Midterm 1 Flashcards
(292 cards)
1
Q
Anatomic (surgical) pathologist vs. Clinical pathologist
A
Based on type of sample that they examine
Anatomic - diagnose based on examination of tissues
Clinical - tend to look at body fluids
2
Q
Etiology
A
the underlying cause of the disease
3
Q
Idiopathic
A
no known etiology
4
Q
Morphology
A
the physical appearance of the disease
5
Q
Gross morphology
A
the appearance to the eye
6
Q
Natural history
A
how the disease progresses with time
7
Q
Sequelea
A
complications associated with the disesase
8
Q
Prevalence vs Incidence
A
Prevalence - total number of cases of that disease within a certain population
Incidence - the number of new cases of that disease within a particular time period (usually one year)
9
Q
Mortality
A
the likelihood of death of an individual with that disease
10
Q
Morbidity
A
the extent to which that disease affects the overall health of an individual
11
Q
Syndrome
A
A disease characterized by the presence of a set of symptoms, signs, and/or lab features that are all related to a particular cause
12
Q
What is the mnemonic for classification of disease?
A
VINDICATED Vascular Inflammatory Neoplastic Deficiency/degenerative Iatrogenic Congenital Autoimmunue/allergic Trauma Endocrine Drug Related
13
Q
Iatrogenic
A
diseases that are due to results of treatment
14
Q
Congenital
A
disease present from birth.
15
Q
Parenchymal vs Stromal tissue
A
Parenchymal - performs function of tissue
Stromal - supportive function
16
Q
What are the 4 types of tissues?
A
Connective - “connects” (hold in place, integrates) organs & systems *includes blood
Epithelial - covers or lines various body parts to protect the body and also is important for absorption, transportation, and secretion
Muscle - capable of contracting and generating tension in response to
stimulation; produces movement
Nervous - capable of sending and receiving impulses through
electrochemical signals; Controls movement etc.
17
Q
Hypertrophy
A
increase in the size of tissue or organ due to increased size of the individual cells
18
Q
Pathologic hypertrophy example
A
cardiac muscle cells enlarge in response to increased pressure in the systemic
circulation (hypertension)
19
Q
Hyperplasia
A
an increase in the size of tissues or organ due to increase in number of cells
20
Q
Pathologic hyperplasia example
A
endometrial hyperplasia is increased number of cells lining endometrial (uterus) cavity
21
Q
Atrophy
A
decrease in size of tissue or organ due to a decrease in number and/or size of cells
22
Q
Pathological atrophy example
A
muscle denervation causes atrophy of skeletal muscle supplied by that nerve
23
Q
Metaplasia
A
a change of one cell type into another cell type
24
Q
Metaplasia example
A
chronic smoking, simple columnar bronchial epithelium squamous epithelium
25
Dystrophic calcification
deposition of calcium in damaged tissue (eg. Atherosclerosis)
26
Metastatic calcification
deposition of calcium in normal tissue when there is hypercalcemia
27
Dysplasia
the presence of cells of an abnormal type within a tissue
28
What are the signs of necrosis in liver (liver damage/hepatitis)?
Liver contains enzymes that are released if cells are injured e.g. Aspartate aminotransferase (AST); Alanine aminotransferase (ALT)
29
What are the signs of necrosis in heart (heart damage/myocardial infarct)?
cardiac myocytes contain proteins that are released if cells are injured e.g. Troponin
30
Coagulative necrosis
– morphologic appearance of boiled meat (coagulated protein)
– most common form of necrosis; due to inactivation of hydrolytic enzymes
– solid internal organs (kidney, liver)
31
Liquefactive necrosis
– necrosis characterized by dissolution of tissue
| – necrotic area is soft and filled with fluid (Brain infarct)
32
Caseous necrosis
– necrotic tissue with appearance of cheese
| – form of coagulative necrosis with limited liquefaction; seen in TB
33
Fat necrosis
– necrosis of fat due to action of enzymes followed by formation of complexes with
calcium; white chalky areas form (especially around pancreas)
34
Fate of necrosis vs. Fate of apoptosis
Necrosis causes an inflammatory reaction, apoptosis does not
35
What are the 5 clinical signs of acute inflammation?
* heat - because of vasodilation
* redness - because of increased blood flow
* edema - inflammation causes vessels to become leaky and allow neutrophils etc to flow
* pain - due to bradykinins
* loss of function
36
What are the events in acute inflammation
• Change in size of caliber of blood vessels
- transient vasoconstriction
- vasodilation (heat, redness)
• Increased vascular permeability
- edema formation
• White blood cells enter site of injury
- kill organisms, mop up debris
37
What are the substances that mediate inflammation?
* Histamine
* Bradykinin
* Complement system
* Arachidonic acid (AA) derivatives
38
What is the source and role of histamine in inflammation?
* increases vessel permeability
| * released by mast cells
39
What is the source and role of bradykinin in inflammation?
* increases vessel permeability
* causes pain
* derived from a plasma protein
40
Transudate vs. exudate
Transudate - fluid pushed through the capillary due to high pressure within the capillary; protein poor fluid containing few cells that forms due to a disturbance in forces across vessels walls
Exudate - fluid that leaks around the cells of the capillaries caused by inflammation; protein rich fluid containing white blood cells
that forms due to inflammation
41
Role of complete blood count in inflammation
to count number of white blood cells (involved in diff responses); e.g. increased neutrophils if inflammation — don’t need to draw blood from the specific location, can draw blood from somewhere else
42
Role and results of examining C-reactive protein (CRP) in inflammation
test does not tell you what is cause, just tells you that there is inflammation
43
What is the complement system?
```
• group of plasma proteins that act to help kill bacteria
• mediate inflammation
• 3 methods of activation
- classical pathway
- alternate pathway
- Lectin pathway
```
44
What are Arachidonic acid (AA) derivatives?
• AA is formed from phospholipids in cell wall
• AA is metabolized to form various substances including leukotrienes,
prostaglandins, prostacyclin and thromboxane each of which affects inflammation
45
What are the cellular components of inflammation?
* Neutrophil (PMN)
* Eosinophils
* Basophils/mast cells
* Macrophages
* Lymphocytes/ Plasma cells
46
What is the role of neutrophils in inflammation?
* first cells to enter site of injury (very mobile)
* able to kill bacteria and engulf material (phagocytosis)
* produce chemicals to attract other cells
* short lived
47
What is the role of eosinophils in inflammation?
* mobile, kill bacteria
* involved in allergic reactions, parasitic infections
* longer lived, present in chronic inflammation
48
What is the role of Basophils/Mast cells in inflammation?
* release histamine
| * basophils when in blood, mast cells when in tissue
49
What is the role of macrophages in inflammation?
* major phagocytes, enter site 3-4 days after injury
| * present in chronic inflammation
50
What is the role of Lymphocytes/Plasma cells in inflammation?
* immune function in chronic inflammation
| * release antibodies
51
What is purulent inflammation (pus)?
Dead neutrophils; inflammatory exudate rich in PMNs usually due to bacterial infection
52
What types of inflammatory exudates are there?
* Serous inflammation
* Fibrinous inflammation
* Purulent inflammation (pus)
53
What is fibrinous inflammation?
• inflammation characterized by exudate rich in fibrin
54
What is serous inflammation?
• inflammation characterized by exudation of clear fluid with few cells
55
What is ulcerative inflammation?
Specific term used to describe acute inflammation:
| • inflammation characterized by loss of an epithelial lining due to the inflammation (ulceration)
56
What is pseudomembranous inflammation?
Specific term used to describe acute inflammation:
• inflammation characterized by ulceration and a fibrinopurulent exudate that forms a
pseudomembrane over the ulcer
57
What are the outcomes of acute inflammation?
There are 4 possible outcomes to acute inflammation:
• Complete resolution - regeneration of cells and restoration of normal function with no residual deficit [ideal outcome]
• Abscess formation - wall off the inflammatory focus within capsule; localized collection of pus
• Healing by fibrosis and scar formation - replacement of usual tissue with fibrous tissue
• Progression to chronic inflammation
58
What is chronic inflammation cell exudate?
lymphocytes, plasma cells and macrophages
59
What is granulomatous inflammation (and granulomas)?
• a specialized form of chronic inflammation
characterized by the formation of granulomas
Granuloma - accumulation of chronic inflammatory cells (lymphocytes, macrophages)
arranged in discrete nodules or aggregates (+/- multi-nucleated giant cells)
60
What is an example of caseating granulomas?
Tuberculosis
61
What is an example of non-caseating granulomas?
Sarcoidosis
62
How do skin wounds heal?
by filling in the defect with granulation tissue and then replacing the
granulation tissue with stronger fibrous tissue; with time the wound contracts due to the contraction of myofibroblasts
63
Describe wound healing by first intention
* the name given to the healing that occurs after a surgical incision
* scab formation, PMN enter and scavenge debris
* formation of granulation tissue
* resorption of granulation tissue and replacement by fibrous scar
64
Describe wound healing by second intention
* gaping wound that is either not closed surgically or can not be closed surgically
* granulation tissue forms and is gradually replaced with fibrous tissue
* with time the wound contracts however the overlying tissue is never the same
65
When do you not want to close a wound?
- Infection
| - Human bites
66
What is the distribution of causes for developmental malformations?
```
– none identified (75%)
– genetic (20%)
– chromosomal (2%)
– infection (2%)
– chemical (1%)
```
67
What are some non-lethal examples of defective growth control genes?
• cleft lip and palate
– multi-factorial inheritance
• achondroplastic dwarfism
– autosomal dominant inheritance
68
What are thalidomide and isotretinoin?
Chemical teratogens (morning sickness and primarily used to treat severe acne)
69
Examples of infectious teratogens
(TORCH)
• Toxoplasmosis (parasite)
– brain microcalcifications, hydrocephaly, skin lesions
• Other (syphilis, listeria, )
• Rubella (German measles virus) (Fig. 5-4)
– microcephaly, congenital heart disease, micropthalmia
– 1st trimester exposure, unimmunized mother
• Cytomegalovirus
– brain microcalcifications, hydrocephaly
– skin lesions
• Herpes simplex virus
70
Aneuploidy
General term for an abnormal number of chromosomes (loss/gain)
71
Monosomy
Loss of a chromosome
Autosomal monosomies = fatal
```
Y only (YO) is fatal
X only (XO) is not fatal (Turner’s syndrome)
```
72
Trisomy
The presence of an extra copy of a chromosome
Autosomal trisomies are not necessarily fatal (e.g. 21, 13, 18)
Additional sex chromosomes are not fatal
73
Down’s syndrome
Trisomy 21
1/800 (most common chromosomal disorder)
True trisomy 21 in 95% of cases
- usually maternal chromosome, increased likelihood with age
Specific typical features
Significant morbidity, increased mortality
74
Turner’s syndrome
```
Monosomy X (XO)
1/3000
Female phenotype
Specific features
Infertile
```
75
Klinefelter’s syndrome
```
Trisomy X (XXY)
1/700
Typical features (Fig. 5-11)
Male phenotype
Infertile (atrophic testes)
```
76
P 11 WAGR
Structural chromosomal abnormality
(Wilma, Aniridia, Genintal malformation, Mental Retardation)
Loss in short arm of chromosome 11
77
q 13 Retinoblastoma
Loss in long arm of chromosome 13
| Causes tumours in retina due to deletion of prevention gene
78
Some Down’s - Translocation
T 21/14
| Extra copy of chromosome 21 due to translocation, not a complete extra chromosome
79
Single gene disorder
Disorder due to defect in particular gene
| Demonstrate patterns of inheritance (Mendelian Patterns)
80
Exceptions to rules of Autosomal dominant disorders
Variable penetrance - % of individuals with gene who express it
Variable expressivity - degree of expression in individual with gene
81
Marfan’s syndrome
Autosomal dominant disorder
1/10 000
Defect in fibrillin gene (structural protein)
Characteristic phenotype (skeletal abnormalities - tall, thin, loose joints; cardiovascular abnormalities - aortic aneurysms, dissections, valves; ocular abnormalities - dislocation of lens, retinal detachment)
Life expectancy shortened
- Death usually to aortic dissection
82
Familial hypercholesterolemia
Autosomal dominant disorder
1/800
Defect in LDL Receptor gene
- insufficient cholesterol removal
Cholesterol deposits in tissue
- premature atherosclerosis, xanthomas in soft tissues and skin
Homozygous have higher LDL than heterozygotes
- develop ischemic heart disease before age 20
83
Cystic fibrosis
```
Autosomal recessive disorder
1/2500
Carrier rate = 1/25
Defect in chloride transport gene
Thick exocrine secretions (obstruction of ducts and infections)
Chloride sweat test to help diagnose
```
84
Lysosomal storage diseases
Autosomal recessive disease
Group of diseases due to defects in different enzymes
Different disease depending on which enzyme disease is defective
Accumulation of materials in lysosomes
E.g. Tay-Sachs, Gaucherie Disease
85
Tay-Sachs
Autosomal recessive - lysosomal storage disease
Defective hexosaminidase
Brain changes, eye changes, 3-5 year life expectancy
86
Gaucher disease
Autosomal recessive - lysosomal storage disease
Defective glucocerebrosidase
Enlarged spleen, anemia, normal life expectancy (type 1)
87
Phenylketonuria (PKU)
Autosomal recessive
Ashkanzi jews
Defective phenylalanine hydrogenase gene
Converts PheA—Tyr
Accumulation of PheA and decreased Tyr result in psychoneural changes
Prevention - heel prick to ID, PheA deficient diet
88
Hemophilia
X linked recessive disorder
Defect in genes coding coagulation proteins
Type A - Factor VIII gene
Type B - Factor IX gene
Bleeding - joint spaces and minor traumas
Secondary complications
Treatment - factor replacement
89
Muscular dystrophy
X-linked recessive disorder
Defective dystrophin protein - attachment of cytoskeleton, weakened cell structure esp. in skeletal muscle
Duchenne = severe, wasting starts early
Becker’s= less severe, later onset
90
Fragile X syndrome
X-linked, non-classic inheritance
A portion of the X chromosome is “fragile” - due to CGG triplet repeats, increased number with each generation, once reached a certain number of repeats get expression
Features - mental retardation, enlarged testes
May not follow Mendelian patterns - pre-mutation is individual who does not have critical number of repeats, increased expression in subsequent generations
91
Dysraphia
Multifactorial inheritance disorder
Incomplete fusion of midline structures, spectrum of abnormalities
E.g. anencephaly, spina bifida, meningocele - each relates to where in the neural tube it had failed to fuse
If one child affected, increased risk
Folate during pregnancy helps decrease risk
92
Anencephaly
Multifactorial inheritance - dysraphia
| Complete absence of brain
93
Spina bifida
Multifactorial inheritance - dysraphia
| Defect in vertebral bones
94
Meningocele
Multifactorial inheritance - dysraphia
| Defect in vertebra, meninges
95
Diabetes Mellitus Type 2
Multifactorial inheritance disorder
| Environmental and genetic components
96
Prenatal diagnosis techniques
Ultrasound = malformation ID
Chorionic villus sampling = biopsy of placental villus, fetal cell for analysis (chromosomal, molecular techniques)
Amniotic fluid
Maternal blood = triple screen
97
IUGR
Underweight baby - Birth weight less than 3200g
98
Causes of premature birth
Maternal - malnutrition, smoking, SA
Fetal - genetics
Placental - insufficiency
99
Neonatal respiratory distress syndrome
Acquired neonatal syndrome
Increasing shortness of breath, usually preterm
Pathophysiology - inadequate surfactant in lungs to decrease surface tension of alveoli, atelectacis (alveolar collapse), hyaline membranes form
Periventricular brain hemorrhage
Long term respiratory difficulties
Can assess levels of surfactant in amniotic fluid before birth
Treatment - corticosteroids before birth
100
Birth injury
```
Acquired neonatal syndrome
Mechanical trauma during delivery
Malposition, large baby
Skull fracture
Intracranial hemorrhage
Etc
```
101
Sudden infant death syndrome
Acquired neonatal syndrome
Sudden, unexpected death
Not understood
Maternal factors - young, low SES, smoking, drug use
Infant factors - low birth weight, male, not first born, prone position
102
What are the cells of the immune system?
T lymphocytes
B lymphocytes
Plasma cells
Natural killer cell lymphocytes
103
Types of T lymphocytes
T helper cells = help B lymphocytes produce antibodies
| T cytotoxic lymphocytes = mediate killing of viral infected or transformed cells
104
B lymphocytes
Immunoglobulin protein on surface (Ab)
| One B lymphocyte and it’s clones produce one antibody
105
Plasma cells
Differentiated B lymphocyte that secretes AB into serum
106
Natural killer cell lymphocytes
Neither B nor T
React against viral infected cells
Kill tumour, foreign cells without prior exposure
107
Antigen presenting cell (APC)
Cell that engulfs Ag, processes that Ag and expresses Ag on cell surface to activate immune response
108
Major Histocompatibility Complex (MHC)
Group of proteins to which processed Ag is attached and then transferred to cell surface
109
IgA
Ab present in secretions, milk
| Dimer
110
IgE
Ag present in tissue (located on surface of mast cells)
| Mediate allergic response (Type I hypersensitivity reaction)
111
IgD
Ab present on surface of B cells
| Involved in activation of lymphocyte response to an Ag
112
IgM
Ab present in blood
First antibody produces in response to Ag
Neutralize microorganisms, activate complement
113
IgG
Ab present in blood
Increased production on re-exposure to particular Ag
Opsonin
****** GO OVER ******
114
Hypersensitivity reactions
```
Classification based on mechanism of immune injury
Type 1 = anaphylactic
Type 2 = cytotoxic type
Type 3 = immune complex
Type 4 = cell mediated (delayed)
```
115
Type I hypersensitivity
Exaggerated immune response due to excessive release of
mast cell derived mediators (Hm)
Mediated by IgE
Increased vascular permeability, edema, cells (eosinophils)
Allergic rhinitis
116
Allergic rhinitis
```
• allergens [pollens (hay fever), cats, dust mites]
• inhaling allergen results in symptoms
• itchy nose, sneeze, watery eyes
• treatment
- antihistamines, other
- desensitization shots
```
117
Atopic dermatitis
Type 1 hypersensitivity example
• contact of allergen with skin
• skin irritation (red, itchy)
118
Asthma (some forms)
Type I hypersensitivity example
• inhale allergen with delayed response
• cough, wheeze
119
Anaphylactic shock
Type I hypersensitivity example
• life threatening systemic reaction to an allergen (bee venom, drugs)
• laryngeal constriction, shock, pulmonary edema
• treat with epinephrine etc.
120
Type II Hypersensitivity
• Exaggerated immune response due to deposition of
antibodies on antigens attached to cells or tissue
• Antigen may be intrinsic or extrinsic
• IgG or IgM binds to the antigen causing disease by:
• activation of complement
• Cell lysis due to direct complement lysis or via opsonization
• activation of cellular destruction
• Cell lysis by non-specific immune cells (PMN, Macrophages, NKcell)
• interfering with receptor function
• some AB bind to receptors on cell surface
• AB binding results in increased or decreased function of those cells
121
Hemolytic anemia
Type II Hypersensitivity example
• AB against protein on surface of rbc
• AB binds causing hemolysis
122
Grave’s disease
* AB against thyroid stimulating hormone receptor on thyroid cells
* AB binds to the TSHR causing increased production of thyroid H
* results in hyperthyroidism
123
Myasthenia gravis
* AB against acetylcholine R on muscle cells
* AB binds to the ACHR blocking the neural impulse
* results in muscle weakness
124
Type III Hypersensitivity
• Exaggerated immune response due to excessive creation of
AB-Ag complexes either in the circulation or in tissue
• AB-Ag complexes pass into various body compartments
with ensuing inflammation in those compartments
125
Systemic lupus erythematosus
Type III Hypersensitivity example;
• autoimmune disease where circulating immune
complexes created due to AB against various antigens
• kidney disease, arthritis, skin disease etc.
126
Post-streptococcal glomerulonephritis
Type III Hypersensitivity example; Multisystemic autoimmune disease
• AB-Ag complexes deposit in BM of glomeruli in kidney
• rare complication of streptococcal upper respiratory tract infection • Etiology and pathogenesis poorly understood
• possibly malfunction of T suppressor cells resulting in polyclonal
activation of B cells with antibody production
• ANA screen is positive, anti dsDNA antibodies, other
antibodies (Extractable Nuclear Antigens)
• Type III hypersensitivity reaction; also Type II
• Variable clinical course
• Treat with immunosuppression
• Kidney failure is most serious complication
127
Polyarteritis nodosa
Type III Hypersensitivity example
• inflammation of medium sized arteries due to formation of immune
complexes in vessel wall
• inflammation of vessel wall weakens wall, thrombosis
• related to chronic Hep B infection
128
Type IV Hypersensitivity
• Exaggerated immune response due to excessive, prolonged
reaction by immune cells to complex Ag
• Ag causes activation (T helper cells etc)
• cytokines cause macrophages to transform
• activated immune cells may create granulomas
• also develop memory to the antigen
129
Tuberculosis
Type IV Hypersensitivity example
• complex antigens of bacteria (Mycobacterium tuberculosis)
• bacteria walled off within granuloma, body develops memory
• TB skin test
• inject tuberculin into the skin, if previous exposure then localized
induration at site of injection
130
Contact dermatitis
• exaggerated cellular mediated immune response to certain
| allergens [latex, poison ivy, gold rings]
131
Allograft
(donor and recipient are not the same)
• requires HLA typing and matching blood groups
• relatives usually best donors
• immunosuppressant drugs to reduce immune response
132
Autograft
(patient is donor and recipient)
| • skin graft, hair transplant, BMT, stem cells
133
Xenograft
(donor and recipient are different species)
| • heart valves, cornea
134
Hyperacute rejection
(occurs within hours of graft)
| • due to preformed AB in the host vs. the donor organ
135
Acute rejection
(occurs within days to weeks of graft)
| • AB and cell mediated immune reaction by host
136
Chronic rejection
(occurs within months to years of graft)
• AB and cell mediated reaction by host
• vascular obstruction and tissue destruction
137
Graft versus host disease (GVHD)
• Graft tissue mounts immune reaction against host
• May occur in allogenic bone marrow transplants
- Donor lymphocytes in donor tissue mount cell-mediated
immune reaction against host tissue
• dermatitis, diarrhea, fever, jaundice
138
Hemolytic Disease of the newborn
* Rh- mother, Rh + father means possible to have Rh+ fetus
* Rh- mother exposed to Rh + blood makes Anti-D (IgG)
* Anti-D is able to cross placenta, results in hemolysis of fetal rbc
* hydrops fetalis, jaundice etc
* immunoprophylaxis
* give anti-D Ig at time of delivery to stop sensitization
* coats D Ag therefore mother not sensitized, doesn’t make anti D
139
AIDS
Syndrome of severe immunodeficiency secondary to
infection of T helper cells and macrophages by HIV
• Transmission by infected body fluids
• IVDA, sexual intercourse, blood transfusions, materno
-fetal
• HIV infection has four stages
• acute viral illness (at time of infection)
• asymptomatic phase
• persistent generalized lymphadenopathy
• opportunistic infections, neoplasia, etc
• Diagnosis of HIV
• identification of HIV antibodies, confirmatory tests
• Monitoring - measure lymphocyte counts (CD
4 and CD8); CD4 cell count drops
• Symptoms - (CNS, mouth, lymph nodes, lung, GI tract, skin) - depends on stage, CD4 count
• Opportunistic infections - pneomocystis carinii, aspergillus, MAI,
• Neoplasms - kaposi sarcoma, lymphoma
• Treatment
- antiretrovirals, prophylaxis vs. opportunistic infection
140
Amyloidosis
• Disease characterized by deposition of abnormal protein
(amyloid) in various organs
• unusual form of protein (Beta pleated sheet)
• various types of amyloid (AL,AA,)
• clinical manifestations vary
• diagnosis by demonstrating amyloid in tissue
141
What is neoplasia?
• Abnormal growth of cells that is not responsive to usual cellular control mechanisms
(autonomous) and is not adaptive
• Usually (not always) produces a mass (neoplasm)
• NOT hyperplasia, hypertrophy, metaplasia or atrophy (cellular adaptations)
• Hyperplasia, metaplasia, hypertrophy and atrophy are potentially reversible.
• Neoplasms are irreversible (autonomous) but rarely may disappear.
142
What is a Neoplasm?
•a neoplasm is a mass of neoplastic cells ( abnormal cells that grows autonomously)
143
What is a tumor (-oma)?
* literally means a swelling (1 of 5 signs of inflammation)
* often used interchangeably with neoplasm
* Includes non-neoplastic masses like cysts etc.
144
What is a mass?
* a mass is a generic term for overgrowth of cells
* Similar meaning to tumor
* may be neoplastic or non-neoplastic
145
What does malignant mean?
• Tending to be severe and become progressively worse, as in malignant hypertension.
• In regard to a neoplasm, having the properties of a malignancy that can invade and destroy nearby tissue
and that may spread (metastasize) to other parts of the body
• Doesn’t just relate to neoplasms
146
What does benign mean?
• Not malignant
• Mild, favorable outlook; not usually tending to cause death
• Benign neoplasm has no tendency to invade adjacent tissues or spread AKA DOES NOT METASTASIZE;
commonly enclosed in a definite capsule.
• May be associated with morbidity and death
147
What is a malignant neoplasm?
•Neoplasm that is malignant has invaded adjacent tissue and therefore has the potential to metastasize
(spread) to other parts of the body
General characteristics of malignant neoplasms
•less well differentiated
•grow quickly (necrotic areas due to ischemic necrosis)
•locally invasive
•irregular infiltrating border, no capsule
•adequate removal requires rim of adjacent tissue (margin)
•able to metastasize
148
Define metastasize
spread of malignant cells from one site to another via invasion of lymphatics or blood
vessels
149
What is cancer?
•generally refers to a malignant neoplasm (malignancy)
150
What is a premalignant neoplasm?
• A neoplasm that may (or is likely to) become malignant
• With respect to epithelial neoplasia a premalignant neoplasm has not invaded past the basement membrane
and therefore is unable to metastasize (spread) to other parts of the body
• Premalignant neoplasms have varying likelihoods of transformation into malignant neoplasms
• Premalignant epithelial neoplasms may or may not produce a mass
151
What is meant by differentiation in relation to neoplasms?
Degree to which neoplastic cells look like normal cells
• Well differentiated - look similar to N
• Poorly differentiated - don’t look at all N
• Anaplastic - can’t tell what type, bad because need to know for type of primary site which allows you determine treatment
152
What is a benign neoplasm?
• Neoplasm that is not malignant; therefore it does not invade the surrounding tissue and does not
metastasize (spread) to other parts of the body
• Benign neoplasms may be associated with significant morbidity and even mortality (bad location)
General characteristics of benign neoplasms
- well differentiated (look like normal tissue)
- slow rate of growth (few mitoses, no necrosis)
- no invasion of adjacent tissue (expansile growth, smooth border, encapsulated, no metastases
153
How are neoplasms named?
• Neoplasms are named on the basis of the cell/tissue of origin and/or differentiation and whether they are
benign or malignant
• The suffix of epithelial and soft tissue neoplasms identifies whether the neoplasm is benign or malignant
- Carcinoma is a malignant epithelial neoplasm
- Sarcoma is a malignant connective tissue neoplasm
• Pre-malignant epithelial neoplasms may be called carcinoma but must be followed by the words in-situ to distinguish them from a true malignancy
154
Nomenclature of epithelial neoplasms
* Benign epithelial neoplasms (-oma)
| * Malignant epithelial neoplasms (carcinoma)
155
Nomenclature of soft tissue neoplasms
* Benign soft tissue neoplasms (oma)
| * Malignant soft tissue neoplasms (osarcoma)
156
Melanoma
malignant neoplasm of melanocytes
157
Lymphoma
malignant neoplasm of lymphocytes
158
Leukemia
malignant neoplasm of hematopoietic cells
159
Carcinoid
malignant neoplasm of neuroendocrine cells
160
Teratoma
neoplasm of germ cells containing different types of tissues, may be benign or
malignant
161
Mixed tumour
neoplasm containing two neoplastic components usually epithelial and mesenchymal
162
Why does neoplasia occur?
* Geographic factors
* Carcinogens
* Age
* Hereditary factors
* Certain clinical conditions of chronic irritation associated with risk of malignancies
* Certain benign neoplasms are associated with increased risk of malignancies
163
What is the most common type of neoplasm?
Epithelial
164
What predicts the likely outcome of a patient with a malignant neoplasm?
Grade and stage
165
Grade of malignant neoplasm
• the degree of differentiation of the malignant cells
- High grade tumours are poorly differentiated
- Low grade tumours are well differentiated
166
Stage of malignant neoplasm
• amount of malignant neoplasm in the body (“tumour burden”)
• TNM system
- T = Size of primary tumour
- N = Amount of tumour in lymph
nodes
- M = Presence or absence of distant metastasis
*M trumps others; In a hollow organ, size less important, what is important is how many layers it has infiltrated
167
What clinical features are associated with neoplasms?
Local effects - neoplasms are space occupying lesions; expansion of the neoplasm causes physical compression of adjacent structures; benign neoplasms may be fatal (eg. Meningioma)
Systemic effects - cachexia (state of general ill health and poor nutrition); weight loss; anorexia
Paraneoplastic syndromes - syndrome of symptoms in patient with cancer not explained by local or distant effects of tumour itself e.g. Hypercalcemia (increased serum calcium), Cushing’s syndrome (production of ACTH), Syndrome of inappropriate antidiuretic hormone (production of ADH)
Hormonal effects - some endocrine neoplasms make hormones
168
Describe chemical carcinogenesis
a multi-step process:
Initiation - chemical induces irreversible change in DNA of cells
Promotion - promoter chemicals induce tumour formation in initiated cells
Progression - acquisition of additional genetic changes, clonal expansion of various cell lines
169
Pro-carcinogen
chemical that must be modified in body to become a carcinogen
170
What are some examples of chemical carcinogens?
- Alkylating agents used to treat cancers may cause other cancers
- Aflatoxin = liver carcinogen produced by fungus
- Polycyclic hydrocarbons = skin, lung carcinogens
- Aniline dyes = bladder carcinogens
- Nitrosamines and amides =
may induce gastric cancer
171
Xeroderma pigmentosa
genetic defect in DNA enzymatic repair system - develop skin cancers at young age
172
How is papllomavirus (HPV) implicated in some cancers?
infects squamous epithelial cells forming warts
- HPV types 16, 18, and 33 associated with cervical cancer
- HPV types 6, and 11 associated with benign cervical lesions
173
How is Epstein Barr virus (EBV) implicated in some cancers?
- infects B lymphocytes
| - association with Burkitt’s lymphoma, nasopharyngeal cancer
174
How is Hepatitis B virus implicated in some cancers?
- associated with increased incidence of liver cancer
175
How is Human T-cell leukemia virus implicated in some cancers?
- associated with rare form of T-cell leukemia
176
Oncogenes vs. Tumour suppressor genes
Oncogenes - mutated genes whose products are associated with formation of neoplasms
Tumour suppressor genes - genes whose products suppress development of tumours; damaged tumour suppressor gene results in increased tumours e.g. retinoblastoma
177
What kind of cancer is most common in females?
Breast
178
What cancer is most common in males?
Prostate
179
What kind of cancer kills the most people?
Lung
180
What are the 3 layers of blood vessels?
Intima – inner layer, primarily endothelium
• almost always thickened in adults, usually by fibroblasts
and collagen
Media – middle later, smooth muscle
• not present in capillaries or lymphatics
Adventitia – outer layer, variably fibrous
* in many vessels, this layer is more theoretical
181
What are the arterial diseases of the intima?
Arteriosclerosis / arteriolosclerosis – intimal scarring, typically
hypertension or aging associated
- stiffening of the arteries
Atherosclerosis – fatty expansion of intima
182
What are the arterial diseases of the media?
Dissection – separation of the media
Raynaud’s disease – abnormal response to cold, causing distal
fingers and toes to become ischemic and blue, manifestation of vasospasm
Vasculitis – inflammation of vessels
183
What arterial diseases can affect all layers?
Aneurysm – dilation of the vessel wall, which predisposes to clots and rupture
Abnormal development (vascular malformations)
Neoplasia (angiomas, angiosarcomas, etc.)
184
What is atherosclerosis?
Fatty expansion of intima
smaller lumen
“Hardened gruel” – deposition of lipids and material in walls of arteries
with resulting narrowing of arteries
Can result in ischemia and thrombosis, with end organ damage
185
What are the causal processes of atherosclerosis?
* Circulating lipids – either high levels or abnormal structures
* Endothelial “dysfunction” – abnormal accumulation of lipids
* Inflammation – progression of lesions
186
How does progression of atherosclerosis go?
Grows outwards then inwards
Fatty streak
- accumulation of lipid in intimate macrophages
Early plaque
- lipid, macrophages, thin fibrous cap
- not much change in lumen size up until now
Mature plaque (fibroatheroma) - stable or unstable
- thick fibrous cap, small necrotic core
- bigger change in lumen size
Rupture, erosion, stenosis, dissection, embolization, etc.
187
Role of foam cells in atherosclerosis
Fat, sedentary macrophages - CAN’t do anything so send out signals to increase # of macrophages, makes things worse
188
What are the target organs of atherosclerosis
Aorta - almost always involved, complications include aneurysm formation and embolism
Renal arteries - cause hypertension because perceived lower blood pressure due to closing off which leads to
Coronary arteries - ischemic heart disease (heart attack)
Cerebrovascular system - stroke
Peripheral vascular system
189
What venous diseases affect the intima?
Deep vein thrombosis (and associated embolism - can cause pulmonary
Thrombophlebitis - inflammation of vein due to thrombus
190
What is congestive heart failure?
Heart unable to pump enough blood to meet tissue demands
Various causes including chronic ischemic damage
n Symptoms include shortness of breath, tiredness, etc.
191
What disease affects all layers of veins?
Varicose veins - dilated
- associated with valve incompetence, increase pressure, and dilation
- leads to thrombus formation, can cause clots
192
What is vasculitis?
Inflammation of the media of any vessel
Classified by clinical presentation, which organs are affected, and which size vessels are affected
Most are autoimmune or idiopathic
193
What are pathologic consequences of hypertension?
* Heart: left ventricular hypertrophy
* Systemic: vascular changes and associated ischemia
* Brain: microinfarcts, strokes
* Eyes - retinal damage
194
What are cardiomyopathies?
Disorders of cardiomyocytes (muscle cells) leading to abnormal heart function
195
What is ischemic heart disease?
Reduced coronary circulation – most commonly atherosclerotic, can
be embolic, rare others
196
How does ischemic heart disease present?
• Angina: transient chest pain due to reversible ischemia
• Myocardial infarct (MI): death of heart muscle due to irreversible
ischemic damage
• Chronic ischemic heart disease: chronic destruction of heart
muscle with progressive dysfunction
• Arrhythmia: can result from ischemia in the conduction system
197
What is a myocardial infarct and it's complication?
Death of heart muscle due to irreversible
ischemic damage
Complications of MI:
• myocardial rupture (5 to 7 days after the MI), possibly with
resulting cardiac tamponade (constriction) - Because wall death due to ischemia
• papillary muscle rupture with mitral regurgitation
• ventricular aneurysm
• mural thrombus and emboli
• arrhythmias
198
How do you diagnose MIs?
clinical features, ECG, lab tests (troponin)
199
What is congestive heart failure?
Heart unable to pump enough blood to meet tissue demands
n Various causes including chronic ischemic damage
n Symptoms include shortness of breath, tiredness, etc.
200
Left vs. right sided congestive heart failure
* Left – failure to get blood out to system, accumulates in lungs
* Right – failure to get to lungs, accumulates in veins (liver, legs, …)
201
Systolic vs. diastolic dysfunction in congestive heart failure
* Systolic – can’t pump the blood out of the heart
| * Diastolic – can’t fill the heart as much as needed
202
Dilated cardiomyopathy
a condition in which the heart's ability to pump blood is decreased because the heart's main pumping chamber, the left ventricle, is enlarged and weakened
Dilated chambers – genetics, past
viral infection, alcohol, chemotherapy (and late ischemic
disease)
203
Hypertrophic cardiomyopathy
thickened walls – electrical signal can't get through. genetic (albeit
about 1/3 spontaneous mutation)
204
Restrictive cardiomyopathy
– reduced ventricular contractility - walls of the heart are rigid (but not thickened)
true idiopathic primary forms in pediatrics, acquired forms in
adults (e.g. amyloidosis)
205
What is Cardiac Neoplasms?
Most common cardiac mass is a thrombus
Most common cardiac neoplasm is metastasis - cancer that spreads to a different part of the body from where it started (typically by venous
spread, e.g. liver or kidney)
Most common primary cardiac neoplasm is myxoma - of primitive connective tissue
```
Most common (albeit very rare) primary malignancy in adult is
probably angiosarcoma
```
Most common (albeit rare) primary malignancy in children is rhabdomyosarcoma
Benign lesions can be excised and all’s well
Malignant lesions typically rapidly fatal
206
RASopathies
mutations in genes of the Ras-MAPK pathway; mimic hypertrophic, plus abnormal vessels
and valves – genetic
207
What is congenital heart disease?
Defects of the heart present at birth
More than 50 well recognized patterns
208
What is Valvular Heart Disease?
Extremely common
Can be stenosis or insufficiency/regurgitation of any valve
Calcific aortic stenosis and mitral regurgitation are clinically
most commonly addressed
Causes include degenerative, prior infection, prior radiation,
autoimmune, and genetic
209
What is Endocarditis?
Inflammation of heart inner lining, usually a heart valve
Typically bacterial, rarely fungal
Acute bacterial endocarditis is caused by virulent organisms that may
infect a normal valve
Subacute bacterial endocarditis is caused by less virulent organisms
that infect an abnormal valve
Complications of all forms include impaired valve function and emboli
210
What is myocarditis?
Inflammation of heart muscle
Includes lymphocytic myocarditis, eosinophilic myocarditis, giant cell myocarditis,
sarcoidosis, etc.
Caused by viruses, toxins, medication, hypersentivity reactions,
autoimmunity, and other infections
211
What is Pericarditis?
Inflammation of epicardium and/or pericardium
Often associated with pericardial effusion, and possibly tamponade
Can be acute (fibrinous), chronic (fibrous), or a mix
Associated with infection, autoimmunity, metastasis, toxic
reactions, prior surgery
If causing tamponade (constriction), surgery required
212
What is Cardiac Neoplasms?
Most common cardiac mass is a thrombus
Most common cardiac neoplasm is metastasis (typically by venous
spread, e.g. liver or kidney)
Most common primary cardiac neoplasm is myxoma
```
Most common (albeit very rare) primary malignancy in adult is
probably angiosarcoma
```
Most common (albeit rare) primary malignancy in children is rhabdomyosarcoma
Benign lesions can be excised and all’s well
Malignant lesions typically rapidly fatal
213
How do fluids move out of capillaries?
hydrostatic pressure in the capillary
osmotic pressure in ECF
214
How do fluids move into capillaries?
oncotic pressure in the vessel
hydrostatic pressure in the ECF
215
Anasarca
severe generalized edema
216
Ascites
excess fluid in abdominal cavity
217
Cyanosis
a bluish discolouration of the lips and skin indicating a lack of oxygen
218
Hydrocardia
excess fluid in pericardial cavity
219
What's the difference between serum and plasma?
```
Plasma = all fluid, no cells
Serum = all fluid, no cells OR clotting proteins (after blood has clotted)
```
220
How is renal disease affected by edema?
plasma proteins lost in urine due to renal diseases (relative increase in osmotic pressure of ECF)
221
Hyperemia
an increased volume of blood in a tissue
222
Active hyperemia
occurs due to dilation of arterioles & capillaries (exercise, inflammation)
223
Passive hyperemia
(congestion) blood going in normally to organ, but there is blockage going out - due to increased venous pressure that occurs with impaired outflow of
blood from the area
224
Cyanosis
a bluish discoloration of the lips and skin indicating a lack of oxygen
225
Terminology for blood entering the body cavity
* hemothorax is blood in thoracic cavity
* hemoperitoneum is blood in peritoneal cavity
* hemopericardium is blood in pericardial cavity
226
What are the steps of plug formation during bleeding?
vessel constriction, platelet plug, reinforced by fibrin
227
Hemoptysis
coughing up blood from lungs
228
hematemesis
refers to vomiting blood from upper GI tract
229
hematochezia
passing bright red blood per rectum
230
melena
passage of dark (black) stools (UGI bleed)
231
hematuria
passage of blood in urine
232
metrorrhagia
excessive menses
233
Shock
inadequate perfusion (blood supply) to tissue; can be a multifactorial process
234
What factors predispose thrombus formation?
(Virchow’s triad)
• stasis of blood (CHF, dehydration)
• hypercoaguable states (inherited, malignancy)
• endothelial injury (thrombogenic surface revealed)
235
What are the 4 major fates of a thrombus?
– lysis of the thrombus removal of thrombus by fibrinolysis
– organization and recanalization replacement of the thrombus by granulation tissue and creation of new
channels through thrombus
– propagation is complete occlusion of a vessel with extension of the thrombus proximal in vein
– embolus formation is detachment of a thrombus and impaction lodge distally
236
Embolus
a thrombus or other movable intravascular mass that may cause obstruction of a
vessel
237
Saddle embolus
prevent the entry of blood into the lung and cause acute anoxia
238
Infarction
Irreversible ischemic necrosis of cells usually due to occlusion of arterial supply
239
Shock
inadequate perfusion (blood supply) to tissue
240
Causes of shock
```
– S septic shock
– H hypovolemic shock
– O obstructive shock
– C cardiogenic shock
– K anaphylactic shock
– S spinal/neurogenic shock
```
241
Cardiogenic shock
– results from heart not pumping adequately
• myocardial infarction
• arrhythmia
242
Hypovolemic shock
– results from loss of blood volume
• hemorrhage
• water loss (burn)
243
Hypotonic shock
– results from pooling of blood in the peripheri
• anaphylaxis
• sepsis
244
Phases of shock
• Compensated (nonprogressive) phase
– compensatory mechanisms able to maintain perfusion
• Decompensated (progressive) phase
– if the problem is not rectified, compensatory mechanisms unable to maintain perfusion
– hypotension, oliguria, acidosis, short of breath
245
Irreversible shock
– circulatory collapse, hypoperfusion of vital organs, loss of vital functions
246
Croup
(3mo -3yo)
• acute viral infection of the larynx in children younger than 3 yo
• barking cough
• due to parainfluenza virus
247
Infections, middle respiratory tract
* Croup (3mo -3yo)
* Acute epiglottitis (3yo-7yo)
* Bronchiolitis
248
Common cold, sore throat, “Flu”
* viral infection of upper respiratory tract with classic symptoms
* rhinovirus, parainfluenza viruses
* self limited, symptomatic relief
249
Pneumonia
Inflammation/ infection of the lungs Symptoms:
• fever, chills, rigors
• dyspnea, cough
• mucopurulent discharge
• chest x-ray, bacterial cultures of sputum, CBC & differential, arterial blood gas
Treatment: antibiotics
250
Mononucleosis
• a viral infection caused by EBV with enlarged nodes, sore throat
251
Diphtheria
• a bacterial infection of the throat with formation of a membrane
252
Pneumonias - Causative agents depend on where infection acquired
• community acquired
- usual bacteria are streptococcus, hemophilus, staphylococcus
• hospital acquired
- usual bacteria are gram negatives
• fungi, parasites and viruses may also cause pneumonia
- travel history is important re possible exposure
- immunocompromised individuals susceptible to unusual organisms
253
Acute epiglottitis
(3yo-7yo)
• acute bacterial infection of the epiglottis due to H. influenzae B
• may be life threatening due to swelling and closure of airway
• immunization
254
Bronchiolitis
(< 2yo)
• inflammation of bronchi and bronchioles due to viral infection
• usually due to Respiratory Syncitial Virus
255
Pneumonia
Inflammation/ infection of the lungs
256
Typical pneumonia
* infection affecting the air spaces characterized by a cough that produces sputum (productive cough)
* Lobar pneumonia is widespread involvement (lobe of lung)
* Bronchopneumonia is more limited involvement
257
Tuberculosis
Chronic respiratory infection due to bacteruium called Mycobacteria tuberculosis (Mtb)
- Mtb causes granulomatous reaction with caseous necrosis
258
Describe the progress of tuberculosis
Initial primary infection
• Ghon complex consists of lung lesion and enlarged hilar nodes
- M. tb bacteria isolated within the granulomas preventing spread
• uncommonly primary infection may progress
Secondary tuberculosis
• reactivation or reinfection
• tissue destruction, extrapulmonary spread
259
Routes of infection for pneumonia
* inhalational
| * hematogenous - originating in or carried by the blood
260
Mycoplasma pneumoniae
* commonest atypical pneumonia
* common in young adults
* may develop extra-pulmonary features
261
Legionella pneumophilia
* cause of Legionnaire’s disease
* prominent non-respiratory symptoms
* uncommon, source is standing water
262
What are come complications of pneumonia?
* Pleuritis: inflammation of the pleural lining
* Pyothorax: pus in the pleural cavity
* Empyema: loculated areas of pus in the pleural cavity
* Abscess
* Bronchiectasis - permanent enlargement of parts of the airways of the lung
* Chronic lung disease
263
Blue bloater
Clinical feature of COPD
• patients with predominant CHRONIC BRONCHITIS
• hypoxemia results in cyanosis “blue”
• frequently obese (“bloater”)
• pulmonary hypertension with resulting right ventricular hypertrophy
264
Diagnosis and treatment of tuberculosis
```
Diagnosis
• non-specific symptoms
• demonstrate presence of bacteria in sputum
• acid fast stain (Ziehl-Nielsen)
• DNA probes
```
Treatment
• multi-drug regimen
• treatment continues for many months
• drug resistant strains arising
265
Obstructive airway diseases
Group of respiratory diseases characterized by symptoms of obstructed airways (↓ flow rate, air
trapping)
```
Major diseases:
• Asthma
• Chronic obstructive pulmonary disease
• emphysema
• chronic bronchitis
• Bronchiectasis
• Cystic fibrosis
```
266
Chronic obstructive pulmonary disease examples
Chronic bronchitis
• disease diagnosed clinically as production of excessive sputum for at least 3 months during 2 consecutive
years
• obstruction is due to narrowing of airways caused by thickened mucosal lining and increased mucus
Emphysema
• destruction and dilation of distal air spaces
• centrilobular emphysema (widening of air spaces in center of a lobule)
• panlobular emphysema (widening of all air spaces in a lobule)
• secondary to deficiency of α-1 anti-trypsin (inactivates proteases)
267
Pink puffer
Clinical feature of COPD
• patients with predominant EMPHYSEMA
• destruction of lung tissue results in overinflation (barrel chest)
• use of accessory muscles of respiration
• hyperventilate to keep blood oxygenated (“puffer”)
268
Blue bloater
Clinical feature of COPD
• patients with predominant CHRONIC BRONCHITIS
• hypoxemia results in cyanosis “blue”
• frequently obese (“bloater”)
• pulmonary hypertension with resulting right ventricular hypertrophy
269
Bronchiectasis
Permanent dilatation of a bronchus due to destruction of the wall
Increased susceptibility to infections
Causes of bronchiectasis include
• obstruction (foreign body, tumor)
• infection (TB, measles, pneumonia)
• impaired defense mechanisms (cystic fibrosis)
270
Asthma
a respiratory disease characterized by increased reactivity of smooth muscle in
airways (reactive airway disease)
271
Extrinsic asthma
* attacks precipitated by exposure to triggering allergens
* Type I Hypersensitivity reaction
* associated with other atopic diseases (eczema, hay fever, allergies)
272
Intrinsic asthma
Intrinsic asthma
• attacks precipitated by non-immune mechanisms
• exercise, stress, infections, temperature, aspirin
273
Pathogenesis of asthma
* stimuli trigger inflammation with release of mediators
* smooth muscle contraction (bronchi constriction)
* leaky vessels
* mucus plugs
274
Sarcoidosis
Multisystemic disease of unknown etiology characterized by non-caseating/non-necrotizing granulomas in various organs
Diagnosis
- biopsy of affected tissue
Treatment
- no specific treatment
- steroids
275
Treatment for asthma
• treat acute attacks with bronchodilators, prevent chronic inflammation with steroids
276
Restrictive lung diseases
• Group of respiratory diseases characterized by symptoms of restrictive lung function (↓ lung
volume, ↓ compliance)
• Major diseases
• hypersensitivity pneumonitis
• pneumoconioses
• sarcoidosis
• Inflammatory process in alveolar walls with fibrosis
• Honeycomb lung is common end stage appearance
277
Hypersensitivity pneumonitis
Respiratory disease due to disordered immune reaction to various inhaled antigens
Acute form (Type III reaction)
Chronic form (Type IV reaction)
Treatment is avoidance of the allergen
278
Pneumoconioses
Respiratory disease due to inhalation of inorganic dusts
279
Sarcoidosis
Multisystemic disease of unknown etiology characterized by non-caseating granulomas in
various organs
280
Drowning
Types of drowning
• wet drowning (90 %)
- aspirated water enters the respiratory tract with resulting anoxia
- sea water results in more pronounced pulmonary edema
• dry drowning (10%)
- reflex laryngospasm with closure of glottis resulting in anoxia
- no water in the lungs
281
Adult respiratory distress syndrome (ARDS)
Clinical condition characterized by acute respiratory failure that does not respond to oxygen
Injury to lung causes leaky capillaries
- fluid enters the air spaces and interstitial space from the capillaries
282
Atelectasis
* term used to describe incomplete expansion of alveoli
* causes
* deficiency of surfactant
* compression of alveoli by external mass
* resorption of air distal to obstruction
283
Dyspnea
• term used to describe subjective feeling of shortness of breath
284
Respiratory Neoplasms
Laryngeal carcinoma
• linked to smoking, alcohol
• squamous cell carcinomas
• symptoms include hoarseness, loss of voice
285
Lung cancer
• number one cause of deaths due to cancer (male and female)
• second most common malignancy (male and female)
Types:
Adenocarcinoma
Squamous cell carcinoma
Small cell carcinoma
286
Adenocarcinoma
* most common primary lung malignancy (>35%)
* equal frequency in smokers and non-smokers
* usually peripheral, solitary nodule
287
Squamous cell carcinoma
* usually smokers
| * typically more centrally located
288
Small cell carcinoma
* usually smokers
* often early spread
* paraneoplastic syndromes (rare disorders that are triggered by an altered immune system response) common
289
Pneumothorax
• entry of air into the pleural cavity with collapse of the lung
290
Pleural effusion
• accumulation of fluid in the pleural cavity
291
Pleuritis
• inflammation of the pleura typically secondary to pneumonia
292
How is distribution of water determined?
• Distribution of water between ICF and ECF compartments is determined by distribution of
electrolytes
• Distribution of water within the ECF between the intra-vascular and interstitial space is
determined by proteins
