CIS questions Flashcards
what is the name of the process that gives the appearance of cachexia?
atrophy
chemical mediator that leads to cachexia?
TNF
elevated TNF-alpha:
-increased gluconeogenesis, lipolysis and proteolysis
- decreased protein, lipid and glycogen synthesis
- decreased appetite and early satiety
precocious puberty
pathologic hypertrophy and hyperplasia
defined as puberty with breast development in a girl less than 6-8 years of age
aging process in breast tissue?
atrophy physiologic
with aging there is a lot of deposition of fat instead of fibrous tissue
process in pregnancy in the breast
physiologic hyperplasia (lobular)
colonic polyps
what is the process occurring
pathologic hyperplasia
what is the name of the process that gives overall expansion of the subcutaneous tissue - obesity
hyperplasia and hypertrophy of the adipose tissue
name the processes that will occur in a fractured area? (3)
necrosis
inflammation
repair
fat cells acquired at an early age….
are there for life
2 month history of left arm pain and associated painful hard mass in his arm
what is the diagnosis
what process gave rise to this lesion
calcified mass inside of muscle on histology
the histo stain shows –> calcium which stains blue so it shows bony spicules
diagnosis- myositis ossificans
process:
-inflammation, hyperplasia, metaplasia
myocytes are terminally differentiated
what cells give rise to myocytes in injury
satellite cells
2 hour history of chest pain left arm pain mild difficulty breathing diaphoresis becomes unresponsive stops breathing no palpable pulse
ECG reveals ventricular fibrillation
diagnosis
process?
MI
ischemic cell injury
decrease in oxidative phosphorylation
leads to decrease in ATP:
-rigor (b/c you can’t relax)
-decreased Na pump–> swelling
- membrane injury–> leakage of enzymes (CK, LDH, increase in ca2+ influx)
- lipid deposition (b/c there is decreased protein synthesis)
- clumping of nuclear chromatin
blebs
what occurs in the first 24 hours in a MI
changes only at the cellular level:
reversible:
-sarcoplasmic edema
-mild swelling of mitochondria
irreversible:
20-30 min of ischemic time***
markedly swollen mitochondria
amorphous Ca2+ deposits in mitochondria from Ca2+ influx
nuclear clumping and margination of chromatin
muscle fiber:
wavy muscle fibers**
deeply eosinophil (red) ** by end of day 1 due to low pH (4-24 hours)
proteins at low pH precipitate so stain is picked up much better
few neutrophils (12-24 hours)
enzyme:
CK around 2 hours
how the neutrophils get to the infarct?
what is the process
stasis
margination
rolling via selectins (upregulated by cytokines)
activation (via cytokines)
adhesion via integrins
diapedesis- across endothelium, BM and into tissues
migration
why does protein denaturation happen in an acute MI
this is because there is hypoxia/ischemia
so there is a build up of lactic acid b/c of glycolysis
the low pH causes protein denaturaiton and makes the cells very eosinophilic (red)
what nuclear change is predominately present in myocytes in an MI
karyyolysis
what nuclear change is present in the neutrophils in an MI
karyorrhexis
what occurs 1-3 days out in acute MI
what cells are present
what happens to myocytes
PMN’s attracted to necrotic myocytes
neutrophils reach maximum levels at 2-3 days***
begin to undergo karryorhexis
myocyte necrosis more prominent
-nuclei disappear
striations less prominent
do enzymes go up with apoptosis of hepatocytes?
yes!
as well as with necrosis
3-10 days out after acute MI
what cells and tissues are present
shift from PMN’s to chronic inflammatory cells
-macrophages digesting dead muscle fibers
lymphcoytes
- granulation tissue***
- proliferation of fibroblasts that begin to lay down collagen
- vascular proliferation
10-14 days after acute MI
what is present
scar tissue replaces granulation tissue from periphery inward
what would you see in an 8 hour old MI
coagulative necrosis with wavy fibers
hypereosinophilia
increased space b/w the myocytes b/c edema/transudate (fluid separating the cells)
2-8 week old MI
more recessation of infallmation
increased collagen
small capillaries that developed with early granulation tissue disappear
8 week old MI
dense scar
what do you see in a viral infection of the heart
lymphocytic myocarditis (infiltrate of lymphocytes rather than neutrophils)
dry gangrene is a type of what necrosis
coagulative necrosis
no inflammatory cells
what do you see in the periphery in liquefactive necrosis
macrophages eating brain stuff (fat mostly)
in what type of fat necrosis do we typically see saponification
pancreatitis
b/c we need the enzymes to break down the fat to combine with the calcium salts
what is the properties required of malignant cells in order to invade and spread to single cells?
collagenase
must lose their adhesive molecules and detach from neighbors
what is the adhesion molecule classically lost in lobular carcinoma of the breast?
E-cadherin
in the breast lobular is distinguished from ductal b/c ductal doesn’t invade as single cells and don’t lose e-cadherin
what is the function of cadherins and integrins ?
specifically cadherins, what cells do they interact with?
cadherins and integrins link cell surface to the cytoskeleton
cadherin. is calcium dependent adhesion protein
participates in interactions between cells of the same type
connect plasma mebmranes of adjacent cells
found in zonula adherens and desmosomes
overdose on paracetomal (Acetominophen)
nausea and right upper abdominal pain
slightly icteric
bile present in the urine
began
hyperventilating
markedly icteric
died
labs: low blood glucose WBC high ALT high bili high
diagnosis?
what process occurred ?
acetaminophen intoxication
process occurred:
chemical cell injury (necrosis)
Acetominophen reduces glutathione
leads to ROS and Nitrogen species that cause oxidative stress
alterations in calcium homeostasis
initiation of signal transduction responses
mitochondrial permeability transition
loss of mitochondrial membrane potential–> loss of ATP production–> necrosis
man with hemoptysis
smoker
losing weight
chest x-ray shows white stufff
diagnosis?
what process gives rise to this process?
what tests should be done next?
TB
process: necrosis
caseating epitheloid granulomas with langhan-type giant cells
take sample of sputum
biopsy
Ziehl-Neelson stain (AFB stain)
showing acid fast bacteria as little red strings
cellulitis is what type of inflammation
purulent suppurative inflammation
what are the 5 types of purulent/suppurative inflammation?
1> cellulitis
- lymphangitic
- abscess *large collection of neutrophils
- ulcerative
- pseudo membranous
what is the subtype of serous inflammation
urticarial
18 month old boy recurrent severe bacterial skin infections lymphadenopathy hepatosplenomegaly foci of skin hypopigmentation silvery hair noted
what do you do next?
Chediak-Higashi syndome
on peripheral slide:
giant granules in neutrophils
anemia-> red blood cells are destroyed
what is defective in chediak higashi syndrome ?
autosomal recessive
defective:
lysosomes of leukocytes leading to infections
dense bodies of platelets leading to bleeding
melanosomes leading to hypopigmentation
neurons leading to cognitive impairment and peripheral neuropathy
The gene LYST codes for lysosomal trafficking and regulator protein associated with microtubule formation
treat–> hematopoietic stem cell or bone marrow transplantation
42 year old male
SOB
doused by formaldehyde
breathing improved but then 2 hours it became suddenly much worse
the patient expired
diagnosis?
etiology?
acute respiratory distress syndrome (hyaline membrane disease)
etiology:
chemical injury
protein leaked out, precipitated on the alveolar membranes–> now oxygen exchange cannot occur
what is acute respiratory distress syndrome characterized by
high levels of IL-1 and TNF
diffuse damage to alveolar walls- capillaries
marked increase in vascular permeabiltiy with protein-rich exudate into alveolar spaces which later form hyaline membranes
decreased diffusion capacity, hypoxia
often results in death or heals with scarring
congo red stain
amyloid is a series of proteins that pick up congo red stain
apple green birefringence is a diagnosis of amyloidosis
viral illnesses such as influenza often produce chronic inflammation that shows up as what in the lungs
interstitial infiltrates ** non productive cough
NOT pleural effusions (this is more seen with heart failure, neoplasia or empyema)
what is the difference b/w viral and bacterial inflammatory response?
viral–> lymphocyte infiltrates
bacterial–> neutrophil infiltrate
anthracotic pigment
black color comes from carbon pigments in dust particles inhaled over many years, engulfed by macrophages and sent via lymphatics to the lymph nodes
looks bad but does not compromise lung function.
smokers have more of this
what color are metastatic lesions?
firm and white
what are russel bodies
intracellular accumulations of immunoglobulins in plasma cells
what might happen in Vitamin A deficiency to the lungs
Vitamin A is necessary to maintain epithelia, and squamous metaplasia of the respiratory tract may occur if there is vitamin A deficiency. The stratified squamous epithelium does not function as well as the normal pseudostratified columnar respiratory epithelium, and there is an increased risk for respiratory infections.
if someone has a traumatic blow to their arm and 3 months go by and they have pain and tenderness and an x-ray that shows brightness what is wrong?
myositis ossificans –> calcification from osseous metaplasia of CT that developed in the healing process
is nuclear pyknosis reversible?
no its irreversible
whereas nuclear chromatin clumping is reversible
trauma to the breast can result in what finding on biopsy
fat necrosis
IL-10
also dampens immune response
