Neoplasia

Front 1

9:16 AM

Neoplasia

Back 1

new growth of abnormal tissue that serves no physiologic function and is independent of normal restraints on orderly growth. Have ability to replicate in the absence of growth factors or may replicate excessively in response to normal stimuli

Front 2

Tumors+

Back 2

always have suffix "-oma". An unmodified suffix generally denotes a benign neoplasm while for malignant neoplasms, the suffix is modified to either carcinoma or sarcoma\

Front 3

Carcinoma

Back 3

refers to epithelial malignancies

Front 4

Sarcoma

Back 4

mesenchymal/connective tissue malignancies

Front 5

Melanoma

Back 5

malignant neoplasm of melanocytes

Front 6

Lymphoma

Back 6

malignant neoplasm of lymphoid tissue

Front 7

Glioma

Back 7

malignant neoplasm of supporting tissue of the CNS

Front 8

Blastoma

Back 8

malignant tumors arising from early, partially differentiated embryonal tissue

Front 9

Teratoma

Back 9

neoplasm which contains cells from more than one embryonic germ cell layer and may be benign or malignant

Front 10

Hamartoma

Back 10

non-neoplastic "tumor" that represents abnormal overgrowth or differentiation of cells native to the tissue of origin

Front 11

Choristoma

Back 11

the presence of normal tissue in an abnormal location; also termed ectopic or heterotopic tissue

Front 12

Prefixes indicating cell or tissue of origin- adeno

Back 12

glandular epithelium

Front 13

Prefixes indicating cell or tissue of origin- transitional

Back 13

transitional epithelium

Front 14

Prefixes indicating cell or tissue of origin- fibro

Back 14

fibrous connective tissue

Front 15

Prefixes indicating cell or tissue of origin- leiomyo

Back 15

smooth mm

Front 16

Prefixes indicating cell or tissue of origin- rhabdomyo

Back 16

skeletal mm

Front 17

Prefixes indicating cell or tissue of origin- hemangio

Back 17

blood vessel

Front 18

Prefixes indicating cell or tissue of origin- chondro

Back 18

cartilage

Front 19

Prefixes indicating cell or tissue of origin- lymphangio

Back 19

lymphatic vessel

Front 20

Prefixes indicating gross features - scirrhous

Back 20

:hard due to excessive production of stroma

Front 21

Prefixes indicating gross features - colloid

Back 21

gelatinous, mucinous

Front 22

Prefixes indicating gross features - cystic

Back 22

fluid or gas filled spaces

Front 23

Prefixes indicating architectural growth pattern - villous

Back 23

forming shaggy, "finger-like" projections

Front 24

Prefixes indicating architectural growth pattern - cribriform

Back 24

pierced by small holes

Front 25

Malignant Neoplastic Cell morphology

Back 25

characterized by cellular and nuclear pleomorphism, increased nuclear/cytoplasmic ration; increased nuclear chromatin which is frequently "clumped", large nucleoli; bizarre mitoses; loss of cellular orientation; loss of normal functional capacity

Front 26

Cellular differentiation

Back 26

the extent to which neoplastic cells resemble their cell of origin histologically. Malig cells often show abnormalities in the number or structure of chromosomes and may vary from complete lack of differentiation (anaplasia) to well differentiated all within the same tumor

Front 27

Mode of growth

Back 27

benign neoplasms grow by expansion and tend to compress surrounding tissue into a capsule. Malig tumors grow by infiltration and invasion of the surrounding tissue and are not confined by a capsule

Front 28

Metastasis

Back 28

spread of a neoplasm to points that are not contiguous with the primary lesion. Benign tumors do not metastasize, but ALL malignant neoplasms have metastatic potential. Metastases occur via lymphatic dissemination, hematogenous dissemination, transcoelomic seeding, and traumatic seeding

Front 29

Lymphatic dissemination

Back 29

most common route of metastasis, esp of epithelial neoplasms (carcinomas) and follow the natural lymphatic drainage of the site of malignancy.

Front 30

Hematogenous dissemination

Back 30

characteristic of connective tissue neoplasms (sarcomas). Carcinomas are also spread by this route since there are vascular-lymphatic anastomoses. Invasion and metastases are more likely to occur via the venous system (not arterial) due to its thin walled structure

Front 31

Traumatic seeding

Back 31

excessive manipulation or cutting into malignant tumors may detach and carry small portions of the tumor to other sites

Front 32

Desmoplasia

Back 32

excessive e production of connective tissue

Front 33

Paraneoplastic syndromes

Back 33

some systemic effects caused by benign or malignant tumors producing hormones or homrone-like substances (hypercalcemia, Cushing's syndrome, inappropriate adh secretion, polycythemia

Front 34

Upper respiratory tract

Back 34

nasal cavities, paranasal sinuses, nasopharynx, oropharynx, and hypopharynx (epiglottis and larynx). Warms the inspired air and filters large particulate matter

Front 35

Lower respiratory air passages

Back 35

trachea and bronchial branches. Trachea > Carina > mainstem bronchi > lobar bronchi > segmental bronchi > intralobar bronchopulmonary segments > subsegmental bronchi > bronchioles > terminal bronchioles > respiratory bronchioles > alveolar ducts > alveolar sacs

Front 36

Pores of Kohn

Back 36

provides communication between adjacent alveolar spaces

Front 37

Acinus

Back 37

the functional gas exchange area of the lung and is composed of a respiratory bronchiole and its branching structures

Front 38

Lobule

Back 38

the smallest discrete portion of lung bounded by fibrous septa and consists of a terminal bronchiole and its branching structures. May contain 25-30 acini.

Front 39

Ventilation

Back 39

the movement and distribution of air within the tracheobronchial system

Front 40

Diffusion

Back 40

the movement of O2 and CO2 between the alveolar space and the capillary blood

Front 41

Perfusion

Back 41

the flow and distribution of blood within the pulmonary vascular bed

Front 42

Compliance

Back 42

stretchability while inhaling

Front 43

Elastic recoil

Back 43

compressibility while exhaling

Front 44

Chronic bronchitis

Back 44

"blue bloaters". Characterized by excessive mucous secretion within the bronchial tree than cannot be explained by either a specific infection or by infiltrative disease. Chronic cough with sputum production for at least three months of the year in at least two consecutive years.

Front 45

Pathogenesis of chronic bronchitis

Back 45

chronic irritation of the tracheobronchial mucosa (smoking) leads to hypertrophy and hyperplasia of the submucosal mucous glands in the large airways with hypersecretion of mucus (increase in sputum production). May also see squamous metaplasia and dysplasia of the surface epithelium. Goblet cell metaplasia of all bronchi and bronchioles also contributes to the excessive mucus production, decreases the number of normal ciliated cells and predisposes to obstruction

Front 46

Clinical signs of chronic bronchitis

Back 46

ventilation/perfusion mismatch (cyanosis), chronic hypoxemia, polycythemia (as RBC production), acidosis. The acidosis promotes pulmonary vasoconstriction which initially tends to correct eh V/Q mismatch by decreasing perfusion, but over time, will result in pulmonary hypertension. Leads to right heart failure, systemic venous congestion, and weight gain. Chest x-ray may be normal

Front 47

Major complications of chronic bronchitis

Back 47

repeated infections, right heart failure, peptic ulcers, and resp failure

Front 48

Emphysema

Back 48

"pink puffers". Abnormal, permanent, destructive lesion of the pulmonary parenchyma which leads to an increase in the size and volume of the air spaces distal to the terminal bronchiole. Causes disruption of the distal airway tissues - destruction with resultant loss of elastic recoil rather than large airway obstruction. The loss of elastic recoil requires a greater expiratory effort of the chest wall to force air out

Front 49

Centrilobular emphysema

Back 49

characterized by destructive changes primarily to the respiratory bronchioles. Often assoc w/ chronic bronchitis b/c of its relation to chronic bronchitis. Particles of cigarette smoke impact in the resp bronchioles and stimulate macrophages which release chemical mediators that are chemotactic for neutrophils. This bronchiolitis is one of the early changes assoc with smoking. Macrophages and neutrophils release proteases that, if not inactivated, will digest the alveolar walls

Front 50

Panlobular emphysema

Back 50

most frequently seen in the lower lobes. Characterized by uniform involvement of the acinus and is seen in patients with inherited or acquired alpha-1 antitrypsin deficiency

Front 51

Clinical signs of emphysema

Back 51

present with a history of progressive dyspnea and weight loss, barrel chest, exhale through pursed lips, less ventilation/perfusion mismatch than in chronic bronchitis. Patients are not cyanotic and blood gas values may be normal until late in the disease, increased radiolucency upon x-ray

Front 52

Bronchial asthma

Back 52

increased sensitivity of the tracheobronchial tree to various stimuli and is manifested by acute, widespread, narrowing of the small airways due to bronchoconstriction and a more chronic narrowing of the small bronchus and bronchioles. Atopic, non-atopic, miscellaneous

Front 53

Atopic asthma

Back 53

(allergic), IgE mediated hypersensitivity reaction (Type I). Can be triggered by a wide variety of allergens. Typically occurs in childhood, often family history. Serum IgE levels are elevated. Upon contact with an allergen, there is an immediate response of wheezing, edema, and increased mucus secretion due to degranulation of mast cells and stimulation of submucosal nerves which cause bronchoconstriction. The interstitial edema reduces overall lung compliance. Can also be a delayed response of persistent bronchospasm resulting from recruitment of inflammatory cells

Front 54

Non=atopic

Back 54

frequently triggered by upper respiratory infections (primarily viral). Mechanism of action is unknown. IgE levels usually normal, no family hx.

Front 55

Bronchiectasis

Back 55

permanent dilatation of bronchi and bronchioles resulting from inflammatory damage to their walls. May be due to bronchial obstruction, necrotizing pneumonia, cystic fibrosis. The inflammatory reaction in the bronchial wall ultimately results in weakening, abnormal dilatation, and fibrosis. Usually assoc with cough and copious production of purulent sputum. Lower lobes usually involved (left more often than the right

Front 56

Cystic fibrosis

Back 56

(mucoviscidosis), inherited chromosome 7 recessive disorder of exocrine glands characterized by abnormally viscous secretions. Manifested by pancreatic insufficiency, chronic resp disease, electrolyte disturbances, infertility, and occas cirrhosis of the liver. The submucous glands in the bronchial tree secrete an atypical viscous mucus which is difficult to clear and which predisposes to obstruction and repeated infection.

Front 57

Restrictive lung diseases

Back 57

characterized by decreased total lung capacity. May be due to loss of lung tissue (surgical resection, pulmonary infarction, atelectasis), filling of alveolar spaces (pneumonia, edema, hemorrhage), or infiltration and thickening of the pulmonary interstitium ( interstitial edema, inflammation, or fibrosis)

Front 58

Atelectasis

Back 58

condition in which there is either collapse of alveoli or incomplete filling of alveoli. Causes a decrease total lung volume and a restrictive pattern of pulmonary fx. Primary - failure of lungs to ventilate at time of birth (when placed in water the lungs will sink b/c there is no air in alveoli). Secondary: acquire, due to deficiency of surfactant (resp distress syndrome), loss of neg intrapleural pressure (chest traumas, pneumothorax), complete obstruction of an airway, direct pressure on lungs, or contraction. Distribution may be local, segmental, or massive. Creates an intrapulmonary right-to-left shunt

Front 59

Carnification

Back 59

complete organization of tissue if the lungs remain collapsed for an extended period of time

Front 60

Type I respiratory distress syndrome

Back 60

Hyaline membrane disease, resp distress of the newborn. Immature development of the lung results in a deficiency of surfactant. Alveoli collapse during expiration. This then requires greater inspiratory effot to expand the airways (nasal flaring and retraction). s/s hypoxia, cyanosis, metabolic acidosis, vasoconstriction. There is exudation of fibrin rich fluid into the interstitium and alveolar space and the formation of hyaline membranes

Front 61

Hyaline membranes

Back 61

fibrinous exudate admixed with necrotic epithelial cell debris

Front 62

Retrolental fibroplasia

Back 62

pressure-induced tissue injury and O2 toxicity caused by ventilation with PEEP

Front 63

Complications of Type I RDS

Back 63

retrolentalfibroplasia and bronchopulmonary dysplasia

Front 64

Type II RDS

Back 64

wide variety of triggering mechanisms (high altitude exposure, anaphylaxis, chem/phys irritants, drugs, o2 tox). The common denominator is widespread microvascular injury.

Front 65

Surfactant

Back 65

the lipid material synthesized by the alveolar cells that is needed to lower the surface tension of the alveoli and help prevent their complete collapse during expiration. The production of the lipid components of surfactant is stimulated by corticosteriod secretion and occurs late in gestation 36-37 weeks.

Front 66

Pneumoconioses

Back 66

occupational diseases from inhalation of inorganic mineral dusts. Dusts elicit inflammation and pulmonary fibrosis. The more soluble particles tend to elicit more of an inflammatory response while the more insoluble materials tend to elicit a fibrotic response. Alveolar macrophage is primary defense

Front 67

Chronic interstitial pneumonias

Back 67

non-infectious. Group of diseases which have alveolitis with subsequent fibrosis. Have difficulty ventilating lungs bc of increased "stiffness" due to fibrosis. End result is honeycomb lung.

Front 68

Honeycomb lung

Back 68

multiple cystic spaces separated by dense fibrous scars. The cystic spaces represent dilated bronchiolescaused by contraction of the fibrous scars and are often filled with mucus and cellular debris

Front 69

Sarcoidosis

Back 69

unknown etiology. Represents an abnormal immunologic response to a variety of non-specific agents. May include hylar lymphadenopathy, miliary sarcoidosis, diffuse fibrosis, or "honeycombing". Presenting symptoms include cough, dyspnea, chest pain, loss of weight, malaise, fatigue.

Front 70

Hilar lymphadenopathy

Back 70

enlargement of the lymph nodes may be so great that the designation "potato nodes" is applied

Front 71

Miliary sarcoidosis

Back 71

gives "snow storm" appearance by x-ray due to the multiple miliary sarcoid lesions throughout the lung parenchyma

Front 72

Bacterial pneumonia

Back 72

streptococcus pneumoniae is most common. Can have lobar or broncho

Front 73

Lobar pneumonia

Back 73

extensive inflammatory consolidation involving an entire lobe or large portion. Before clinical symptoms, there is rapid proliferation of bacteria in the alveolar spaces which triggers the early stage of the inflammaroty response (vascular hyperemia and exudation). Neutrophils swarm into alveolar spaces to combat bacteria along with rbc's and a fibrinous exudate

Front 74

Bronchopneumonia

Back 74

less extensive than lobar, but possibly more destructive. Inflammtory consolidation occurs in patches throughout a lobe (often following viral bronchitis). The bacteria colonize the airways and elicit inflammatory response which extends out into surrounding lung parenchyma w/ tissue destruction, microabscess formatoin, and scarring.

Front 75

Clinical presentation for both pneumos

Back 75

sudden onset. Shaking chills, followed by high fever. At first, dry cough. Later, sputum becomes thick, purulent, and hemorrhagic ("rusty"). Pleuritic pain and friction rub, poss pleural effusion. Leukocytosis 15,000 to 40,000. complications include abscesses, empyema, and sepsis.

Front 76

Mycoplasma/viral pneumo

Back 76

caused by mycoplasma pneumoniae. Lesions are peribronchiolar and interstitial (w/in alveolar walls). Alveolar spaces are generally free of significant cellular exudate. Often hx of recent uri and may be an irregular fever with myalgia and malaise. Persistent, racking, sparsely productive cough may be present. May be severe frontal headache, worsened during coughing. Substernal chest pain. * pleuritic pain, effusions, dyspnea, and cyanosis are rare.

Front 77

Mycotic pneumonias

Back 77

fungi. Cause tissue damage primarily by hypersensitivity rx by the host. Induce a chronic granulomatous inflammatory rx. Pneumocystis carinii is most common opportunistic agent producing pneumo in AIDS patients. The organisms proliferate in the alveolar spaces and are assoc with a characteristic "frothy-appearing" intraalveolar edema. (think of yeast)

Front 78

Primary TB

Back 78

most common route of infection is through inhalation of aerosol droplets. Usually settles in the middle of the lung - called the Ghon focus. Central caseous necrosis is seen. Can spread to hilar lymph nodes

Front 79

Primary Ghon complex

Back 79

combination of the subpleural lesion and the hilar node involvement in TB

Front 80

Secondary TB

Back 80

hypersensitivity reexposure to organism that produces a prompt granulomatous tissue response often with caseous necrosis. This usually occurs in the apices of the upper lobes. In some cases, the lesions may remian active, erode into neighboring airways and cavitate. Cavitation is considered the anatomic hallmark of secondary TB. Complications include massive hemoptysis, loss of ventilating capacity, and TB empyema,.

Front 81

Chemical pneumonia

Back 81

aspiration is most frequent cause. If sufficient volume with low pH is aspirated, a distinct clinical picture ensues 2 to 5 hours after aspiration with the onset of cyanosis, dyspnea, tachypnea, tachycardia and shock, bloody frothy sputum, marked pulm congestion and edema.

Front 82

Pulmonary abscess

Back 82

aspiration I smost common cause b/c it inoculates the lower resp tract by anaerobic organisms from the oral cavity. Occur most frequently on the right side. Also caused by bacterial pneumo, bronchial obstruction, septic emboli, penetrating chest wounds. Consists of liquefaction necrosis of lung parenchyma. s/s are fever w/ prominent cough accompby foul smelling or bloody sputum

Front 83

Bronchiogenic carcinoma

Back 83

leading cause fo cancer deaths. Surgery may be effecive. Smoking is prob morst important factor. Can be squamous cell carcinoma, adenocarcinoma, small cell undifferentiated carcinoma. When symptomatic, presentaton consists of chronic cough w/ hemoptysis, chest pain, anorexia and weight loss, and dyspnea. Metastatic neoplasms are far more common than primary neoplasms and tend to present as multiple nodules usually in the lung periphery.

Front 84

Squamous cell carcinoma

Back 84

cancer most closely assoc w/ smoking. Tumors may cavitate and can simulate the appearance of tb or infectious lung abscess

Front 85

Adenocarcinoma

Back 85

mostly peripheral lesions that tend to spread to hilar lymph nodes. May remain silent until s/s of metastases occur. Rare variety is called bronchioloalveolar carcinoma that arises from bronchiolar epithelium

Front 86

Small cell undifferentiated carcinoma

Back 86

oat cell. Almost always a central lesion. These tumors are notorious for producing hormone-like substances that cause paraneoplastic syndromes. Surgery is seldom an option.

Front 87

Acute cystitis
(inflammatory)

Back 87

Bladder infection
• Residual urine
• stasis of urine
• mucosal trauma leading to infection.
• Usually E. coli
• Frequency
• Dysuria
• lower abd/pelvic pain
Neutrophils and red blood cells in urine
Females > Males
Mucosa is edematous, hyperemic , exudates, ulcerations, hemorrhage
Antibiotics

Front 88

Chronic interstitial cystitis
(inflammatory)

Back 88

Hunner ulcer
Unknown etiology
• Suprapubic pain
• Frequency
• Urgency
• Dysuria
• Dyspareunia
• malaise
Chronic inflammation
Middle aged women
Mucosa is edematous with petechial hemorrhages and ulcerations.
Fibrosis of muscular wall of bladder
Symptomatic
• Irritability
• Personality changes
• depression

Front 89

Renal agenesis

Back 89

Hereditary
• Pulmonary hypoplasia
• Oligohydramnios
• Potter's syndrome

More often males

Incompatible with life

Front 90

Simple cysts

Back 90

Congenital or acquired

No clinical significance

Lesions arising from the cortex of kidney
Variable sizes

Must differentiate from a renal tumor for dx

Front 91

Adult polycystic kidney

Back 91

Autosomal dominant
• Hematuria (from hemmorhage into cysts)

30-40 yrs
Almost always bilateral
Enlarged kidney w/ many cysts

Chronic renal failure

Front 92

Calculi
(inflammatory)

Back 92

Bladder stones
Promoted by bacteria that make urine alkaline
May be no symptoms
Recurrent infections

More often men
Drink 6-8 glasses water/day
lithotripsy

Front 93

Renal calculi

Back 93

Kidney stones
Excessive Ca in serum or urine
Urinary stasis/retention
Extreme colicky abd pain radiating from flank to groin
Can have infection and hematuria

Front 94

Urinary obstruction

Back 94

Stones
Prostatic hypertrophy
Congenital defects
Tumors
Pregnancy
Pain if acute
Can be asymptomatic if gradual
Hydronephrosis (dilitation of renal pelvis)
Atrophy of kidney



May be unilateral or bilateral

Changes irreversible after about 3 wks of complete obstruction

Front 95

Acute proliferative glomerulonephritis

(nephritic syndrome)

Back 95

Post-infectious glomerulonephritis

Common in children 1-3 weeks after strep throat
Type III immune hypersensitivity rx
Malaise
Fever
Oliguria
Hematuria
Nausea
Periorbiltal edema
Hypertension
Red blood cell casts
Mild proteinuria (<1 gm)
Azotemia (↑bun and creatinine)
Immune mediated damage

95% recover fully
May progress to chronic glomerulonephritis

Front 96

Rapidly progressive glomerulonephritis
(nephritic syndrome)

Back 96

Ubrupt onset of oliguria and hematuria
Lesser degree of htn, edema, protenuria
Immune mediated damage
Azotemia (↑bun and creatinine)

Rapid progression to renal failure w/in weeks of onset of symptoms

Front 97

Nephrotic syndrome

Back 97

Proteinuria (>3.5 gm/day)
Hypoalbuminemia
Hyperlipidemia
edema

Infections due to loss of immunoglobulins and complement
Thrombosis due to loss of anticoagulant factors

Front 98

Minimal change disease
(nephrotic syndrome)

Back 98

Lipoid nephrosis,
Nil disease
Unknown cause


This disease is most common cause of nephrotic syndrome in children
Very little morphologic change to the glomeruli
Children respond dramatically to steroid tx

Front 99

Membranous glomerulonephropathy
(nephrotic syndrome)

Back 99

Not inflammatory


------------------------------
Over time develop increasing BUN, HTN
Most common cause of nephrotic syndrome in adults
Characterized by thickening of the glomerular capillary basement membranes


Progressive renal failure

Front 100

Acute pyelonepheritis

Back 100

Urinary obstruction, foley, vesicoureteral reflux, pregnancy, prior renal disease, diabetes
Usually caused by E. coli - bacterial ascension from bladder
Acute onset of fever and maliase
Costovertebral angle pain
Dysuria
Frequency
Urgency
Pyuria
WBC casts
Positive urine cultures



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



--------------------------------------------
Antibiotic therapy
Necrotizing papillitis
Pyonephrosis
Perinephric abscess
High incidence of recurrence

Front 101

Chronic pyelonephritis

Back 101

Chronic obstruction leading to recurrent infections or result of backward reflux of urine from the bladder to kidney (reflux nephropathy)
Repeated bouts of acute pyelonephritis or insidious w/ renal insufficiency and htn.
Polyuria and nocturia


Kidneys are small with broad irregular cortical scars and deformed blunted calyces

Front 102

Neoplasms

Back 102

Transitional cell carcinoma
Cigarette smoking
Exposure to dyes
Chronic mucosal irritation
• Painless hematuria
• Generally asymptomatic

Males 3:1
Multifocal

Front 103

Renal cell carcinoma

Back 103

May be asymptomatic until tumor is bigger
May have hematuria with or without a palpable mass
Paraneoplastic effects: polycythemia, hypercalcemia, htn
Most frequent form of renal cancer in adults 2:1 males
60-70 yrs
Tumor is solitary, bulky, unilateral, yellow w/ foci of necrosis and hemorrhage
Nephrectomy is tx of choice
Metastisis mostly in lung and bone

Front 104

Wilms' tumor

Back 104

Present as abd swelling or lrg unilateral masses w/ or w/out abd pain and gross hematuria


--------------------
Most common primary renal malignancy of childhood

Used to be uniformly fatal
Metastasis to lung and liver

Front 105

Transitional cell carcinoma

Back 105

Arises from epithelium which lines the calycs and pelvis of the kidney
b/c of location, tend to produce early hematuria, so identified earlier than renal cell carcinoma


Presence of multicentric lesions suggests this may be effects of a carcinogen in urine
Multifocal tumors in urinary tract

Front 106

Acute renal failure

Back 106

Acute tubular necrosis
Ischemic or toxic damage to renal tubules
Onset begins 24-36 hrs after initiating insult
Oliguria
Decreased blood filtration by glomeruli leads to fluid overload, uremia, electrolyte retention


dialysis
During recovery may have large amounts of urine output before fx returns to normal

Front 107

Chronic renal failure

Back 107

Azotemia, htn

Uremic syndrome: "urine in blood", leads to disfx of multiple organ systems, depression of CNS, and coma