obstructive pulmonary diseases

A

group of diseases that results in airflow limitation or obstruction

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7
Q

4 disorders of obstructive pulmonary diseases

A

emphysema, chronic bronchitis, bronchiectasis, and asthma

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8
Q

what is COPD

A

emphysema and chronic bronchitis combined

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9
Q

what does emphysema result in

A

alveolar wall destruction and overinflation, alveolar parenchymal destruction,

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10
Q

what does chronic bronchitis result in

A

productive cough and airway inflammation

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11
Q

what does asthma result in?

is asthma a reversible or irreversible obstruction

A 
asthma= bronchial hyperresponsiveness triggered by allergens, infections, etc
Asthma= reversible obstruction
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12
Q

what is emphysema?
major cause?
genetic causes?

A

emphysema is a permanent enlargement of the distal small air spaces due to destruction of alveolar septal walls
major cause- smoking
genetic causes: TGF B1 polymorphisms and a1 antitrypsin deficiency

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13
Q

clinical aspects of emphysema

path:

A

Emphysema: dyspnea, cough, prolonged exhalation= pink puffers
path: imbalance between protease and ant protease enzymes

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14
Q

What is centriacinar emphysema

A

centriacinar: involves the central portion of the acini usually affects upper lobes most often related to smoking

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15
Q

what is panacean emphysema:?

A

paracinar: involves entire acini unit from respiratory bronchioles to terminal alveoli usually affects lower lobes and seen in pts with a1 AT deficiency

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16
Q

What says a pt has chronic bronchitis

A

pt has cough + sputum production in 3 consecutive months in 2 consecutive years

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17
Q

what may pts w chronic bronchitis have

A

may have hypoxemia and cyanosis aka BLUE Bloaters

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18
Q

Chronic bronchitis
pathogenesis:
pathology:

A

pathogenesis: chronic irritation (smoking) and infections
path: INC mucus gland layer, chronic inflammation, fibrosis, and narrowing of airways. Edema, seromucous gland hypertrophy and excessive secretions

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19
Q

Chronic bronchitis and emphysema predisposing factor smoking: what does smoking cause in lungs?

A

smoking! causes mucus gland hypertrophy, INC smooth m tone, inhibits cilia, inhibits phagocytosis, induces squamous metaplasia

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20
Q

Chronic bronchitis and emphysema predisposing factors

A

smoking, atmosphere pollutants, infections, genetic factors= CF and a1 AT deficiency

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21
Q

what is bronchiectasis

A

bronchiectasis is chronic infection w permanent major airway dilation secondary to obstruction infection or both

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22
Q

clinical aspects of bronchiectasis:

complications of bronchiectasis

A

clinical: severe cough, bloody mucoid expectoration, dyspnea
complications: abscess, pneumonia, bronchopleural fistula and empyema

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23
Q

predisposing factors to bronchiectasis

A

obstructive tumors, foreign bodies, cystic fibrosis (mucus plugs), other COPD, CF: supportive or necrotizing pneumonia

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24
Q

pathology of bronchiectasis

A

dilated distal bronchi and bronchioles, chronic infection w inflammation and variable purulence

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25
Q

what is asthma?

what does asthma lead to

A

asthma: INC irritability and prominence of smooth m in bronchi and bronchioles
asthma leads to marked reversible episodes of contraction and airway constriction

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26
Q

what are the initiating factors of asthma

what percentage of adults? children? and where is it

A

allergies, infections, exercise, drugs, emotions

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27
Q

Clinical symptoms of asthma

A

asthma: wheezing, long exhalation, hyperinflation of lungs

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28
Q

Two types of asthma and describe each type

A

Atopic asthma: allergic, extrinsic, type 1 hypersensitivity (IgE), environmental antigen and family history is common
Non atopic= intrinsic, may be initiated by viruses, air pollutants

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29
Q

What can atopic and non atopic asthma both be triggered by

A

emotional stress, exercise, cold temps

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30
Q

Asthma pathology

A

Asthma - INC mucus glands, smooth m hypertrophy w inflammation w eosinophils and type 2 helper T cells

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31
Q

Pathogenesis of Asthma:

A

Antigen binds to surface of IgE on mast cells releasing a large number of mediators including histamine and leukotrienes

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32
Q

Treatment of asthma

A

attack may subside spontaneously if not: inhalation bronchodilators for immediate relief (albuterol) and controller medications (corticosteroids)

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33
Q

What is a leading cause of death and often complicates other chronic debilitating diseases? w
what can it be caused by

A

Pneuomia: can be caused by any organism: bacterial, viral, fungal, parasites

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34
Q

Predisposing factors to bacterial pneumonia

A

loss of cough reflex, injury to cilia, DEC phagocytosis, pulmonary edema, immunocompromised condition

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35
Q

Clinical aspects of Bacterial pneumonia

A

Clinically bacterial pneumonia leads to cough dyspnea, fever, chills, and sputum production

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36
Q

what is bronchopneumonia? what organism?

occurs in who?

A

Bacterial!

bronchopneumonia: patchy process, begins around the small bronchi common in very young and old

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37
Q

what is lobar pneumonia? what organism

occurs in who?

A

bacterial! occurs in healthy adults

lobar pneumonia: involves an entire lobe= 90% Streptococcus pneumonia

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38
Q

patchy areas of consolidation is what

A

bronchopneumonia

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39
Q

describe the stages of inflammation in lobar pneumonia

A
  1. congestion.
  2. red hepatization
  3. gray hepatization
  4. resolution
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40
Q

Complications of pneumonia

A

emphyema, abscess, pericarditis, bacteremia

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41
Q

What is seen with mycoplasma pneumonia and viruses

A

Atypical Interstitial Pneumonia

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42
Q

What is clinically seen with atypical interstitial pneumonia

A

highly variable, mild fever to headache, dry cough, myalgia to life threatening

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43
Q

Pathology of Atypical (interstitial) Pneumonia

A

interstitial inflammation, mononuclear cells, congestion, hyaline membranes (diffuse alveolar damage)

44
Q

What is Acute Respiratory Distress?

what causes ARDS

A

ARDS is a rapidly developing serious condition with some histologic features as interstitial pneumonia
ARDS causes by shock, infections, trauma, Drug OD, irritants, etc

45
Q

What does ARDS cause

A

ARDS= injury to endothelium and alveolar epithelium and INC endothelial permeability = leaky!

46
Q

what is the mortality rate of ARDS

A

30%!!

47
Q

What are the clinical symptoms of a pulmonary abscess?

whats the course of a PA?

A

Pulmonary abscess clinically: cough, fever, purulent sputum

course: scar. cavitation, progressive enlargement

48
Q

what are the predisposing factors to a pulmonary abscess

A

PA disposing factors = bronchiectasis, aspiration, septic emboli, airway obstruction, dental sepsis

49
Q

What is caused by Mycobacterium Tuberculosis? How much of the world is infected by this?

A

M Tuberculosis = TUBERCULOSIS

infects 1/3 of the world!

50
Q

what is the most common cause of death from an infectious disease? how many deaths per year?

A

Tuberculosis= 3 million deaths per year

51
Q

What has been the trend of TB in the US?

What causes an INC in TB infection?

A

US: mid 80s TB cases slowly rose but have been declining since late 90s
HIV, overcrowding, poor living conditions and immigrants INC risk of TB infection

52
Q

Describe the bio of Mycobacterium Tuberculosis.

whats the classic result of TB

A

M TB= bacillus rod, aerobe, non motile, slow growing w a waxy coat that resists acid destaining = acid fast bacillus = AFB
result of TB= caveating granulomatous inflammation

53
Q

TB pathogenesis: what is at the site of an early TB infection, how is it acquired

A

acquired by inhalation
Ghon lesion= site of early infection
Ghon complex - lung lesion + hilar lymph nodes

54
Q

what is Cavitary TB

A

Cavitary TB is TB at the apex of the lungs that results in significant scarring, may seed the large airways, lymph nodes, or blood and lead to an effusion (direct extension to the pleura)

55
Q

What does reactivation of TB lead to?

What is TB called that widely disseminates and what might happen with this TB

A

Reactivation of TB induces Type 4 hypersensitivity and tissue necrosis
widely disseminated TB = miliary TB can lead to multi organ involvement

56
Q

What does Miliary TB result from? what is the name for what causes Miliary TB?

A

Miliary TB results from spread via lymphatics or blood

caused by Millet seeds

57
Q

What can cause Granulomatous lung disease

A

TB, fungal infections like histoplasmosis, and sarcoidosis

58
Q

What is the leading cause of cancer deaths? what are the risk factors for this cancer

A

LUNG cancer= leading cancer killer!

risk factors= smoking, asbestos, radon, nickel, chromates, pollutants, lung scar

59
Q

Clinical symptoms of Lung Cancer? What may lung cancer tumors do?

A

Clinical of lung cancer: cough, weight loss, chest pain, hemoptysis
Lung cancers may produce hormones like ADH, ACTH, PTH, etc

60
Q

what is the 5 year survival for lung cancer?

if localized?

A

all types = 16%

if localized = 45%

61
Q

What are Pneumoconioses?

what size particle inhalation is the most dangerous and why

A

Pneumoconioses are a group of lung disorders caused by inhalation of dusts/ particles
particle size, shape, concentration all important
particles 1-5 micrometers most dangerous bc they lead to fibrosis scarring

62
Q

what is the most prevalent form of occupational disease?

A

Silicosis

63
Q

Autosomal dominant disorders: expression can be identified in all affected persons but to differing extents, what is this called

A

variable expressivity

64
Q

What is a AD disease that is relatively common and has highly variable expressivity but shows a nearly 100% penetrance (everyone shows it who has it)

A

Neurofibromatosis

65
Q

Age of onset is often early in life with these disorders, complete penetrance is common and many of the disorders conditions are enzyme defects leading to metabolic dysfunction

A

Autosomal Recessive Disorders: heterzygous pts typically have reduced but adequate levels of normal functional enzyme

66
Q

what sex chromosomes carries all sex linked disorders?

what does the other chromosome have?

A

X chromosome = all sex linked disorders!

Y chromosome has SRY gene and 1 trait for hairy ears. Y = no diseases

67
Q

What does unfavorable lyonization do to a female

A

results in X linked disease expression in a heterozygous female

68
Q

what is a AD disorder that is a mutation of the FBN1 gene resulting in abnormal fibrillin?
what is its prevalence

A

Marfan syndrome= abnormal elastic production due to FBN1 mutation
occurs 1/5000 people= Abe Lincoln

69
Q

What does Marfan syndrome result in?

A

tall thin body, abnormally long legs, arachnodactyly, dislocation of eyes, aortic aneurysm and dissection leading to heart failure and aortic rupture

70
Q

what is a disorder w dominant and recessive forms that results in problem with collagen synthesis

A

Ehlers Danlos Syndrome

71
Q

What are two diseases caused by mutations in genes encoding receptor proteins or channels? name the protein or channel for both

A

Familial Hypercholesterolemia: LDL receptor

Cystic Fibrosis: chloride channel protein

72
Q

what is a common AD inherited disorder that results from mutation of the gene that encodes the LDL receptor?
what is its frequency?
what does it result in?

A

Familial Hypercholesterolemia
1 in 500 people
results in impaired metabolism and INC LDL cholesterol in plasma

73
Q

What an Familial Hypercholesterolemia cause (2)?
Describe the difference in LDL levels between heterozygotes and homozygote
what drug is used for TX

A

multiple xanthomas of the skin and premature atherosclerosis
hetero= 2-3x INC LDL
homo- 5X INC LDL, often die by MI by age of 20
lomitapid

74
Q

what are 3 diseases caused by mutations in enzyme proteins

A

Phenylketonuria, Galactosemia, and Lysosomal storage disease

75
Q

What is an AR disorder that leads to hyperphenylalaninemia and PKU eventually causing mental retardation by 6 months of age?
what do affected pts lack?
prevalence

A

Phenylketonuria
1:10,000 caucasians
Lack of phenylalanine hydroxylase

76
Q

what do storage diseases lead to?

What is a frequent involvement of storage diseases that leads to what?

A

Storage diseases lead to accumulation of large, insoluble molecules (sphingolipids, mucopolysaccharides) in macrophages which leads to hepatosplenomegaly
frequent involvement w CNS leading to neuronal damage, retardation and early death

77
Q

name the 4 lysosomal storage diseases

A

Tay sachs
Niemman Pick
Gaucher
Mucopolysaccharidoses

78
Q

Mucopolysaccharide storage disease is inherited how>
due to what?
affected Pts have what

A

AR! Mucopolysaccharide storage disease
Due to lack of enzyme to degrade mucopolysaccharides
affected pts have coarse facial features, clouding of cornea, joint stiffness and mental retardation

79
Q

what is AR, caused by deficiency of Alpha L iduronidase w a life expectancy of 6-10 years?
how is it treated

A

HURLER DISEASE = deficient alpha L iduronidase

tx: bone marrow transplant or enzyme for 300 k per year

80
Q

what is an X linked disorder with a deficiency of L iduronate sulfatase

A

Hunter syndrome- no corneal clouding and a milder clinical course otherwise similar to Hurler syndrome

81
Q

What can down syndrome cause

A

Mental retardation, epicanthic folds, flat facial profile, cardiac malformations, INC susceptibility to infection. LARGE TONGUE, INC risk for acute leukemia

82
Q

what is Klinefelter syndrome:

A

male hypogonadism when there are at least 2 X chromosomes and 1 or more & chromosome - most are 47 XXY

83
Q

what is turner syndrome

A

partial or complete absence of one of the X chromosomes = 45X

84
Q

what does Klinefelter syndrome result in

A

Phenotypically = male
INC length of lower limb, reduced body hair, gynecomastia, hypogonadism, usually male sterility
Dentally: INC freq of TAURODONTISM

85
Q

Turner syndrome results in what?

A

short stature, webbing of neck, low posterior hairline, shield like chest, high arched palate, congenital cardio malformations, failure to develop secondary sex characteristics, primary amenorrhea

86
Q

What is a distinctive cell of Hodgkin lymphoma?

What is hodgkins tx with

A

Hodgkins= reed sternberg cell

tx with chemo and radiotherapy is highly curable

87
Q

what is specific to Hodgkin lymphoma about its distribution amongst the population

A

Hodgkin Lymphoma is bimodal age distribution 20-30 y/os and greater than 50 y/os

88
Q

these two things characterize Hodgkins lymphoma

A

painless lymphadenopathy and splenomegaly

89
Q

describe the reed sternberg cell

what percentage of lymph node cells are RS cells? whats the origin of RS cells? what is often present in RS cell?

A

reed sternberg cell is a large cell with mirror image nuclei and prominent nuclei, compromises about 2% of cells in involved lymph node, Germinal center B lymphocyte origin and Epstein Barr Virus is present is 70% of RS cells

90
Q

describe low stage Hodgkins and tx

describe high stage hodgkins and tx

A

low stage: localized= chemo and radiation

high stage: wide spread disease w distant or bone marrow involvement= chemo

91
Q

with hodgkins what are B signs/ symptoms? what are they associated with

A

B signs/ symptoms= fever, night sweats, unexplained weight loss
B signs= worse prognosis, most often with stage 3 and 4 disease

92
Q

what is tx of Hodgkins associated with?

A

Hodgkins tx puts pt at low risk of development of secondary tx related acute leukemia

93
Q

what is NON hodgkin lymphoma, percent that are of B cell origin? when does incidence INC?

A

Non hodgkin lymphoma is neoplastic lymphocytes originating in lymph nodes or extranodal lymphoid tissue. 85% are of B Cell origin (rest T cell), Incidence rises steadily after age 40

94
Q

Clinical aspects of NON hodgkin lymphoma

A

painless lymph node enlargement, systemic symptoms in 30% of pts, immune abnormalities, splenomegaly, may involve GI tract, bones, CNS

95
Q

Non Hodgkins lymphoma what is better: nodular or diffuse, small or large

A

Nodular better than diffuse

Small cell better than large

96
Q

with Non Hodgkins lymphoma what is an exception to the normal prognosis rule

A

with NHL you use grading (sub typing) instead of staging which is normally used in prognosis

97
Q

describe the differences between acute and chronic leukemias

A

acute: rapid onset, survival may be months, mostly circulating blasts, INC WBC and INC blasts in bone marrow
chronic: slow indolent onset, survival years/ decades, mostly mature forms INC WBC, and normal blasts in bone marrow

98
Q

what is the most frequent cancer in those 15 and younger with INC WBC and thrombocytopenia. What may these pts have?
what pts have good prognosis? what pts have bad prognosis?

A

Acute Lymphoblastic Leukemia, pts may have lymphadenopathy and splenomegaly
children have good prognosis
adults have bad prognosis

99
Q

what leukemia is more common in adults with INC WBC count often accompanied by anemia and thrombocytopenia? what is it a clonal proliferation of

A

Acute Myelogenous Leukemia= clonal proliferation of primitive myeloid cell

100
Q

what is present in the cytoplasm of acute myelogenus leukemia?
tx of it? what percent of patients have remission but many relapse

A

Acute Myelogenous Leukemia= myeloperoxidase present in the cytoplasm . tx w chemo, 70% of pts have remission but many relapse

101
Q

what is the most common adult leukemia that expresses surface IgM with kappa light chain restriction? what doe this leukemia expression? who does this favor?

A

Chronic lymphocytic leukemia- clonal proliferation of Mature b lymphocytes identical to small lymphocytic lymphoma.
High expression of BCL2
favors males. adults over 60

102
Q

what does chronic lymphocytic leukemia present with? what develops as it progresses. what does its tumor cells do and cause?

A

chronic lymphocytic leukemia presents with splenomegaly and lymphadenopathy,
leads to anemia and thrombocytopenia
Its tumor cells suppress normal B cells leading to HYPOgammaglobulinemia

103
Q

What is a stem cell disorder of clonal proliferation of immature granulocytes?
Leads to INC In what?
Presents with what?

A

Chronic myelogenous leukemia- profil of granulocytes may have thrombocytosis and anemia and splenomegaly

104
Q

chronic myelogenous leukemia is a cytogentic abnormality of what?
mutation of what genes?
chemo targets what?

A

Chronic myelogenous leukemia= philadelphia chromosome
fusion of BCR and ABL genes
chemo targets blockage of bcr-abl tyrosine kinase

105
Q

what is a clonal proliferation of monoclonal plasma cells leading to monoclonal heavy and light chain production with IgG being most common

A

Multiple Myeloma- disease of late middle age to elderly

106
Q

what are the lab/ clinical findings of multiple myeloma

A 
lytic bones lesions, hypercalcemia
bone marrow infiltration by plasma cells
INC serum monoclonal protein
Bence Jones proteinuria
Renal failure
infections
107
Q

Blood and marrow findings of multiple myeloma

A

circulating plasma cells in blood are uncommon.
RBC show stacking (ROULEAUX formation)
marrow plasma cell infiltrates in single cells and sheets

Pathology Sp 16 (7 decks)

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