Review Flashcards
1
Q
Aphthous Ulcers ( Canker Sores)
A
Small, painful, shallow ulcers
2
Q
Canker sores triggers
A
stress, fever, ingestion of certain foods, activation of inflammatory disease
3
Q
Canker Sores clinical course
A
self-limiting, usually heals without scarring but may recur in same/different location
4
Q
What are canker sores covered by?
A
covered by fibrinopurulent exudate with underlaying infiltrate with mononuclear and polymorphonuclear leukocytes
5
Q
Leukoplakia what is it? where is it found? How does it look like?
A
preneoplastic epithelial lesion— well-defined, demarcated.
Found on buccal mucosa, tongue, floor
A white plaque that cannot be scrapped off or identified as other disease
6
Q
leukoplakia association
A
tobacco, pipe smoking, smokeless tobacco
7
Q
Banal hyperkeratosis
A
varies from leukoplakia ( no underlying dysplasia to mild/sever dysplasia, potential carcinoma in situ)
8
Q
Can leukoplakia go through malignant transformation?
A
Yea, to squamous cell carcinoma in 3-25%
9
Q
Erythroplakia
A
red-equivalent to leukoplakia.
less common
10
Q
Erythroplakia can go through malignant transformation?
A
Yea, greater than 50%
11
Q
how does eythroplakia looks like?
A
red, velvety, often granular, circumscribed
12
Q
Pleomorphic Adenoma
A
Most common salivary gland tumor esp. in superficial parotid gland
13
Q
can pleomorphic adenoma be surgically removed?
Can a malignant mixed tumor arise?
A
yea, but may recur
yea, it has a 30-50% year mortality rate
14
Q
Pleomorphic Adenoma characteristics
A
admixture of epithelial and stromal elements (heterogeneity)
Forms slowly growing, painless, movable, encapsulated firm mass with smooth surface
15
Q
Mucuoepidermoid Carcinoma
A
most common primary malignant tumor of the salivary glands
malignant salivary gland tumor with neoplastic epidermal cells, mucus secreting cells, and epithelial cells of the intermediate type
16
Q
Where does the mucuoepidermoid carcinoma originates? How is the differentiation?
What are the ‘nests’ composed of?
A
originates in the ductal epithelium
differentiation variable and clinical course depends on grades
‘Nests’ composed of squamous cells as well as clear vacuolated cells with mucin.
17
Q
Esophageal varices: causes? clinical?
A
dilation of esophageal and periumbilical veins dues to portal hypertension
causes cirrhosis and portal hypertension, often diue to alcohol abuse.
Hepatic schistosomiasis is the second most common cause of varices
varices greater than 5mm prone to rupture, leading to life-threatening hemorrhage
18
Q
what are esophageal varices?
A
dilated veins beneath the mucosa with a tendency to rupture and hemorrhage due to extra blood volume, connecting the intra-abdominal and systemic venous circulation
19
Q
cancers of the esophagus?
A
1) adenocarcinoma
2) squamous cell carcinoma
20
Q
adenocarcinoma of the esophagus
A
occurs in the Distal end!
- Risk with dysplasia, tobacco use, obesity, radiation, therapy.
- Fresh fruits/veggies lower risk
- Pain/difficulty, progressive weight loss, hematemesis, chest pain, vomiting.
- usually has spread to submucosal lymphatics upon discovery
- 5 year survival rate is less than 25%
21
Q
Squamous cell Carcinoma of the esophagus
A
- occurs in MIddle Third where it commonly causes strictures
- Risk from alcohol and tobacco, esophageal injury, achalasia, radiation therapy.
- Begins as squamous dysplasia
- ranges from well-differentiated with epithelial pears to poorly differentiated tumors
- presents with dysphasia (difficulty in swallowing), but by time of discovery, tumors are unresectable
22
Q
Gastric cancer
A
- mainly adenocarcinomas
- many environmental/dietary factors are associated
- loss of E-cadherin function seems to be a key step
23
Q
what are the the two types of Adenocarcinomas of gastric cancer?
A
1) Intestinal type
2) Diffuse (Infiltrating) type
24
Q
intestinal Type gastric cancer
A
Bulky tumor composed of glandular structures, elevated mass with heaped-up borders and central ulcerations.
predominant in high risk area and develops from precursor lesions including dysplasia and adenomas.
Depth of invasion and extent of metastasis (staging) most powerful prognostic indicator for gastric cancers.
Remarkable decrease in gastric cancer only applies to intestinal type
25
Diffuse (Infiltrating) Type gastric cancer
no true tumor seen--- Do not form glands
Large mucin vacuoles that expand cytoplasm and push nucleus to the edge, looking like a "signet-ring"
evoke desmoplastic reaction that stiffens gastric wall. Rigid thickening of wall of the whole stomach creating the appearance of a water bottle ---Litinis plastic
26
Barrett Esophagus: cause? clinical?
metaplastic replacement of squamous epithelium by columnar epithelium
cause: results from gastroesophageal reflux--- involves lower third of esophagus
clinical: increases risk of esophageal adenocarcinoma-- 30-100x greater risk
27
barret esophagus morphology
"intestinal metaplastic epithelium" goblet cells with gastric foveolar cells
Dysplasia classified low or high grade
28
Sialadenitis: what? cause? clinical tx?
inflammation of the salivary gland
cause: mucocele (blockage/rupture of salivary gland duct often due to trauma)
clinical tx: excision of cyst with the minor salivary gland
29
Sialadenitis Morphology
cyst-like space with inflammatory granulation tissue filled with mucin and macrophages
30
Acute gastritis: what? cause? associated with? clinical?
acute mucosal inflammatory process, usually transient with mucosal necrosis
cause: disruption of mucosal layer, stimulation of acid secretion, decreased bicarbonate production, reduced mucosal blood flow, direct epithelial damage
Associated with: NSAID, aspirin, alcohol, smoking, chemo, ischemic injury
clinical: complete restitution if stimulus removed
31
Acute gastritis morphology
localized or diffuse superficial inflammation---concurrent erosion and hemorrhage. mucosal edema and inflammatory infiltrate of neutrophils and chronic inflammatory cell
32
Celiac Disease: what? characterized by? diagnosis based on?
immune response to Gluten. Gliadin particles interact with immune system leading to killing of eneterocytes and damage to mucosal epithelium
characterized by: generalized malabsorption mucosal lesions
Diagnosis based on: prompt clinical/histological response withdrawal of gluten containing foods.
33
Celiac Disease histology
atrophy/loss of villi. eosinophils in lamina propria but not deeper
34
Pseudomembranous colitis: what? causes(4)?
classic example of infectious enterocolitus
caused by: C. difficile--following administration of antibiotics, resulting in cytotoxin release.= causes
(1) disruption of epithelial cytoskeleton,
(2) tight junction loss,
(3) cytokine production, and
(4) apoptosis
35
what is pseudomembrane?
is adhesion of fibrinopurulent debris and mucus to damaged superficial mucosa
36
Pseudomembranous colitis histology
denuded with an infiltrate of neutrophils-- superficially damaged crypts with exudate released resembles a "volcano"
37
Crohn diseases Vs Ulcerative colitis
Crohn: chronic, segmental, transmural inflammation of the intestine
Ulcerative colitis: chronic, superficial inflammation of the colon and rectum
38
Crohn disease vs ulcerative disease? location?
Crohn: principally in distal small intestine but can be anywhere in digestive tract and discontinuous "skip lesions"---colon particularly the right one can be affected
ulcerative colitis: continuos colonic involvement beginning on the rectum---limited to the colon and rectum
39
Crohn's disease histology
affects all wall layers (transmural inflammatory disease.) Granulomas in 40-60% of cases
early lesions as aphthous ulcers which later become deeper and look like fissures
40
ulcerative colitis histology: name and describe the 3 stages.
Early: mucosal surface raw, red, granular, crypt abscesses dilated with crypt filled neutrophils
Progressive: mucosal folds are lost. Fragments of mucosa between ulcers form pseudopolyps -- granulation tissue is denuded areas but no stricture.
Advanced: large bowel shortened. Mucosal folds indistinct. mucosa atrophied
41
Crohn vs Ulcerative colitis: clinical
Crohn: abdominal pain and diarrhea, colonic bleeding and intestinal obstruction and fistulas
Ulcerative colitis: diarrhea, rectal bleeding (risk of moderate anemia) with intermittent attacks.-- Severe colitis occurs with 20 bloody bowl movement daily with massive hemorrhage being life threatening
Toxic megacolon-- extreme dilation of colon and risk of perforation (dangerous complication)
42
Crohn vs Ulcerative colitis: neoplastic pottnial
Crohn: predisposition to colorectal cancer
ulcerative colitis: higher risk of colorectal cancer than general population
43
Colorectal cancer: what? risk? clinical?
mostly adenocarcinomas-- A classical example of neoplastic progression with multistep carcinogenesis
two possible mechanisms involved
risk factors: age, chronic inflammatory bowel disease, diet, genetics
clinical: occult blood in the stool, iron deficiency anemia, obstruction.--- Metastasis through direct extension or vascular/lymphatics invasion (particularly for liver)
44
polyps of the small and large intestines
non neoplastic or premalignant lesions within the mucosa
| neoplastic potential: some hyperplastic polyps on the right side of the colon are precursors to colorectal cancer
45
villous adenoma (polyps)
a) large, broad based elevated lesions made of thin, tall finger like processes that superficially look like villi.
b) Variable degrees of dysplasia.
c) Foci of carcinomas occur more often than tubular type
d) >1/3 resected villous adenomas contain invasive carcinomas
46
Tubular Adenomas (polyps)
a) smooth surface lesions with as stalk covered by normal colonic mucosa
b) Head has neoplastic epithelium with branching glands
c) All degrees of dysplasia can be encountered from contained cancer in mucosa to invasive carcinoma in submucosa
d) Cancer risk correlates to size
47
Histogenesis of the polyps
non-neoplastic type occurs sporadically and increase in frequency with age. Most are hyperplastic polyps... adenomatous type arises from mucosa
48
jaundice: what? possible causes?
retention of bile results from abnormal processing of bilirubin and its retention (bilirubin metabolism:production, uptake, conjugation and transport.)
possible causes of hepatocellular jaundice: anything that interferes with uptake, conjugation, and transport
other plausible causes: excessive production, impaired excretion, obstruction
49
Cholestasis: cuases?
systemic retention of bilirubin and other solutes eliminated in the bile due to decreased bile flow through canaculi, reducing secretion of water, bilirubin, and bile acids
causes: intrinsic liver disease (intrahepatic cholestasis), obstruction of bile ducts (extrahepatic cholestasis)
50
Cholestasis histological changes
presence of brownish pigment within dilated canaliculi and hepatocytes ot "bile lakes"
bile ductular proliferation,edema, bile pigment retention, inflammatory infiltrate
51
what is the diagnosis of cholestasis?
elevated serum alkaline phosphatase
52
Portal hypertension
often caused by cirrhosis; severely compromises ability to deliver blood, leading to blood flow to other locations. causes esophageal varices, ascites, and splenomegaly among other factors.
53
esophageal varices
"caput- Medusae" collateral veins of lower esophagus and upper stomach used and dilated. Rupture can lead to death
54
Ascites
accumulation of fluid from not enough albumin produced by liver leading to decreased oncotic pressure. Liver "weeps" lymph into abdomen. Renal retention of sodium and water.
55
Splenomegaly
hypertrophy of spleen- decreased life span and reduction of red/white cells. Spleen is firm, large. uniformly deep red with inapparent white pulp
56
what are the result of hypodonagium in women?
oligomenorrhea, amenorrhea, and sterility are frequent
57
Acute/ Chronic hepatitis
infection of hepatocytes by hepatotropic viruses named from A to G that produce necrosis and inflammation
58
Acute Hepatitis morphology (4)
(1) Scattered necrosis of single cells.
(2) ballooned hepatocytes (degeneration involving diffuse swelling of cells).
(3) Councilman bodies (apoptotic liver cells that are small, deeply, eosinophilic.)
(4) Infiltration of macrophages.
Cholestasis is common.
Regenerative changes
59
Chronic Hepatitis morphology (4)
(1) Piecemeal periportal necrosis (fragmented necrosis that looks like it was "moth-eaten",
(2) intralobular and portal tract inflammation,
(3) bridging necrosis (formation of connective tissue septa between adjacent portal tracts),
(4) ground-glass hepatocytes (have large granular cytoplasm with HBsAg)
60
Alcoholic hepatitis: name the three morphologic and clinical entities
alcoholic liver disease
1) Fatty change: acculumulation of fat in hepatocytes steatosis
2) Hepatitis: necrosis of hepatocytes in the central zone, cytoplasms hyaline inclusions hepatocytes
3) Mallory bodies" alcoholic hyaline, collagen deposition around central vein
Cirrhosis
61
Hepatocellular Carcinomas
malignant primary tumor derived from hepatocytes. one of the most common worldwide tumors which appears as a soft, hemorrhagic mass in the liver
62
Hepatocellular Carcinoma association? histology?
- Associated with HBC, HCV, metabolic conditions (hemochromatosis dues to iron helping with free radical production, cirrhosis) and environmental agents (alpha-toxin B1)
- Histology variable--will try to invade vascular channels
-Alpha-fetoprotein is a tumor marker
prognosis is dismal
63
Cholelithiasis
- Gall stones
| - presence of stones within lumen of gall bladder or extra-hepatic biliary tree
64
composition of Gall stones
1) most gallstones are composed of cholesterol
| 2) pigmented gallstones are composed of calcium bilirubinate or other calcium salts
65
Cholecystitis
- Gall bladder inflammation
| - Usually secondary to obstruction by gall stones
66
Cholecystitis chronic (3)
1. thickening of muscular wall,
2. presence of chronic inflammatory cells.
3. mucosa ulcerated and atrophic or may be intact
67
Cholecystitis Acute (2)
1. neutrophils in epithelium and lamina propia,
| 2. mucosa fiery red to purple
68
Ischemic Bowel disease
- injury from decreased intestinal blood flow.
| - Acute intestinal ischemia is the most common type
69
three levels of severity of IBD
1) mucosal
2) mural
mucosal/mural secondary to acute/chronic hypo-perfusion
3) transmural infarcts- due to acute occlusion
70
IBD predisposing conditions
a) Obstruction: atherosclerosis, aortic aneurysm, hypercoagulable states, oral contraceptive use, embolization of cardia vegetations, aortic atheromas
b) Hypoperfusion: Cardiac failure, shock, dehydration, vasoconstrictive drugs, systemic vasculitides, portal hypertension, compression by masses
71
IBD results
- a range from mucosal necrosis to transmural bowel infarction.
- Occlusion of one of the three major vessels may lead to extensive infarction, although rich anastomoses may prevent affect
72
Cirrhosis
End stage of chronic liver disease characterized by bridging fibrous septa, parenchymal nodules, and disruption of the normal architecture of the entire liver
73
What happens in Cirrhosis (3)
1. death of hepatocytes,
2. extracellular matrix deposition,
3. vascular reorganization
74
Clinical Cirrhosis
silent, but symptoms may be anorexia, weight loss, weakness, and in advanced disease, frank debilitation.
Ultimately leads to death through liver failure, portal hypertension complication, or hepatocarcinoma
75
Cirrhosis morphology
a) type I and III collagen deposited in space of disse, vascular architecture disruption leading to scarring, shunting of blood, loss of fenestration, impairment of exchange.
b) Fibrosis due to proliferation of hepatic stellate cells activated to become myofibroblasts
c) Nodule formation from surviving hepatocytes stimulated to regenerate rather than normal "pineapple" shape
76
Pancreatitis
injury to acini cells in the exocrine portion of the pancreas leading to an inflammatory reaction
77
Acute pancreatitis
varies from mild. self-limited with inflammation and stromal edema to severe, acute hemorrhagic disorder . dystrophic calcification
will return to normal if cause is removed
78
Chronic pancreatitis
results from repeated acute pancreatitis leading to recurrent attacks of severe abdominal pain, progressive fibrosis, and pancreatic insufficiency
79
Causes of pancreatitis
1) inappropriate activation of pancreatic enzymes- injuries to acinar cells lead to trypsin activation leading to proteolytic enzyme activation. tissue destruction and fat necrosis
2) overwhelmed anti-activation mechanisms
3) secretion against obstruction: any condition that narrows the pancreatic duct or prevents outflow of enzymes (ex. neoplasms, anatomical anomalies) leading to inappropriate activation
4) gallstones: 45% pts with pancreatitis have them, sick 25x higher than general population---not always seen though
5) alcohol consumption: 1/3 cases associated in acute, ethanol possibly causing spasm or acute edema. may stimulate secretion from intestine, triggering release of pancreatic juice
6) other: viral infection, drugs, trauma
7) unknown causes: 10-20%
80
pancreatitis: macroscopic changes
fat necrosis, chalky calcium deposits, hemorrhage
81
Pancreatitis: Microscopic changes
Acute: fat necrosis, calcium deposits, saponification, destruction of blood vessels leading to hemorrhage, parenchymal destruction, inflammatory response, edema, acini cell necrosis
Chronic: fibrosis, reduction in functional parenchyma (endo-exocrine components reduced in number/size, acinar and islet size) ducts dilated
82
pancreatitis clinical
acute: severe upper back pain, nausea and vomiting, vascular collapse/shock, elevated serum amylase/lipase. Gram-negative bacteria infection. Usually mild/self-limiting, but 20% severe and a medical emergency
Chronic : repeated episodes of acute pancreatitis in 5% of pts. Continuos/intermittent pain wight loss, jaundice , calcification is visible in radiographs
1/5 pts die
83
Serous Cystadenomas
1/4 of all pancreatic cystic adenomas
- Glycogen rich cuboidal cells surrounding cysts with clear, straw-colored fluid.
- Begins in 7th decade of life: female/male ration of 2:1
84
Mucinous Cystic adenomas
cystic tumor with thick mucin --- almost always in women
85
mucin. cystic adenomas found in?
in body or tail
86
Mucin. cystic adenomas tumor
is a cystic space filled with thick, tenacious mucin. lined by columnar mucinous epithelium with dense cellular stroma
87
can Mucin cystic adenomas be benign, borderline malignant or malignant ?
Yea
88
Insulinomas
most common islet cell neoplasm--most are benign lesions in the body/tail
89
describe the clinical aspect of insulinomas
severe hypoglycemia, sweating, nervousness, hunger eventually becoming confusion, lethargy, and coma--- high levels of insulin in blood and tumor cells
90
morphology of insulinomas
resemble normal beta cells but form trabecular and solid patterns---- amyloid found in stroma
91
islet cell tumors name (5)
account of 10% of pancreatic neoplasms
| (1) gastrinomas (2) Glucagonomas (3) somatostatinomas (3) vasointestinal (5) insulinomas
92
gastrinomas
G cells--- intractable gastric hypersecretion leading to peptic ulceration of duodenum and jejunum--most more malignant
93
glucagonomas
Alpha cells--- mild diabetes, necrotizing migratory, erythematous rash, anemia, venous thrombosis
Glucagon levels 30x higher than normal 2/3 malignant
94
Somatostatinomas
delta cella--- mild diabetes, gallstones, steatorrhea--- most malignant
95
Vasointestinal polypeptide secreting tumors (VIPoma)
elevated levels of VIP. Explosive diarrhea
| Most malignant
96
Pancreatic Cancer
4th most common cause of cancer death-- 5 year survival rate of 5%--- occurs later in life
97
90% of all pancreatic cancers
Ductal adenocarcinoma
98
Pancreatic cancer: Where is it found? give me %?
1) head- 60%
2) body- 10%
3) tail- 5%
rest is diffused
99
do cancers of the body and tail impinge on the biliary tract?
nope
100
pancreatic cancers association?
a) smoking- 25% of cases
| b) 80% of patients with pancreatic, evidence of DM (increased risk)
101
Pancreatic cancer: classical neoplastic progression name (4)
```
accumulation of mutations:
i) K-RAS
ii) p16 gene
iiI) SMAD4
iv) p53
```
102
p53 (PC)
tumor suppressor gene inactivated in 50-70% of cases
103
SMAD4 (PC)
- tumor suppressor gene inactivated in 55% of cases
104
p16 (PC)
most frequently inactivated tumor supressor gene
105
K-RAS (PC)
most frequent altered oncogenes
106
Pancreatic cancer clinical (4)
1. jaundice,
2. migratory thrombophlebitis especially in body/tail adenocarcinoma (paraneoplastic syndrome related to hyper-coagulability)
3. early metastasis: by the time of diagnosis.
4. Courvoisier sign-- acute, painless gallbladder dilation accompanied by jaundice due to bile duct obstruction by tumor
107
Oral thrush
a fungal infection of the oral cavity resulting in a scrapable, white plaque
108
what causes oral thrush?
Caused by candida albicans in combination with some impairments of usual protection such as diabetes mellitus, anemia, antibiotic/glucocorticoid therapy, HIV infection, disseminated cancer
109
how does it oral thrush looks like?
white, circumscribed plaque-- pseudomembrane of fungal organisms superficially attached (and thus can be scrapped off)
110
Can oral thrush spread to esophagus?
Yea, life threatening if disseminated
111
xenobiotic metabolism
intake of chemicals which further become metabolized either to safe or unsafe forms
112
how are exogenous chemicals absorbed?
through inhalation, ingestion, skin contact
113
chemicals
can be excreted or can accumulate
114
most solvents and drugs are
lipophilic
115
cys p450
the most !. detoxifies or activates xenobiotics in phase I.
| Variations in individuals can be due to induces or genetic polymorphisms
116
What does grapefruit do?
it inactivates Cyp3A4 in intestines reducing metabolism of some oral drugs and increase bioavailability
117
Phase I of xenobiotic metabolism
hydrolysis, oxidation and reduction resulting in "primary metabolite"
118
Phase II of xenobiotic metabolism
conversion into water soluble compounds by glucoronidation, sulfuration, methylation, conjugation with glutathione
readily excreted
119
lead
chemical which interferes greatly with skeletal, blood, renal system, and especially neuro system
120
is air pollution classified a carcinogen?
yep
121
lead in children
major hazard
| causes central effects: low IQ, behavioral problems, generally irreversible.
122
what is the maximum allowable for lead?
10 ug/dL but subclinical lead poison may happen in children with less than 10
123
in adults with lead poisoning
peripheral neuropathies predominante
124
effects in lead poisoning in skeletal system
interferes with normal remodeling, resulting in "lead lines" along the epiphyses, cartilage mineralization delayed
125
effects in lead poisoning in hematopoietic
microcytic, hypo-chromic anemia. Basophilic stippling (dotting of RBC). hemolytic anemia due to increased fragility of cell membranes
126
effects in lead poisoning in Nervous system
brain damage, especially in children---peripheral neuropathies
127
effects in lead poisoning in kidneys
tubular damage
128
Tx. for lead poisoning?
Nope, only tx is to remove from source and chelation therapy for severe symptoms
129
alcohol
it is the cause and solution to all of life's problems
130
what happens to the liver with drinking alcohol?
fatty liver, alcoholic hepatitis, cirrhosis, portal hypertension, increased risk of hepatocellular carcinoma
131
alcohol can also result in
gastritis, gastric ulcers, peripheral neuropathies. cardiomyopathies, acute/chronic pancreatitis
132
alcohol increases risk of
cancers of the oral cavity, pharynx, larynx, esophagus
risk is greatly increased by concurrent smoking or use of smokeless tobacco
133
exogenous estrogens
administered for post-menopausal and for birth control
134
Oral contraceptives
major complications include thromboembolism, cardiovascular diseases, and hepatic adenoma
135
Hormone replacement therapy
used for distressing menopausal symptoms or to prevent/slow osteoporosis
increases risk of: endometrial carcinoma (mainly estrogen, less with estrogen and progesterone together) and breast cancer (estrogen and progesterone together) as well as thromboembolism
little evidence that it protects against MI
136
do burns depend on the depth of penetration in the dermis?
yea! there are three!
137
First degree burn
only epidermis is injured
138
second degree burn
necrosis extends to upper dermis but skin appendages such as hair follicle and sebaceous gland are spared
139
Third degree burns
necrosis extends to deep dermis, subcutis may be involved, skin appendages are destroyed
140
marasmus
calorie deficiency
141
what do you see in marasmus?
growth retardation
somatic protein affected result in muscle loss while visceral protein is barely reduced
serum albumin is normal
subcutaneous fat is mobilized
142
marasmus leads to
extremities thin and weak while head is disproportionately larger
anemia, multivitamin deficiencies, immun deficiency, concurrent infection
143
kwashiorkor
protein reduction rather than just total caloric reduction
144
in kwashiorkor
there is muscle mass and subcutaneous fat spared, visceral protein affected, resulting in hypoalbuminemia and consequent edema
145
we see in kwashiorkor
zones of hyperpigmentation in skin and hypopigmentation "flaky paint"
Hair changes: loss of color or pattern of pale and dark hair
loss of firm attachment to skull, straightened, fine texture
146
kwashiorkor results in
fatty liver, apathy, listlessness, loss of appetite--- sequelae are multivitamin D efficiency, immune deficiency, secondary infections
147
vitamin D deficiency
basic derangements for rickets and osteomalacia
148
rickets
children "bowing of legs"
149
osteomalacia
adults " unmineralized matrix"
150
Atelectasis
pulmonary collapse, inadequate expansion of airspaces
Hypoxemia- low arterial oxygen sue to shunting of the oxygenated blood from pulmonary arteries into veins
151
Resorption Atelectasis
obstruction of airway, collapse of alveoli distal to obstruction
152
Which atelectasis are reversible? which are not?
Reversible : Resorption and compression
| Irreversible: Contraction
153
Resorption atelectasis: causes and involves?
Causes: Mucus (CF), tumor (Mass Effect), foreign bodies (aspiration)
Involves: the entire lung, complete lobe, or one or more segments
154
Compression Atelectasis
external pressure leads to mechanical collapse
155
Compression atelectasis causes?
pneumothorax (air); hemothorax (blood); effusion (fluid); mass effect (neoplasm); Basal (posture)
156
Contraction Atelectasis
interstitial fibrosis interferes with expansion--- low compliance indicates a stiff lung
157
ARDS
progressive respiratory insufficiency caused by diffused alveolar damages in the setting of sepsis, severe trauma,and diffused pulmonary infections
"Shock lung"
158
Causes of ARDS
Shock, pneumonia with sepsis, endotoxins, near drowning, ischemia, aspiration
159
ARDS pathogenesis
- diffuse alveolar damage with endothelial/epithelial cell injury
- more pro than anti-inflammatory mediators activated
- Neutrophils
160
What are the two steps of ARDS progression?
1) Acute
| 2) Organizing
161
Acute ARDS
lungs dark red, airless, heavy
| Necrosis, edema, collection of neutrophils with alveolar ducts lined with hyaline membranes
162
Organizing ARDS
proliferation of type II pneumocytes and fibroblasts, removal hyaline membrane by macrophages
Resolution is unusual, and fibrin organizes leading to fibrosis
163
ARDS clinical
arterial hypoxemia, cyanosis, mult. organ failure
scarred lung--sequelae
Tx methods: mechanical ventilation for hypoxemia
164
obstructive airway disease
limitation of airflow -- increase in resistance by partial or complete obstruction
165
Obstructive disease examples
emphysema, chronic bronchitis, bronchiectasis and asthma
166
Obstructive disease characteristics
total lung capacity is normal
| decreased maximal airflow rates during forced expiration
167
Restrictive disease
reduced expansion of lung parenchyma accompanied by decreased total lung capacity
168
restrictive disease examples
1) chest wall disorder in the presence of normal lungs-- severe obesity, diseases of the pleura, neuromuscular disorders
2) acute or chronic interstitial lung diseases --- ARD, pneumoconioses, sarcoidosis
169
restrictive diseases characteristics
reduced total lung capacity
| expiratory flow rate is normal or reduced proportionately
170
emphysema
a form of COPD with irreversible airflow obstruction--- permanent dilation
alveolar wall destruction w/out fibrosis
overinflation
171
lobule
terminal bronchiole and distal structures
172
acinus
respiratory bronchiole and distal structures
173
what are the two types of emphysema
1) centriacinar
| 2) Panlobular
174
Centriacinar
most common, seen in smokers, upper lobes, and apical segments
distal alveoli spared!!
175
Panlobular
non-smokers, alpha-1-antrypsin deficiency, affects lower lung zones
176
emphysema pathogenesis
insufficient tissue repair---- inflammation because of cytokines, elstases, MMOs, oxidants
homeostasis imbalance between pro/anti- inflammatory mediators
177
Emphysema diagnosis
-expiratory airflow limitations
-"pink puffer"
barrel chested, pursed lips, hunched over
178
Emphysema complications
bullous formation, pulmonary hypertension, CHD, cor pulmonale
death due respiratory acidosis, right- side heart failure
179
Chronic Bronchitis
form of COPD with irreversible airflow obstruction
persistent cough
180
Chronic Bronchitis (4) morphology
(1) hyper-secretion of mucous
(2) hyperplasia/ hypertrophy of goblet cells
(3) Reid index increases
(4) inflammatory cells : mononuclear and neutrophils
181
Chronic bronchitis clinical
Productive cough
blue bloater- combination of cyanosis and edema
cor pulmonale
may be seen with emphysema
182
Asthma
form of Obstructive pulmonary disease with reversible airflow obstruction
183
asthma caused by?
reversible bronchoconstriction caused by airway hyper-responsiveness
184
Main features of asthma? (4)
1- intermittent/reversible
2- eosinophils
3- SMC hypertrophy/hyperactivity
4- airway remodeling
185
Differences between extrinsic and intrinsic asthma?
extrinsic- majority asthma cases, caused by Th2 and IgE
intrinsic- non-immune stimuli (aspirin, cold, stress...)
186
Asthma Morphology (5)
1. Mucus plugs
2. cellular infiltrate- eosinophils
3. curshmann spirals
4. charcot-leyden crystals
5. airway remodeling:
- thickening of BM
- edema
- increase of submucosal glands
- hypertrophy of walls
187
Asthma clinical
dyspenia w/ wheezing
difficulty in expiration
188
Bronchiectasis
permanent dilation of branchi and bronchiole--- destruction of SMC and elastic supporting tissues
189
Causes of bronchiectasis
bronchial obstruction such as tumors and foreign bodies
pneumonia- S. aureus
congenital/ hereditary conditions like cystic fibrosis
190
Morphology of bronchiectasis (5)
1) lower lobes
2) airways dilated
3) intense acute and chronic inflammatory
4) chronic cases lead to fibrosis
5) lung abscess may form
191
Bronchiectasis clinical
severe, persistent cough, expectoration, infection
192
restrictive lung diseases of diffuse interstitial (4)
restrictive disorders which affect lung movement during respiration
1. usual interstitial pneumonia
2. pneumoconioses
3. Asbestosis
4. sarcoidosis
193
usual interstitial pneumonia
idiopathic pulmonary fibrosis
pleura has cobblestones appearance
fibroblastic foci, honeycomb fibrosis
heterogeneity of both early and late lesions
clinical: dsypenia, cyanosis.. lung transplant only therapy
194
pneumoconioses
chronic interstitial restrictive pulmonary diseases caused by particle inhalation
reactivity depends on size, shape, solubility, reactivity
particles that are 1-5 um are the most dangerous b/c they get lodged at bifurcation of airways
most particles removed by mucociliary clearance
tobacco smoking worsens the effects of all inhaled mineral dusts
195
Asbestosis
classical example of pneumoconiosis:
| very fibrogenic particles
196
Morphology of asbestosis
diffuse interstitial fibrosis, asbestos bodies in the lungs--- iron-protein coat
golden brown stains w/ prussian blue
197
Asbestosis clinical
pleural plaques: well circumscribed of dense collagen
mesotheliomas: bronchogenic carcinomas, fibrosis, pleural effusions
cigarette smoking increases risk of lung cancer in comb. with this
worsening dspenia
198
sarcoidosis
non-caseating granulomatous diseases of type IV hypersensitivity: steroid bodies and shaumann bodies
199
in diffuse interstitial lung disease the ________ ________ ___ is involved
pulmonary connective tissue
200
Diffuse interstitial lung disease
- reduced compliance
- fibrosis may or may not see honeycombing
- presence of macrophages
- alveolitis is the initial manisfetation
201
Pneumonia name the two clasess
infection of the lungs
1) bronchopneumonia
2) lobar pneumonia
202
Morphology of lobar pneumonia (4) steps if not stopped with antibiotics
affects the entire lobe:
(1) congestion- lobes red, heavy and soggy. vascular congestion w/ proteinaceous fluid, neutrophils
(2) red hepatization- liver like consistency-- alveoli have neutrophils, red cells, fibrin
(3) gray hepatization- dry, gray, firm due to red cell lysing---- fibrinosuppurative exudate in the alveoli
(4) resolution- happens in uncomlicated cases--- exudate that was digested produced granular, semifluid debris that is reabsorbed and ingested by MQ or coughed up
203
Morphology of Bronchopneumonia (4)
(1) distributed in patches
(2) focal suppurative exudate
(3) complete restitution of tx properly
(4) complications: abscess, emphysema, organization, bacteremic dissemination
204
pulmonary neoplasms
lung is frequent site of metastasis---
| primary tumors are a leading cause of death
205
Bronchial epi. is site of ____ of lung carcinomas
95%
206
___ are miscellaneous bronchial carcinoids
5%
207
what are the four types of Carcinomas of the lung? name also the two therapies?
(1) squamous cell
(2) Adenocarcinomas
(3) large cell
(4) small cell
i. SCLC-- small cell, likely have already metastasized and it is treated with chemo
ii. NSCLC-- non-small cell, responds poorly to chemo and it better tx with surgery
208
Squamous cell carcinoma
3-% of lung cancers, arises in major bronchi and associated smoking
smoking forces regeneration in the form of squamous metaplasia and it follows same sequence of dysplasia (carcinoma in situ)-- metaplastic mucosa
209
Adenocarcinomas
1/3 of lung cancer and most common form of cancer in women and non-smokers
210
adenocarcinomas appears in the _____ and associated w/ ___ ____ and ___ ___, resulting in pleural ____
occurs in the periphery
ass. w/ pleural fibrosis and pleural scars
pleural puckering
211
adenocarcinomas characterized
moderate to well differentiated tumors--- mucin droplets in tumor cytoplasm
212
precursor of adenocarcarcinomas
atypical adenomatous hyperplasia -- prolif. of cuboidal to low columnar cells resembling clara/type 2 cells
213
small cell carcinoma
20% of lung cancers and strong assoc. w/ smoking
small cells w/ neuroendocrine features
highly malignant-- 70%
214
small cell carcinoma are assoc. with paraneopladtic syndromes except
hypercalcemia and hematologic type
215
Large cell carcinoma
10% of lung cancer, evolves from poorly differentiated adenocarcinomas/ squamous cell carcinomas
216
Bronchial carcinoids
low- grade malignant tumors (centrally located) composed of neuroendocrine cells though to arise from kulchitsky cells that line bronchial mucosa and resemble intestinal carcinoids
often resectable and curable
217
Large cell carcinoma have
large nuclei, prominent nucleoli and moderate cytoplasm
218
______ _______ epithelial tumors w/out cytologic features of small-cell and glandular or squamous differentiation
undifferentiated malignant
219
bronchial carcinoids appear at an ____ ____ and represent about ____ of pulmonary tumors
early age, 5%
220
bronchial carcinoids show no gender predilection? what about assoc, with smoking?
no gender p. and no assoc. with smoking
221
Bronchial carcinoids tumor cells
contain dense- core neurosecretory granules in the cytoplasm
test positive for : synaptophysin
most of the mare endocrinologically silent and rarely secrete hormonally active polypeptides
222
hypercalcemia most often encountered with
squamous cell neoplasams
| secrete PTH
223
hematologic syndromes encountered w/
adenocarcinomas
224
malignant mesothelioma
neoplasm of mesothelial cells in the pleura
combination w/ cigarette smoking does not increase meo but does carci
225
malignant mesothelioma assoc. w/
asbestos exposure
226
malignant mesothelioma have a ____ latency. The tumor cells often ______ and ______ the lung
latency, encase and compress "pleural rind' looks like an orange peel
227
malignant mesothelioma have
extensive pleural fibrosis and plaque formation and tx is largely ineffective and prognosis is poor
228
signs of cholestasis
jaundice, pruritus due to deposition of bile acid on skin
229
portal hypertension causes
Esophageal varices, ascites, splenomegaly
230
pseudocysts are a common aftermath of pancreatitis
they are delimited by Connective tissue with degraded blood, debris, necrotic pancreatic tissue
has no epithelial lining and may become infected
75% of all pancreatic cysts
231
Vitamin A is important for
vision, cell growt/ differentiation, metabolism, resistance to infection, photo-protection and antioxidation
232
Vit. A deficiency
leads to night blindness, dry eye, Bitot's spots (keratin debris plaques and keratomalacia (cornea erosion)
233
Vit. A def. principally results in _____ ______
Squamous metaplasia-- hyperkeratinization immune dificiency
234
Vitamin C
normally helps out with hydroxylation and amidation (collagen)
w/out, collagen is more vulnerable to enzymatic degradation-- functions as an oxidant
235
vit. C deficiency
impaired collagen formation leading to bleeding (poor vascular support), inadequate osteoid matrix formation and impaired wound healing
236
Malnutrition
inability/ insufficient intake of energy, amino acids, vitamins and minerals
237
protein compartments in the body are regulated separately name them and explain
1. somatic: proteins in skeletal muscles
| 2. Visceral: proteins in the viscera, primarily in liver
238
primary malnutrition
missing some component of appropriate diet
239
Secondary malnutrition
from nutrient supply sufficient but malabsorbed, impaired utilization or storage, excess nutrient loss or need for nutrients
240
hyperthermia
prolonged exposure to elevated ambient temperature can have detrimental effects on the body
241
Heat cramps
loss of electrolytes via sweating -- normal core temp, cramping of voluntary muscles during exercise
242
Heat exhaustion
sudden onset and collapse--- CV cannot compensate for loss of fluid---- equilibrium spont. reestablished
can progress to heat stroke
243
Heat stroke
heat regulation fails, sweating ceases, core temperature rises,
peripheral vasodilation, pooling of blood, decreased effective circulating blood volume
244
with hyperthermia can you have a change in mental status, arrhythmias, intravascular coagulation?
yep
245
hyperthermia can be a risk for
the elderly, people with CV disease, and healthy people doing stressful things
246
sialadenitis assoc. with
viral infection- paramyxovirus, mumps
bacterial infection- ductual obstruction
sjogren syndrome- dry eyes/ mouth; immunological destruction
247
colorectal cancer
mostly adenocarcinomas-- classical examples of neoplastic progression with multistep carcinogenesis
248
what are the two possible pathways involved in colorectal cancer
1. beta catenin
| 2. microsatellite instability
249
risk factors of colorectal cancer
age, chronic inflammatory bowel disease, diet, genetics
250
colorectal cancer clinical
occult blood in stool, iron deficiency anemia, obstruction-- metastasis through direct extension or vascular lymphatic invasion (part. in liver)
his friend that walks in boston commons got this!
251
acetaminophen
normally taken as a pain reliever, if overdoses metabolism can lead to toxicity
252
what is the antidote for acetaminophen?
N- Acetylcysteine which restores GSH
253
acetaminophen although generally detoxified by phase ___ enzymes, it is also metabolized by ____ which produces ____ which can be conjugated with _______
II, CYP2E1, NAPQ, glutathione- GSH
254
Depletion of reduced GSH results in
free radical damage and cell death leading to centrilobular necrosis of hepatic lobules
255
chronic gastritis
H. Pylori gastritis-- chronic inflammatory changes
256
what are the chronic inflammatory changes assoc. w/
mucosa leading to mucosal atrophy and epithelial metaplasia-- results from imbalance btw. gastroduodenal mucosal defenses and damaging forces tat overcome these defenses
257
cellular infiltrate of chronic gastritis
intraepithelial neutrophils and subepithelial plasma cells
258
over time in chronic gastritis, will extend to involve the bosy and funsus of the stomach and bc. ____. Assoc. w/ ____ with germinal centers can transform into ______
atrophic, MALT, lymphomas
259
Clinical Chronic Gastritis
combination Tx of antibiotic eliminate H.Pylori and proton pump inhibitors-- less acid
260
peptic ulcer disease
ulcers penetrate the mucosa, often as a result of H. pylory and NSAIDs
261
Peptic Ulcer dis. is seen in the ______ and _______ ( more common in later)
stomach and duodenum
262
peptic ulcer dis. gross
round to oval "punched- out" defect. Mucosal margin level w/ surrounding mucosa. base of ulcer smooth and clean, blood vessels may be evident
263
Peptic ulcer dis. histological
thin layer of fibrinoid debris w/ neutrophil infiltrate.
granulation tissue infiltrated with mononuclear lymphocytes and fibrous/ collagenous scar. vessels walls in the scar are thickened and thrombosed
264
Peptic ulcer dis. clinical
bleeding-- potentially life-threatening- perforation
265
herpetic stomatitis
common viral infection of the oral cavity
266
herpetic stomatitis caused by
HSV1 or HSV2
267
herpetic stomatitis mprphology
inclusion and polykaryons detected with Tzanck test---- vesicles filled with exudate
268
Cancers of the oral cavity and tongue
are mostly squamous cell carcinomas risk factors included tobacco
they are moderately to well- differentiated keratinizing tumors
"keratin pearls"--- early lesions
may progress to dysplasia
269
ionizing radiation
DNA damage through a direct/indirect effect with indirect effect creating free radicals
270
What can happen in ionizing radiation?
Damage DNA: rapidly dividing cells such as germ cell, bone marrow, GI sensitive to radiation.
inadequate repair of DNA can lead to neoplastic transformation
271
ionizing radiation factors influencing effects (5)
1. higher rate of cell turnover
2. vascular damage-- late manifestation--- replacement of fibrous tissue
3. rate of delivery-- single/fractional doses
4. hypoxic tissues more resistant
5. large/small doses more potent than small/large
272
Acute radiation syndrome
different modes of death dependent on radiation dosage
273
acute radiation syndrome- small dosage
hemopoietic-- 2 week latency, death in 3 weeks
kills bone marrow, resultant leukopenia,
274
acute radiation syndrome- medium dosage
intestinal- 3 day latency--- death in 2 weeks
GI epithelium necrosis and ulceration, infection, and diarrhea
275
acute radiation syndrome- large dosage
Cerebral- 1 hour latency-- death in 1 day
cerebral edema, neuronal necrosis, vasculitis, coma
