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MT1 GOOD Flashcards

1
Q

In ischemia leading to cell injury, decreased O2 impairs _____ in ____. This effects the plasma membrane because it decreases ___ which decreases ability of membrane to maintain homeostasis. Can also cause detachment of _____ from ____

A
  • oxydative phosphorylation in mitochrondria
  • Decreases ATP.
  • Detachment of ribosomes from RER
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2
Q

When ROS leads to cell injury, these occur…

lipid _____, protein (membrane) _____, reacts with ____ and ____ to induce ______

A

-lipid perOXYdation
-protein cross-linking
-thymidine and guanine
=induces single strand DNA breaks

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3
Q

What is the “final” common pathway in cell injury?

What does it activate?

A
  • Increased cytoplasmic Ca2+

- Activates degradative enzymes (phospholipases, proteases, ATPase)

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4
Q

What does a cell that has reversible cell injury look like? Why?

A
  • Pale and swollen

- Plasma membrane injury leads to increased intracellular Na+ that leads to gain in water

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5
Q

A cell doesn’t show a nucleus, but retained an eosinophilic outline of cell, which kind of necrosis is this?

A

Coagulative necrosis

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6
Q

A cell looks like a amorphous pink granular material within a ring of granulomatous inflammation, which kind of necrosis is this?
What does the tissue look like (gross)?
Which disease is this associated with?

A

Caseous necrosis

  • White and cheesy
  • TB
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7
Q

Which kind of necrosis causes tissue to look totally digested by lysosomal enzymes during acute inflammatory response?
What is this often associated with?

A

Liquefactive necrosis

-bacterial/fungal infections (abscesses and gangrene)

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8
Q

You look in microscope and see “soap bubbles”, what kind of necrosis?

A

fat necrosis

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9
Q 
Necrosis vs. Apoptosis..
Which is multiple cells:
Which causes cell swelling:
Which is ATP dependent:
Which causes inflammation:
A

multiple cells: necrosis
swelling: necrosis
ATP dependent: apoptosis
Inflammation: necrosis

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10
Q

What does the Bcl-2 gene family regulate?
What do BCL-2 and BCL-x genes do?
Bax and Bak?

A
  • Membrane permeability of mitochondria
  • INHIBIT apoptosis
  • STIMULATE apoptosis
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11
Q

Cytochrome-c is released from _____.
Serves to:
In the end, what effect does it have on apoptosis?

A
  • outer mitochondrial membrane
  • disrupts Bcl-2
  • FAVORS apoptosis
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12
Q

What are capsases?

A

the executioner of apoptosis

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13
Q

Patient has iron deficiency, what type of cellular “growth” will he have in his thyroid?

A

hypertrophy

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14
Q

Hyperplasia can be secondary to:

A

estrogen treatment for prostate cancer

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15
Q

Erythrocyte ______ can follow ectopic production of erythropoietin renal cell carcinoma

A

hyperplasia

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16
Q

Vitamin A deficiency can cause (hypertrophy/hyperplasia/metaplasia)

A

metaplasia

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17
Q

What is steatosis?

A

Fat accumulation (Fatty liver)

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18
Q

Where does cholesterol accumulate and what can it cause?

A

In macrophages

-Xanthoma in skin

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19
Q

Alzheimer’s disease is an accumulation of ____

A

protein

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20
Q

Glucose/glycogen accumulation is abnormal glycogen metabolism due to ______

A

enzyme deficiency

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21
Q

Pigment accumulations..
Lipofuscin is due to:
Hemosiderin:
Bilirubin:

A

Lipofuscin: ROS peroxidation
Hemosiderin: excess iron locally due to hemorrhage
Bilirubin: end product of heme metabolism. Obstructed bile flow

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22
Q

Vascular changes of inflammation:
Chemical

What is fever mediated by?

A

Vascular: heat, redness, swelling
Chemical: pain, loss of function

-IL-1, TNF, PGE2

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23
Q

During inflammation what causes vasodilation? what maintains it?

A

NO

prostaglandins (PG_)

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24
Q

Transudate:
Exudate:

A

Trans: low protein. Fluid accumulates due to change in pressure

Ex: HIGH protein. Indicative of tissue and endothelial cell damage

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25
Q

Cellular changes during inflammation…
Endothelial cells are activated by:
Leukocyte extravasion is mediated by:
Leukocytes are activated by:

A
  • histamine, thrombin
  • Integrins (ICAM, VCAM)
  • Arachidonic acid
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26
Q

Phagocytosis attachment is mediated by _____ on targets and specific ____ receptors.

What happens to lysosome when it fuses with phagosome?

A

Opsonins
Leukocyte

-degranulation

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27
Q

What are the first cells of inflammation?
After phagocytosis and digestion, they undergo ____.
They release ____ and ____

A

Neutrophils (PMNs)

  • Apoptosis
  • ROS and Lysozyme
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28
Q

Which cells of inflammation present antigen to T cell

A

Monocytes (macrophages/histocytes)

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29
Q

Granulomous inflammation (chronic inflammation) is linked to ______ hypersensitivity immune reaction.

What kind of cells will it form?
How is it healed?
What can cause it?

A

delayed-type IV

  • multinucleated giant cells (Langhans)
  • fibrosis
  • TB, cat scratch fever
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30
Q

What is the source of histamine?

Causes vaso___ and ____ vascular permeability

A

Mast cells

  • vasodilation
  • INCREASES vascular permeability
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31
Q

First vs second intention wound healing.

In second intention, wound contraction is due to:

A

First intention is blood clot–> neutrophils..etc.

Second has more inflammation and more granulation tissue

-myofibroblasts

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32
Q

What is thrombosis?

Arterial thrombi are which color?
Where do the tend to occur?

Venous thrombi are which color?
Where do they tend to occur?

A

BLOOD CLOT

Arterial= pale white
Occur at sites of turbulence and lodge in smaller arteries causing infarction

Venous= red
Occur in deep veins in legs

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33
Q 
Fate of thrombi...
Propagation:
Embolization:
Dissolution:
Organization:
A
  • Propagation: enlarged by additional fibrin/platelet deposition
  • embolization: thrombus breaks loose
  • dissolution: lysis by fibrinolytic activity
  • organization: ingrowth of fibroblasts and smooth muscle cells, leads to deposition of collagen (replacing the fibrin) and recanalization, which may reestablish flow through thrombus
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34
Q

DIC ends up accumulating:

A

fibrin split products

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35
Q

Thromboemboli that lodge in _____ arteries usually arise from _____

A

pulmonary

deep veins in the legs

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36
Q

What predisposes fat emboli?
Air emboli:
Amniotic fluid:
Atherosclerotic (hardening of arteries):

A

fat: fracture of large long bone
Air: chest wall injury, decompression sickness (bends)
Amniotic: associated with DIC
Atherosclerotic: debris from central core of atherosclerotic plaque

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37
Q

What color infarcts occur in solid organs (where tissue density limits blood seepage from adjacent vascularization)

What color infarcts are caused by venous occlusion

A

White infarcts

red infarcts

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38
Q

What kind of necrosis results from infarcts in the brain?

A

liquefactive (NOT coagulative)

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39
Q

Anaphylactic shock is mediated by:

What kind of shock is caused by anesthesia?

A

IgE

neurogenic shock

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40
Q

Nonprogressive stage of shock:

Progressive stage:

A

Nonprogressive: compensatory

Progressive: inadequate perfusion w/ metabolic imbalances such as acidosis (increased lactic acid)

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41
Q

What are the two most common areas of ischemic necrosis in the brain?

A

Hippocampus and cerebellum

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42
Q

Clinical manifestations of shock:

A

tachycardia, HYPOtension, cool clammy skin, decreased urinary output, confusion , acidosis (increased lactic acid)

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43
Q

Nephrotic syndrome is an example of which edema?

A

Decrease in plasma osmotic pressure

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44
Q

What is congestion and what is it often accompanied by?

Examples of congestion?

A

Congestion: increased RBCs (impaired venous return)
-Accompanied by edema

-CHF, tourniquet

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45
Q

Types of hemorrhages..

Petechia, purpura, ecchymoses

A

Petechia: 1-2mm
Purpura: 3-9mm
Ecchymoses: >1cm

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46
Q

What is the cofactor for binding platelets to collagen (platelet adhesion).

Platelet secretion is mediated by

A

von Willebrand factor

-ADP + thromboxane A2

47
Q

Thrombomodulin binds to ____ and this complex activates _____

A

thrombin

protein C

48
Q

FibrinoLYSIS occurs by the activation of _____.

What does plasmin do?

A

Plasmin

Breaks down fibrin (hence the lysis…)

49
Q

How does lead-induced anemia work?

What kind of anemia do they develop?

What does lead compete with?

A

lead has high affinity for enzymes involved in the synthesis of hemoglobin, which blocks or hinders the incorporation of iron into the molecule.

  • Microcytic hypochromic anemia
  • Competes with Ca2+
50
Q

Radiation injury…
TARGET effect:
Indirect effect:

A

Target: direct hit on DNA, causing mutations

Indirect: production of free radicals

51
Q

Marasmus is deficiency of ____. ____compartment is depleted. Can cause ____ and ___deficiency (especially T cell). What is a common finding?

A

Marasmus: deficiency of Caloric intake (starvation).

  • Somatic protein compartment (skeletal m.)
  • Can cause anemia and immune deficiency.
  • Common finding=thrush
52
Q

Kwashiorkor is:
This is the most common form of ___ in Africa. Is this more or less severe than marasmus?
What organ does this mess with?

A

greater deficiency of protein than total calories.

  • most common form of Protein-Energy Malnutrition
  • MORE severe
  • Liver
53
Q

What is Protein-Energy Malnutrition in cancer patients called?

A

Cachexia

54
Q

If you have dry eye, and can also affect respiratory/urinary tracts, and immune system (can cause measles, pneumonia, etc.), what is wrong with you?

A

Vitamin A DEFICIENCY

55
Q

If you have blurred vision and fissured lips, what’s wrong?

A

Vitamin A TOXICITY

56
Q

If you have impaired collagen synthesis –> impaired capillaries + venules (hemorrhage in gingiva…wound healing is impaired), what’s wrong with you?

A

Vitamin C DEFICIENCY

57
Q

What causes scurvy?

A

Vitamin C DEFICIENCY

58
Q

What can give some protection from gastric and esophageal cancers (and enhance iron absorption)?

A

Vitamin C

59
Q

What is special about pulmonary (lung) blood supply?

A

Dual blood supply (pulmonary and bronchial)

60
Q

Vocal cords are lined with:

Large airways lined with:

A
  • Vocal cords: stratified squamous epi (SSE)

- Large airways: psuedostratified ciliated columnar epi (PCCE)

61
Q

Where is the mucociliary apparatus?

Where are the alveolar macrophages?

A

lower airway

lymphoid tissues

62
Q 
Clinical manifestations of pulmonary disease..
Hemoptysis:
Dyspnea:
Atelectasis:
Pneumothorax:
Pleural effusion:
A

Hemoptysis: coughing up blood
Dyspnea: shortness of breath
Atelectasis: loss of lung volume (inadequate expansion of airspaces)

63
Q

Causes of pulmonary edema:

A

Increased vascular pressure
Hypoproteinemia (low protein)
Vascular damage

64
Q

Px is having trouble exhaling, what’s the mechanism?

A

(emphysema) imbalance between protease and anti-protease enzymes

65
Q

What is the disease when you have increased mucus glands, chronic inflammation, fibrosis, narrowing of airways

A

Chronic bronchitis

66
Q

What is a chronic infection w/ permanent (large) airway dilation

A

bronchiectasis

67
Q

Asthma is increased irritability of ___ in bronchi. Inflammation caused by ______. Antigen binds to surface ____

A

S.m.
Eosinophils
IgE

68
Q

What pulmonary infection affects full lobe of lung

A 
bacterial pneumonia (streptococcus pneumoniae). 
This affects HEALTHY adults
69
Q

What pulmonary infection causes interstitial inflammation, mononuclear cells, congestion and hyaline membranes (diffuse alveolar damage)

A

viral (walking) pneumonia

70
Q

What pulmonary infection develops rapidly and causes injury to endothelium and alveolar epi

A

ARDS (acute respiratory distress syndrome)

71
Q

Which pulmonary infection can cause cough and fever. Caused by ASPIRATION

A

Pulmonary abscess

72
Q

What is the most common infectious cause of death in the world?

A

TB

73
Q

Which pulmonary infection causes a caseating granuloma and Ghon lesion

A

TB

74
Q

Granulomatous inflammation is common in TB, but is associated w/ many fungal infections such as _______ and

A

histoplasmosis

sarcoidosis

75
Q

Squamous cell carcinoma and small (oat) cell are common cancers of:

A

the lung

76
Q

What is pneumoconioses?

A

Inhaled particles induce fibrosis (scarring). 1-5um is the worst.

77
Q

What is the most prevalent form of occupational disease?

A

silicosis (silicon dust)

78
Q

In cancer, which component determines the biological behavior of the neoplasm?

A

Parenchymal

79
Q

For cancer, what is stroma

A

supporting tissue of tumor (supplied by host)

80
Q

Benign tumors suffix:
Malignant mesenchymal suffix:
Malignancy of epithelial origin:

A

“oma”
“sarcoma”
“carcinoma”

81
Q

Definitions…
Hamartoma:
Choristoma:
Teratoma:

A
  • Hamartoma: proliferation of tissue normally found at that site
  • Choristoma: collection of tissue not normally found at that site
  • Teratoma: neoplasm derived from more than one germ layer
82
Q

Are high grade/anaplastic malignancies poorly or highly differentiated

A

poorly

83
Q

Well-differentiated (low-grade) malignancies resemble:

A

normal tissue

84
Q

Difference of dysplasia and anaplasia in malignancies

A

dysplasia is disorderly, but non-neoplastic growth.

Anaplasia is most extreme distrubance in cell growth…poorly differentiated…faster growing

85
Q

Which tumors have a fibrous capsule, benign or malignant

A

benign

86
Q

What is the hallmark of malignancy

A

metastasis (secondary deposits of tumor at distant sites).

The larger and more anaplastic it is, the more likely to metastisis

87
Q

What are the 3 methods of metastasis

A
  • Seeding within body cavities (pluera)
  • Lymphatic spread (carcinomas)
  • Hematogenous spread (sarcomas…affects liver and lungs)
88
Q

Inherited cancer syndromes are usually due to:
Autosomal ___

Some examples:

Defective DNA repair syndromes are autosomal ____
Example?

A

single gene mutation
autosomal DOMINANT

-retinoblastoma,

  • recessive
  • xeroderma pigmentosum
89
Q

What are growth promoting cancer cells called.

Are they controlled?

A

protooncogenes

NO, they are UNcontrolled promoters of growth

90
Q

What is the most common growth promoting signal-transducing protein in cancer?

What does it do?

A

RAS oncogene.

Normally inactive, but when mutated, stimulates constant cell proliferation

91
Q

What growth promoting gene mutation causes Burkitts lymphoma (most common nuclear transcription factor).

What happens when it’s mutated?

A

MYC

Activates a kinase, therefore causing cells to divide rampantly

92
Q

RAS and MYC are both growth____

A

promoting

93
Q

Which cancer needs 2 “hits” and is a key player in regulation of the cell cycle

A

retinoblastoma

94
Q

Most common target for genetic alteration in human tumors (found in every type of cancer):

Is that gene growth promoting or inhibiting

With loss/mutation of this drug, what happens to damaged DNA

A

TP53

Inhibiting (suppressor)

It goes unfixed

95
Q

Overexpressed BCL-2 protein protects cells from apoptosis, which can result in

A

low-grade (well differentiated…slower growing) lymphoma

96
Q

Are cancers usually one mutation or more

A

MORE, or everyone would have cancer!

97
Q

~__% of newly diagnosed patients with solid tumors will present with metastasis

A

30%

98
Q

Is carcinogenesis lethal/nonlethal genetic damage

A

NONlethal

99
Q

Cancer cell proliferation….

What are CDKs important for?

A

important in determining whether a cell is going to enter the cell cycle.

100
Q

Have atypical cells invaded into the host with carcinoma in-situ?

A

NO

101
Q

Which cancers have lymphatic spread?

A

carcinomas

102
Q

***End products of metabolic conversion in cancer are termed ____ carcinogens

A

ultimate

103
Q

**What does prostacyclin do?

A

inhibit adhesion

104
Q

Overall 5 year survival rate for all cancer types is

A

16%

105
Q

Difference of a carcinogen (chemical) and promoter in cancer

A

carcinogen: initiator of mutation
promoter: drives replication

106
Q

What is the latent time for radiation exposure to time of cancer

A

7-12 years

107
Q

EBV (epstein-barr virus) is implicated in the pathogenesis of several malignancies including:

A

Burkitt’s lymphoma, B-cell lymphoma, Hodgkins lymphoma..

EBV=LYMPHOMA!!!!

108
Q

Hep B virus is liked to development of:

A

hepatocellular carcinoma

109
Q

What is an example of a paraneoplastic syndrome?

A

Non-bacterial thrombic endocarditis (NBDTE)

110
Q

Cancer develops in immune competent patients by:

A

selective outgrowth of antigen-negative variants

111
Q

Cancer Grading vs staging.

Which is more valuable in determining prognosis?

A

grading= aggressiveness (grade IV being least differentiated….worst)

Staging=extent/size/metastasis (IV is most disseminated..worst)

Staging is more important for prognosis

112
Q

A mutation in the genes for adhesion molecules would NOT affect:

A

margination (slowing of blood)

113
Q

What’s the problem with frozen section biopsy?

A

Prone to errors. Must do it right at time of surgery

114
Q

What is a contusion

A

Bruise. Doesn’t break skin.

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