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MT1 Flashcards

1
Q

Decreased oxygen in the cell impairs _____ in the _____. Reduced ATP reduces the ability of the plasma membrane to maintain homeostasis. This leads to a net ___ of ___ and isosmotic ___ in ____water

A
  • oxydative phosphorylation
  • mitochondria
  • gain of solute
  • isosmotic gain in cytoplasmic water
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2
Q

An isosmotic gain in water leads to:

Dilation of ER leads to ____ of ribosomes from RER and dissociation of ____ and a decrease in _______. This can lead to increased _____

A

-Cell, mitochondria, and endoplasmic reticulum swelling

  • Detachment
  • polysomes
  • protein synthesis
  • lipid deposition
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3
Q

REDUCED oxidative phosphorylation leads to _____ glycolysis.

Increased glycolysis produces _____ and ____ that decrease _____ leading to ____ clumping

A

-INCREASED

  • lactic acid and inorganic phosphates
  • Intracellular pH
  • Chromatin clumping
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4
Q

Does hypoglycemia (reduced substrate for ATP production) have the same patterns as hypoxia?

A

YES

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5
Q

Where do oxidative reactions take place that produce ROS

A

Plasma membrane, mitochondria, cytoplasm, and peroxisomes

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6
Q

What inactivates Superoxide?
What inactivates Hydrogen peroxide?
Hydroxyl radicals are GENERATED by?

A
  • Inactivated spontaneously or by superoxide dismutase (SOD) to form H2O2
  • Detoxified by glutathione peroxidase and catalase
  • Hydrolysis of water by ionizing radiation or by transitional metals such as Fe2+ or Cu2+
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7
Q

3 ways ROS damages cells:

A
  • Lipid peroxidation
  • Protein cross-linking
  • Reaction w/ thymidine and guanine to induce single strand DNA breaks
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8
Q

Antioxidant systems act to reduce the effects of ___.
Intracellular antioxidant systems include:
Extracellular antioxidant systems include:

A
  • ROS
  • SOD (superoxide dismutase), catalase, and glutathione peroxidase
  • Vitamins A,C,E, iron binding proteins (transferrin, ferritin) and copper (ceruplasmin)
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9
Q

What is the final common pathway of cell injury?

Which degradative enzymes does it activate?

A
  • Increased cytoplasmic Ca2+

- phospholipase, protease, endonucleases, ATPase

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10
Q

Which complement proteins can cause cell membrane injury?

A

C5-C9 membrane attack complex

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11
Q

In cell injury, which occurs first, biochemical alterations or morphological?

A

Biochemical BEFORE morphologic

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12
Q

REVERSIBLE cell injury.. plasma membrane injury leads to increased intracellular __ which leads to an isosmotic __ of water.

What does this make the cell look like?

A
  • Na+ leading to GAIN of water

- Pale and swollen

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13
Q

What are the 2 MORPHOLOGIC forms of cell death

A

necrosis and apoptosis

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14
Q

If a cell has a glassy homogenous pink staining cytoplasm, it most likely is:

A

necrosed

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15
Q

During coagulative necrosis, the ___ is lost but the eosinophilic outline of the cell is retained prior to being removed by inflammatory response

A

nucleus

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16
Q

What kind of necrosis is when the tissue is totally digested by the release of lysosomal enzymes during the acute inflammatory response.

Often associated with:

A
  • Liquefactive necrosis (“pus”)

- bacteria, fungal infections (abscesses/gangrene), also central nervous system

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17
Q

Caseous necrosis is associated with:

Tissue appearance:

A
  • Tuberculosis

- White and “cheesy” appearance

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18
Q

Which necrosis give a “soap bubble” appearance?

Common in trauma to:

A
  • Fat necrosis

- breast or pancreatitis

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19
Q

In morphologic apoptosis (programmed cell death), chromatin condensation is followed by ____

A

fragmentation

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20
Q

What is a Fas-ligand

A

“death signal” for apoptosis

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21
Q

For apoptosis, what is a removal of a trophic signal?

A

removal of hormones

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22
Q
  • For apoptosis what does Bcl-2 and Bcl-x do?
  • What do Bax and Bak do?

How do all these work?

A
  • INHIBIT apoptosis
  • STIMULATE apoptosis

-on/off switches that regulate membrane permeability of the mitochondria

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23
Q

What is released from the mitochondria membrane to disrupt inhibitory Bcl-2 (so it FAVORS apoptosis)

A

Cytochrome-C

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24
Q
  • Caspases are considered the:

- Their substrates include:

A
  • “executioner” of apoptosis

- matrix and transcription proteins, DNase

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25
Q

Besides capsases, what’s another apoptosis executioner

A

mitochondria release of Ca2+ that activates various enzymes

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26
Q

What are the 2 stimuli for necrosis?

2 stimuli for apoptosis?

A
  • Hypoxia and toxins

- Physiologic and Pathologic

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27
Q

Which one effects multiple cells, necrosis or apoptosis

A

NECROSIS

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28
Q

Which causes cell swelling, necrosis or apoptosis

A

NECROSIS

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29
Q

Which mechanism of DNA destruction is ATP DEPENDENT (necrosis/apoptosis)

A

APOPTOSIS

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30
Q

Does apoptosis cause inflammation?

A

NO, only necrosis does

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31
Q
  • Hypertrophy:
  • Hyperplasia:
  • Metaplasia:
A
  • cell size
  • cell number
  • cell differentiation
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32
Q

What can cause cellular hypertrophy (increase in cell size)

A
  • hormones (i.e. smooth muscle hypertrophy in pregnant uterus)– GOOD
  • Overproduction of TSH due to iodine deficiency induces thyroid follicle hypertrophy (goiter) – BAD
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33
Q

Is a goiter (thyroid) hypertrophy, hyperplasia, or metaplasia?

A

HYPERTROPHY (overproduction of TSH b/c of iodine deficiency)

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34
Q

Exercise causes muscle ____

A

hypertrophy

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35
Q

Endometrial glandular cells during menstruation is (hypertrophy/hyperplasia/metaplasia)

A

HYPERPLASIA (increase in cell number)

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36
Q

What can hyperplasia increase the risk of?

A

neoplasia

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37
Q

Wound healing is (hypertrophy/hyperplasia/metaplasia) of connective tissue walls and epithlium

A

HYPERPLASIA (increase in cell number)

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38
Q

Callus’s on hands are (hypertrophy/hyperplasia/metaplasia) of epidermal cells

A

HYPERPLASIA

39
Q

When an adult cell type is replaced by another adult cell type in response to chronic stress, this is called:

A

METAPLASIA

40
Q

When normal epithelium in intestines is replaced with goblet cells and other mucosal cells this is (hypertrophy/hyperplasia/metaplasia) —SIMILAR TO BARRET’S ESOPHAGUS

A

METAPLASIA

41
Q

If you are a chronic smoker, or have a vitamin A deficiency, your cells will adapt, this is (hypertrophy/hyperplasia/metaplasia)

A

METAPLASIA

42
Q

What is steatosis?

What can cause it?

A
  • Fatty liver. An abnormal accumulation of triglycerides within cells.
  • Obesity, diabetes, anorexia
43
Q

Where does cholesterol primarily accumulate?

A

Macrophages (foam cells)

44
Q

Protein cellular accumulations…
a1-anti-trypsin deficiency:
Mallory bodies:
Neurofibrillary tangle in Alzheimer’s:

A
  • impaired folding due to gene mutation
  • impaired secretion due to improper folding or precipitation
  • accumulations of microtubule-associated proteins and neurofilaments
45
Q

What is the “wear and tear brown-yellow granular pigment”, a lipoprotein complex due to ROS peroxidation of membranes

A

lipofuscin

46
Q

What is the black-brown pigment produced by melanocytes but accumulated in adjacent epidermal cells and macrophages

A

Melanin

47
Q

What is Hemosiderin?
Where does its accumulation arise from?
What is hemochromatosis?

A
  • A yellow-brown pigment that represents aggregates of ferritin micelles.
  • Excess iron locally due to hemorrhage
  • Genetic disease associated with cell death due to uncompensated hemosiderin accumulation
48
Q

What is the yellow-brown pigment that’s the end product of heme metabolism?
Where does it accumulate?

A
  • Bilirubin

- In hepatocytes and bile ducts due to hemolysis, obstructed bile flow, and/or hepatocellular disease

49
Q

For inflammation….Heat, redness, and swelling are due to ____, while pain and loss of function are due to ______

A
  • vascular changes

- chemical mediators and leukocytes

50
Q

Neutrophils are characterized in ___ inflammation, while lymphocytes, macrophages, and plasma cells are characterized in ____

A
  • acute inflammation (hours-days)

- chronic inflammation (days-years)

51
Q

Fever is mediated by:

A

IL-1, TNF, and PGE2

52
Q

In acute inflammation , where does vasodilation begin?
What is it mediated by?
—What does this induce?
-Vasodilation is maintained by?

A
  • precapillary arterioles
  • NO
  • –Vascular smooth muscle relaxation and mast cell release of histamine
  • Prostaglandins (PG_)
53
Q

During acute inflammation, vascular permeability ___ which results in movement of fluid ___ the micovasculature. The blood becomes ____ concentrated and flow ___ (stasis)

A
  • increases
  • out of
  • more concentrated
  • flow slows
54
Q

In acute inflammation, what level does movement of inflammatory cells out the vessels (diapedesis) occur at?

A

Post-capillary venules

55
Q

In inflammation…endothelial cell CONTRACTION forms intercullular ___ due to reversible ___. This occurs (how fast)___ and lasts for ___.

Contraction is mediated by:

A
  • intercellular gaps
  • reversible contractions
  • occurs rapidly
  • lasts for 15-30 minutes

-Histamine and bradykinin

56
Q

In inflammation…endothelial cell RETRACTION due to restructuring of _____ is mediated by ________. This takes _____ to develop and lasts for ___

A
  • cytoskeletal proteins
  • IL-1, TNF, IFN-y
  • 4-6hrs
  • Lasts 24 hours or more
57
Q

What is the order of leukocyte extravasion?

A

margination, rolling, adhesion, emigration, chemotaxis (MRAEC)

58
Q

Cell adhesion molecules mediate the processes involved in the movement of ____ from the blood stream into extravascular tissue

A

leukocytes

59
Q

Leukocyte margination:
Rolling:
Adhesion:

A
  • mechanical process due to slowing of blood
  • selectins mediate a weak, transient, sticking that slows the cells forward progression
  • mediated by integrins (ICAM/VCAM)
60
Q

Is chemotaxis random or non-random movement of leukocytes to the site of injury
-What are the 2 potent chemotactic factors

A

NON-random

-PAF and LTB4

61
Q

Activation of leukocytes is characterized by production of ___ and ___ from ____

A

leukotrienes and prostaglandins from arachidonic acid

62
Q

Phagocyte attachment is mediated by ____ on targets and specific leukocyte receptors

A

opsonins

63
Q

What is the morphologic hallmark of acute inflammation?

A

Neutrophils (PMNs)

64
Q

What do neutrophils release for acute inflammation

A

ROS and lysosomal enzymes

65
Q

What end up replacing neutrophils in acute inflammation within 48 hours?

What is their half life?

A

Monocytes (macrophages/histiocytes)

-months

66
Q

Which immune cell reacts to allergic reactions and parasitic infections

A

eosinophils

67
Q

An abscess is a localized area of:

A

liquefactive necrosis

68
Q

Acute inflammation relies on ___ immunity while chronic relies on ____

A

innate

specific/adaptive

69
Q

Granulomatous inflammation is linked to the delayed-type ___ hypersensitivity immune reaction

A

IV

70
Q

Granulomatous inflammation includes epitheloid (activated) ___. They are healed by ___

A
  • histiocytes

- fibrosis

71
Q

NSAIDs inhibit release of ____ from cell membrane phospholipids

A

arachidonic acid

72
Q

While prostaglandins generally cause vasodilation, _______ causes vasoconstriction

A

thromboxane A2

73
Q

When is peak neovascularization during wound healing

A

DAY 5

74
Q

Arterial thrombi have a ____ appearance with distinct lines of ___.

Venous thrombi have a ___ appearance. They often form in:

A

Pale/white
lines of Zahn

  • red
  • deep veins of legs
75
Q

Sterile (non-infectious) thrombi on heart valves are called:

A

Nonbacterial thrombotic endocarditis (NBTE)

76
Q 
Fate of thrombi...
Propagation:
Embolization:
Dissolution:
Organization:
A
  • Propagation: enlarge by additional fibrin/platelt deposition
  • Embolization: entire thrombus dislodges or a piece 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 some flow through the thrombus
77
Q

Disseminated Intravascular Coagulation (DIC) is the widespread activation of the coagulation cascade and fibrinolytic system leading to depletion of ______ and ____ and accumulation of ____split products. This can be associated with formation of ____and risk of ____

A
  • depletion of coagulation factors and platelets
  • formation of fibrin split products
  • risk of of hemorrhage
78
Q

Embolism defintion:

A

A solid, liquid, or gas carried from one point to another in the vascular system

79
Q

Thrombo-emboli that lodge in pulmonary arteries usually arise from where?

A

deep veins in the legs

80
Q

Do small embolisms cause ischemia? Why/why not

A

No, cuz of double blood supply in the lungs

81
Q

What is a saddle embolus?

A

Sudden death due to large emboli straddling the bifurcation of the pulmonary arterial trunk

82
Q

Can gradual obstruction of many small pulmonary arteries by repeated embolization over time result in in pulmonary hypertension?

A

yes

83
Q

What’s a paradoxical embolus?

A

embolus that arises in a systemic vein and crosses a communication from the venous side to the arterial side

84
Q

Usual origin of systemic embolization?

Can they travel to any systemic artery?

A

Left atrium, left ventricle, or ulcerated atherosclerotic plaque.
-YES

85
Q

What kind emboli is caused by fracture of large long bone?

A

fat emboli

86
Q

Infarction definition:
Usually due to:
Less often due to:

A

-ischemic (restriction of blood supply to tissue –>shortage of oxygen) necrosis of an organ. (AKA an are of dead tissue resulting from failure of blood supply)

  • Due to arterial obstruction
  • less often because of shock or vessel twisting
87
Q

Infarcts tend to be ____shaped with the wedge at the site of ______

A

wedge

arterial obstruction

88
Q

The histologic changes of coagulation necrosis do not develop for (how long) after the infarct has occurred.

Infarction is followed by ______ that peaks at ___days. Healing occurs by ________, starting at the _____ of the infarct, followed by ____

A

Several hours (NOT immediately)

  • acute inflammation
  • 2-3 days
  • granulation tissue ingrowth
  • edge
  • scar formation
89
Q

Infarcts in the brain result in ____ necrosis and heal with formation of a ____

A
  • liquefactive necrosis (NOT coagulative)

- cystic space

90
Q

What’s more vulnerable to hypoxia…brain/heart or arm/leg

A

brain/heart

91
Q

Shock definition

A

systemic hypoperfusion (decreased blood flow) of tissues

92
Q 
What is cardiogenic shock?
hypovolemic?
septic?
Anaphylactic?
Neurogenic?
A
  • cardiogenic: loss of pumping capacity of the heart
  • hypovolemic: blood loss
  • septic: bacterial
  • hypersensitivity reaction mediated by IgE
  • neurogenic: loss of vascular tone (anesthesia/spinal cord injury)
93
Q

During septic (bacterial shock), _____ bind to ____ on ___and ___ mediating the release of ___ and ___ .

This causes vaso____, ____tension, (increased/decreased) myocardial contractility

A
  • PAMPS
  • bind to toll-like receptors (TLRs)
  • on monocytes and neutrophils
  • release of IL-1 and TNF

-vasoDILATION, HYPOtension, decreased

94
Q

Difference of nonprogressive and progressive stages of shock

A

nonprogressive: compensatory mechanisms maintain tissue perfusion
progressive: leads to reduced perfusion and hypoxic injury leading to DIC (intravascular coagulation)

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