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PBD > CIS questions > Flashcards

CIS questions Flashcards

1
Q

what is the name of the process that gives the appearance of cachexia?

A

atrophy

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2
Q

chemical mediator that leads to cachexia?

A

TNF

elevated TNF-alpha:
-increased gluconeogenesis, lipolysis and proteolysis

  • decreased protein, lipid and glycogen synthesis
  • decreased appetite and early satiety
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3
Q

precocious puberty

A

pathologic hypertrophy and hyperplasia

defined as puberty with breast development in a girl less than 6-8 years of age

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4
Q

aging process in breast tissue?

A

atrophy physiologic

with aging there is a lot of deposition of fat instead of fibrous tissue

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5
Q

process in pregnancy in the breast

A

physiologic hyperplasia (lobular)

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6
Q

colonic polyps

what is the process occurring

A

pathologic hyperplasia

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7
Q

what is the name of the process that gives overall expansion of the subcutaneous tissue - obesity

A

hyperplasia and hypertrophy of the adipose tissue

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8
Q

name the processes that will occur in a fractured area? (3)

A

necrosis
inflammation
repair

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9
Q

fat cells acquired at an early age….

A

are there for life

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10
Q

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

A

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

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11
Q

myocytes are terminally differentiated

what cells give rise to myocytes in injury

A

satellite cells

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12
Q 
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?

A

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

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13
Q

what occurs in the first 24 hours in a MI

A

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

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14
Q

how the neutrophils get to the infarct?

what is the process

A

stasis
margination

rolling via selectins (upregulated by cytokines)

activation (via cytokines)
adhesion via integrins

diapedesis- across endothelium, BM and into tissues

migration

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15
Q

why does protein denaturation happen in an acute MI

A

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)

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16
Q

what nuclear change is predominately present in myocytes in an MI

A

karyyolysis

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17
Q

what nuclear change is present in the neutrophils in an MI

A

karyorrhexis

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18
Q

what occurs 1-3 days out in acute MI

what cells are present
what happens to myocytes

A

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

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19
Q

do enzymes go up with apoptosis of hepatocytes?

A

yes!

as well as with necrosis

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20
Q

3-10 days out after acute MI

what cells and tissues are present

A

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
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21
Q

10-14 days after acute MI

what is present

A

scar tissue replaces granulation tissue from periphery inward

22
Q

what would you see in an 8 hour old MI

A

coagulative necrosis with wavy fibers
hypereosinophilia
increased space b/w the myocytes b/c edema/transudate (fluid separating the cells)

23
Q

2-8 week old MI

A

more recessation of infallmation
increased collagen
small capillaries that developed with early granulation tissue disappear

24
Q

8 week old MI

A

dense scar

25
Q

what do you see in a viral infection of the heart

A

lymphocytic myocarditis (infiltrate of lymphocytes rather than neutrophils)

26
Q

dry gangrene is a type of what necrosis

A

coagulative necrosis

no inflammatory cells

27
Q

what do you see in the periphery in liquefactive necrosis

A

macrophages eating brain stuff (fat mostly)

28
Q

in what type of fat necrosis do we typically see saponification

A

pancreatitis

b/c we need the enzymes to break down the fat to combine with the calcium salts

29
Q

what is the properties required of malignant cells in order to invade and spread to single cells?

A

collagenase

must lose their adhesive molecules and detach from neighbors

30
Q

what is the adhesion molecule classically lost in lobular carcinoma of the breast?

A

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

31
Q

what is the function of cadherins and integrins ?

specifically cadherins, what cells do they interact with?

A

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

32
Q

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 ?

A

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

33
Q

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?

A

TB

process: necrosis
caseating epitheloid granulomas with langhan-type giant cells

take sample of sputum
biopsy

34
Q

Ziehl-Neelson stain (AFB stain)

A

showing acid fast bacteria as little red strings

35
Q

cellulitis is what type of inflammation

A

purulent suppurative inflammation

36
Q

what are the 5 types of purulent/suppurative inflammation?

A

1> cellulitis

  1. lymphangitic
  2. abscess *large collection of neutrophils
  3. ulcerative
  4. pseudo membranous
37
Q

what is the subtype of serous inflammation

A

urticarial

38
Q 
18 month old boy
recurrent severe bacterial skin infections
lymphadenopathy
hepatosplenomegaly
foci of skin hypopigmentation
silvery hair noted

what do you do next?

A

Chediak-Higashi syndome

on peripheral slide:
giant granules in neutrophils

anemia-> red blood cells are destroyed

39
Q

what is defective in chediak higashi syndrome ?

A

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

40
Q

42 year old male
SOB
doused by formaldehyde
breathing improved but then 2 hours it became suddenly much worse

the patient expired

diagnosis?
etiology?

A

acute respiratory distress syndrome (hyaline membrane disease)

etiology:
chemical injury
protein leaked out, precipitated on the alveolar membranes–> now oxygen exchange cannot occur

41
Q

what is acute respiratory distress syndrome characterized by

A

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

42
Q

congo red stain

A

amyloid is a series of proteins that pick up congo red stain

apple green birefringence is a diagnosis of amyloidosis

43
Q

viral illnesses such as influenza often produce chronic inflammation that shows up as what in the lungs

A

interstitial infiltrates ** non productive cough

NOT pleural effusions (this is more seen with heart failure, neoplasia or empyema)

44
Q

what is the difference b/w viral and bacterial inflammatory response?

A

viral–> lymphocyte infiltrates

bacterial–> neutrophil infiltrate

45
Q

anthracotic pigment

A

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

46
Q

what color are metastatic lesions?

A

firm and white

47
Q

what are russel bodies

A

intracellular accumulations of immunoglobulins in plasma cells

48
Q

what might happen in Vitamin A deficiency to the lungs

A

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.

49
Q

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?

A

myositis ossificans –> calcification from osseous metaplasia of CT that developed in the healing process

50
Q

is nuclear pyknosis reversible?

A

no its irreversible

whereas nuclear chromatin clumping is reversible

51
Q

trauma to the breast can result in what finding on biopsy

A

fat necrosis

52
Q

IL-10

A

also dampens immune response

PBD (7 decks)

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