Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology, Exam 1 > Pathology > Flashcards

Pathology Flashcards

1
Q

Immunohistochemsitry Autopsy is

A

Done for unknown tumors, infectious dx and brain tissue in the case of dementria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Microbiology Autopsy

A 
When COD is suspected to be infectious dx
Includes
- lung tissue culture
- Viral nasal swab culture
- Blood culture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What type of autopsies utilize a blood culture?

A

microbiology and toxicology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Toxicology Autopsy

A

Blood, urine, and vitreous humor in cases of overdose, motor vehicle accidents or sudden / unexplained death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cytogenetic Autopsy

A

Take skin, pericardium and placenta in the case of miscarriage or still birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Radiology Autopsy

A

Gunshot wound
Child abuse
Suspected pneumothorax / air embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Forensic Autopy

A 
Sexual assault testing
Bullets
Pellets
Nail clippings
Trace evidence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is a coroner autopsy

A

Performed by a coroner / medical examiner

  • forensic pathologist prosects
  • next of kin consent NOT needed
  • death outside of hospital
  • MAJORITY of natural deaths
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Medical Autopsy

A

Pathologist + Resident prosect
Next of kin CONSENT NEEDED
Death often in hospital or nursing home
Majority of natural deaths

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cell Injury

A

When a cell is stimulated by severe stress and the cell’s adaptive capabilites are exceeded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What would result in an increase in protein degradation -to-synthesis ration?

A

Atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When one adult cell type is replaced by another, less vulnerable one capable of withstanding more stress this is an example of?

A

Metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The replacement of columner EPI by squamous in the respiratory tract of a smoker is an example of…

A

Metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Metaplasia involves reprogramming of what?

A

Stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When squamous cells are replaced by columnar cells in the the throat of someone with acid reflux, there is an example of?

A

Metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

The glassy pink appearance seen in H&E staining as a result of intracellular or extracellular acccumulations of protein is called?

A

Hyaline change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are Russell Bodies?

A

Immunoglobins in plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Whati s anthracosis?

A

Black discoloration of lung tissue and lymph nodes draining it.
This is due to carbon being phagocytosed by alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are CASPASES

A

A family of cysteine proteases that exist as pro-enzymes until cleaved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

A pathological form of cell death associated with damage from an external source is?

A

Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is congulative necrosis?

A

Dead tissue architecture is preserved for a few days b/c proteolytic enzymes are denatured

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Saponification is an example of (is)

A

Fat necrosis: areas of fat destruction in which fat products combine with Calcium to produce chalky-white areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Ischemia is caused by which type of necrosis?

A

Coagulative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When dead cells are completley digested and leave only viscous fluid this is known as?

A

Liquefactive necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Hypoxic tissue damage in the CNS is an example of what type of necrosis?

A

Liquefactive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Pancreatitis and leakage of pancreatic lipase into adjacent tissue is an example of

A

Fat necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

TB is an example of what type of necrosis?

A

Caseous Necrosis: when dead tissue is transformed to ‘cheesy’ granular material

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Small, dark chromatin due to chromatin condensation and cleavage into fragments during apoptosis is what?

A

Pyknosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Karyorrhexis is

A

Chromatin fragmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Fading of chromatin is

A

Karyolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Molecules with an unpaired electron in their outer orbit are

A

Free Radicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Deposition of calcium salts in dying tissues despite NORMAL Serum Ca levels is

A

Dystrophic Caclification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What initiates Ca concentration in cellular vesicles?

A

Membrane damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Ca++ salts are deeply ________ and are seen in areas of _________

A

Basophilic (dark blue / purple)

Atherosclerosis (agining/damaged heart valves)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does dystrophic calcification signify?

A

Prior cell damage but it can contribute to further organ dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How do dystrophic and metastatic calcification differ?

A

Metastatic is NOT initatied by cell damage or death; occurs when there is increased serum Ca++ in normal tissue
** This will have the same histology as dystrophic calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

The widing of heart walls due to HT (Hypertension) is an example of what?

A

Pathological Hypertrophy (exercise and muscle growth would be an example of physiological)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

When a normal, endogenous substance is produced at a normal or increased rate, but metabolism is inadequate to remove it, this is called?

A

Intracellular Accumulations (extracellular too?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

When you have intracellular accumulation of TGs you have

A

Steatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

When you have extracellular accumulation of cholesterol you have?

A

Atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Intracellular Accumulations can be caused in 4 ways

A

1) Normal endogenous, produced at normal rate, but bad metabolism
2) Abnormal endogenous accumulates because cellular machinery cannot package, transport or secrete it
3) Normal endogenous substance accumulates because of defects in ENZYMES for its metabolism
4) Abnormal exogenous substance accumulates due to lack of cellular machinery to degrade or transport it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Necrosis is always what?

A

Pathological and also associated with cell membrane disruption and therefore INFLAMMATION

43
Q

Apoptosis differs from necrosis how?

A

It is regulated and does not incur membrane distruption and therefore does not elicit an inflammatory response.

It may or may not be caused by cell injury

44
Q

The intrinsic pathway of apoptosis is also known as the

A

Mitochondrial pathway

45
Q

What happens in intrinsic apoptosis?

A

Proteins normally in the MITO (cytochrome C) are released into the cytoplasm

46
Q

What controls the release of cytochrome C into the cytoplasm during intrinsic apoptosis?

A

Release is controlled by BCL proteins with BOTH pro and Anti apoptotic members
The balance between these two controls whether apoptosis occurs or not

47
Q

When the PRO member of the BCL protein dominate what happens?

A

The from a channel into the MITO so proteins can leave and when this protein (cyto C) leaves it activates Caspases

48
Q

Extrinsic Pathway for apoptosis

A

The plasma membrane death receptors receive signals from outside the cell

FAS R: binding of Fas Ligand expressed by T Lymphocytes brings together caspases that trigger the caspase cascade

49
Q

What does Fas R Do?

A

This is part of the extrinsic pathway

When it binds (comes from T Lymphocytes) it brings together caspases that trigger the caspase cascade

50
Q

What are some of the major causes of cell injury?

A

1) Hypoxia / Ichemia
2) Physical Agents: trauma, temp., pressure, radiation, electric shock
3) Chemical Agents / Drugs: some are fine at low concentrations (smoking, alcohol, etc)
4) Infection
5) Lesser: immunologic, genetic, nutritional

51
Q

Which is more damaging: hypoxia/Ischemia?

A

Ischemia b/c there is no O2, glucose and other metabolic substances

52
Q

What are 4 targets of cell damage? (Think: BCG P (Please))

A

B: Biochemical machinery of aerobic respiration
C: Cell Membrane
G: Genetic Apparatus
P: Protein Synthesis

53
Q

One mechanism of cell damage is Depletion of ATP. Explain this

A

you lose the Na/K ATPase - the Na builds up and there is low K. The cell swells

Also inhibit glycolysis: build up of lactic acid and low glycogen stores

See a failure of Ca++ Pump so an influx of Ca

Damage to protein synthesis apparatus: reduction in synthesis

Abnormal protein folding

54
Q

What type of cell damage results in the build up of lactic acid and low glycogen stores?

A

Depletion of ATP

55
Q

How can MITO be damaged?

A

1) increased cytosolic Ca++
2) Increased ROSs
3) Ischemia

These will all from the MITO permeability transition pore and destroy MITO membrane potential for oxidative phosphorylation.

MITO protein leakage would also result in apoptosis

56
Q

Loss of Ca++ homeostasis is a major mechanism of cell damage. What happens here?

A

1) You can activate enzymes like phospholipases, proteases, endonucleases and ATPases
2) Activation of caspases

57
Q

Oxidative stress can result from:

A

1) Hydroxyl Radicals
2) Superoxide Anion
3) Hydrogen Peroxide
4) Peroxynitrite

58
Q

When there is lipid peroxidation in the membrane from unsaturated FAs rxing what is yielded and what happens?

A

1) Yields Lipid Peroxides which disrupt the membrane

59
Q

When there is oxidative modification of proteins what can happen?

A

This can cause damage to the proteins active site or conformation

60
Q

What is the morphology of apoptosis (what will it look like?)

A

Cell Shrinkage
Increased Density of cytoplasm (dark Pink on H&E)
Nuclear Pynknosis: Small dark chromatin
Cytoplasmic Blebs: Apoptic bodies that are rapidly cleared by phagocytosis

61
Q

When would you see dark pink on an H&E?

A

Apoptosis

62
Q

Electron Microscope shows: Loss of microvilli, mito swelling, dilation of ER and Plasma Membrane Blebbing. What is doing on?

A

Reversible cell injury (necrosis)

63
Q

Light microscope is showing cell swelling, clear cytoplasmic vacuoles, and fatty change. What is going on?

A

Reversible Cell injury

64
Q

EM is showing membrane discontinuity, MITO swelling, myelin figure of whorled phospholipid masses. What is going on?

A

Irreversible injury (necrosis)

**Both reversible and irreversible have MITO swelling

65
Q

LM is showing: dark pink cytoplasm (cytosplasmic eosinophilia), dystrophic calcification, Karyolysis (fading of chromatin) and pyknosis (small dark chromatiin) and loss of nucleus as well as chromatin fragmentation. What is going on?

A

Irreversible injury (necrosis)

66
Q

What involves rubor, calor, dolor and tumor?

A

Inflammation

67
Q

What is a non-specific rxn of the body to stimulus perceived to be injurious to the host?

A

Inflammation

68
Q

What is categorized as innate immunity?

A

Skin barriers and inflammatory response

69
Q

What is categorized as acquired immunity?

A

Antibodies produced for a specific antigetn

70
Q

What can lead to inflammation?

A

1) Infections and microbial toxins
2) Trauma
3) Tissue necrosis (secondary to ischemia)
4) Foreign Bodies (Splinters, dirt, sutures, metal)
5) Immunie Rxns (hypersensitivity, autoimmune)
6) On-going inflammation (can lead to more inflammation – ha!)

71
Q

What makes up 50-70% of WBC in the blood?

A

Neutrophils

72
Q

Describe the characteristics of a neutrophil?

A

1) Segmented nucleus with 3-5 lobes
2) Cytoplasmic granules containing acid hydrolases
3) MOTILE phagocytes

73
Q

What is the primary responder to acute inflammation?

A

Neutrophils

74
Q

What makes up 25-35% of WBCs?

A

Lymphcoytes

75
Q

What are the characteristics of Lymphocytes?

A

1) Very little cytoplasm

2) One nucleus

76
Q

What is involved with chronic inflammation and acquired immunity?

A

Lymphocytes

77
Q

What do lymphocytes produce?

A

1) Cytokines and immunoglobins to help eliminate foreign material

78
Q

What makes up 4-6% of WBC?

A

Monocytes

79
Q

What makes monocytes unique?

A

1) Produced in Bone marrow
2) Stay in blood for ~1 day (then go to tissue near blood vessels and are called macrophages
3) HORSESHOE shaped nucleus and granules
4) These are motile phagocytes with granules containing toxic substances

80
Q

What is involved with acute and chronic inflammation and considered a bridge from innate to acquired immunity?

A

Monocytes

81
Q

What do monocytes do?

A

They phagocytose foreign material and present it to lymphocytes

82
Q

What become macrophages?

A

Monocytes (once they get to tissue near BVs)

83
Q

What are involved in the inflammatory rxns to allergens and parasites?

A

Eosinophils

84
Q

What make up 1-3% of WBCs and have bi or tri lobed nucleus

A

Eosinophils

85
Q

What do eosinophilic granules contain?

A

1) HA
2) Proteolytic Enzymes
3) Major basic proteins

86
Q

What are called mast cells when they are in tissue?

A

Basophils

87
Q

What makes up .4-1% of WBCs and has a bilobed nucleus that is difficult to see due to the huge amount of granules

A

Basophils

88
Q

What to basophilic granules contain?

A

1) HA
2) Proteoglycans
3) Proteolyic enzymes
4) Lipid mediators of inflammation

89
Q

What area the slow reacting substances of anaphylaxis?

A

Lipid mediators of inflammation (from basophils which become mast cells)

90
Q

Where are mast cells (formerly basophils) located?

A

Near

1) vessels
2) Mucosae
3) dermis

91
Q

What are anuclear fragments of megakaryocytes with many granules but very litte in the way of organelles?

A

Plateletes

92
Q

What contain platelet activating factors which affetec ALL features of inflammation?

A

Platelets

93
Q

What are the two types of chemical mediators in inflammation?

A

1) Plasma Derived

2) Cell Derived

94
Q

Where are the plasma derived chemical mediators of inflammation produces?

A

Liver

* Always present in plasma in pro-form and require activation

95
Q

What are the plasma derived mediators of inflammation? (Think FKCC)

A

1) F: Factor XII (Hageman Factor)
2) Kinins
3) Complement Proteins
4) Clotting Proteins

96
Q

When are cell derived chemical mediators made?

A

They exist in organelles or are made upon stimulation

97
Q

What are the cell derived chemical mediators of inflammation? (Think: At the V-AA CC said NO to LYSO’s RSO)

A 
V = Vasoactive Amines (HA and 5-HT)
AA = Arachidonic Acid Metabolites
CC = Cytokines and chemokines
NO = Nitrous Oxide
Lyso = Lysosomal Contents
RSO = Reactive Oxygen Species??
98
Q

Aspects of Acute Inflammation

A

1) Immediate Onset
2) Short duration (only as long as stimulus lasts)
3) BVs allows WBCs to leave and go into tissues

99
Q

What is chronic inflammation?

A

1) prolonged onset and duration

2) Typically follows acute but it can be insidious

100
Q

What are the principle cells of chronic inflammation?

A

Lymphocytes, plasma cells and macrophages

101
Q

What are the vasoactive mediators in inflammation?

A

Bradykinin
Substance P
HA
Also Cytokines (IL-1, IFN-TFN)

102
Q

During inflammation, how are endothelial gaps widened?

A

Via constriction of endothelial cells

103
Q

Where is the the inflammation response most important?

A

In the efferent venule (dilation there) versus the afferent arteriole

Pathology, Exam 1 (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions