Brainscape's Knowledge GenomeTM

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


See full index

Pathology- Inflammation > Inflammation > Flashcards

Inflammation Flashcards

0
Q

What is the intrinsic apoptosis pathway and when does it occur?

A

The intrinsic pathway occurs during embryogenesis, menstruation, menopause, radiation, toxins, and hypoxia.

Increase in Bax (pro-apoptotic) and decrease in Bcl-2 (anti-apoptotic) lead to increased mitochondrial permeability and cytochrome c release which activates cytosolic caspases.

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

What is apoptosis, does it require ATP, or inflammation and what is it characterized by?What are the 2 apoptotic pathways?

A

Apoptosis is genetically programmed cell death. It is characterized by cell shrinkage, nuclear shrinkage, and basophilia (pyknosis), membrane blebbing, nuclear fragmentation (karyorrhexis), nuclear fading (karyolysis), and formation of apoptotic bodies, which are phagocytosed. It requires ATP. No significant inflammation. It consists of intrinsic and extrinsic pathways which activates caspases that mediate cellular breakdown.

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

What is the extrinsic apoptosis pathway and when does it occur?

A

(2)extrinsic pathways activate caspases:
1- ligand receptor interactions (Fas Ligand -FasR CD95): cancers use it

2- immune Killer T-cell attacks virus infected cells: perforin (creates pores in cell membrane) & Granzyme B (enters to activate caspases).

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

What is necrosis and how does it differ from apoptosis?

A

Necrosis is enzymatic degradation & protein denaturing of cells resulting from exogenous injury. Intracellular components extravasate. Unlike apoptosis it is an inflammatory process.

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

What are the 6 types of necrosis?

A

Coagulative, liquefactive, caseous, fatty, fibrinoid, & gangrenous.

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

What are characteristics of Coagulative & Liquifactive?

A

Coagulative necrosis can happen in any tissue except the brain. The kidney/liver/heart remains firm, nucleus of cells disappears but the overall shape is normal.
Liquefactive necrosis is basically pus (neutrophils + cell debri) and happens in bacterial abscess, in the Brain, and pleural effusion.

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

What are characteristics of Caseous and Fatty necrosis?

A

Caseous necrosis is a combination of coagulative & liquifactive necrosis: it is characterized by caseating granuloma (pathogen, macrophage, B cells, T cells) and happens in TB & systemic fungi.
Fatty necrosis occurs in breast trauma and pancreatitis (lipase saponification). It is chalky white debri with bluish cast of Calcium & basophilic.

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

What are characteristics of Fibrinoid & Gangrenous necrosis?

A

Fibrinoid necrosis occurs in blood vessels and are microscopic changes which consist of fibrin + Ig complexes.
Gangrenous necrosis is common in limbs and the GI tract. It can be Dry (ischemic coagulation) or Wet (liquefaction with bacteria).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Characterize cell injury: reversible

A

Reversible (with O2) is characterized by decreased ATP synthesis, cellular swelling due to impaired Na/K pump, nuclear chromatin clumping (acidosis), decreased glycogen, fatty change, and ribosomal detachment which causes decreased protein synthesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Characterize cell injury: irreversible

A

Irreversible cell injury is mainly characterized by plasma membrane damage. 3 stages: pyknosis ( nuclear condensed basophilia), karyorrhexis (nuclear fragmentation), and karyolysis (nuclear fading/dissolved). Calcium influx activates caspases. Lysosomal rupture causes hydrolytic enzymes to leak. Mitochondrial permeability cause electron transport lost & cytochrome c leaks into cytosol activates caspases causing apoptosis.

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

What causes increased erythrocyte sedimentation rate (ESR)?

What decreases erythrocyte sedimentation rate (ESR)?

A

Inflammation, Infections, cancer, pregnancy, & SLE cause increased ESR:
Products of inflammation such as fibrinogen coat RBCs and cause aggregation so they fall at a faster rate within the test tube.

Decreased ESR occurs in sickle cell (altered shape), polycythemia (too many), CHF (unknown ).

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

Compare Transudate vs Exudate.

A

Transudate: hypo cellular, protein poor, specific gravity < 1.012. Caused by increased hydrostatic pressure, decreased oncotic pressure, and Na retention.

Exudate: cellular, protein rich, specific gravity > 1.020. Caused by lymphatic obstruction or inflammation.

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

What is the mechanism of granulomatous disease?

A

Th1 cells secrete gamma interferon, activate macrophages which secrete TNFalpha which induces and maintains granuloma formation. Anti-TNF drugs can break down granuloma a causing spread/disseminated disease

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

What are 9 causes of Granulomatous diseases?

A
  1. TB - caseating
  2. Fungal infections (ie histoplasmosis)
  3. Syphilis (Treponema pallidum)
  4. Leprosy (M. Leprae)
  5. Cat scratch disease (Bartonella henselae) - suppurative
  6. Sarcoidosis - sorry its noncaseating
  7. Berylliosis (lung;inhalation of Berium)
  8. Chron’s disease.
  9. Rheumatoid Arthritis - necrotizing ‘bumps’
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is one of the leading causes of fatality from toxicological agents in children, the mechanism, and symptoms?

A

Iron poisoning causes cell death by peroxidation of membrane lipids.
Acute iron poisoning causes GI bleeding as result of perforation.
Chronic iron poisoning causes metabolic acidosis, and scarring leading to GI obstruction.

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

What is amyloidosis and the gross characteristic of the tissue?

A

Misfolded protein deposits in the extra cellular space damages tissues: systemic/localized.
Beta pleated sheet demonstrated by apple-green bifringence of Congo red stain under polarized light. Affected tissue has “waxy appearance.”

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

What 2 types of amyloidosis are systemic and what is the protein in each & and where is it derived from?

A

Bence Jones (primary)= is caused by AL derived from Ig light chains in multiple myeloma.

Secondary= is caused by AA (acute phase reactant) derived from Serum Amyloid Associated (SAA) protein in chronic inflammatory disease.

Both are DX via tissue biopsy

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

What are localized causes of amyloidosis?

A 
Senile cardiac
Familial Amyloid Cardiomyopathy 
T2DM
Medullary carcinoma of the thyroid
Alzheimer's disease
Dialysis associated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is senile cardiac amyloidosis, the protein involved and where it’s derived from?

A

Occurs in old people about 25% of 80 yo. The protein deposit is AF derived from Transthyretin

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

What is Familial Amyloid Cardiomyopathy and the protein involved?

A

Familial Amyloid Cardiomyopathy is mutated Transthyretin deposits in the heart that lead to Restrictive Cardiomyopathy.

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

What is T2DM amyloidosis, the protein involved and where it’s derived from?

A

T2DM Amyloidosis involves AE (E for Endocrine) deposits derived from Amylin (insulin part).

21
Q

What is medullary carcinoma of the thyroid amyloidosis, what protein is involved and where is it derived from?

A

The protein deposit is A-CAL derived from CALcitonin produced by tumor cells. The tumor cells are soaked in an amyloid background.

22
Q

What is Alzheimer’s disease amyloidosis, what is the protein involved, where is it derived from, and which patient population are at highest risk to have it by age 40?

A

Alzheimer’s disease Amyloidosis involves Beta-amyloid deposits in the brain which are derived from Amyloid precursor protein (5-APP) located on chromosome 21 so most Down syndrome patients develop Alzheimer’s by age 40!

23
Q

What is Dialysis associated amyloidosis, what protein is involved, and where is it derived from?

A

Dialysis associated amyloidosis is caused by deposits in the joints of Beta2-microglobulin derived from MHC class I proteins.

24
Q

What is a keloid and what characterizes it?

A

A keloid is (defective wound healing) excess production of scar tissue that is out of proportion to the size of the scar. It is made of excess Type 3 collagen (not the permanent tensile type 1), has a genetic predisposition in Blacks. It classically affects the earlobes, face, and upper extremity.

25
Q

What are the 3 stages of wound healing?

A
  1. Inflammatory (immediate)
  2. Proliferative (2-3 days post injury)
  3. Remodeling (1 week post injury)
26
Q

What are the mediators and characteristics of the first phase of wound healing?

A

The mediators if the inflammatory phase are platelets, neutrophils, and macrophages. It involves clot formation, increased veno permeability and neutrophil migration into the tissue. Macrophages clear debris 2 days later.

27
Q

What are the mediators and characteristics of the second phase of wound healing?

A

The mediators of the proliferative phase of wound healing are fibroblasts (from macrophage growth factor secretion), myofibroblasts, endothelial cells, and keratinocytes. It consists of deposition of granulation tissue and collagen, angiogenesis, epithelial cells which crawl from basal layer to proliferate, dissolution of clots, and wound contraction of the wound via myofibroblasts.

28
Q

What are the mediators and characteristics of the last phase of wound healing?

A

The remodeling phase mediators are only fibroblasts which commit apoptosis when they are done with collagen formation. Type 3 collagen is removed by collegenase (cofactor is zinc) and replaced by cross linked Type 1 collagen (Vitamin C dependent). The tensile strength of the tissue is great.

29
Q

What are the two types of shock and their characteristics?

A

Hypovolemic/cardiogenic shock = low output failure with increased TPR, low cardiac output, cold clammy patient.

Septic shock = high output failure with decreased TPR, dilated arterioles & high venous return, hot patient (fever).

30
Q

What are the differences between a red and a pale infarct?

A

REd infarct is due to REperfusion injury (free radical damage) or due to loose tissues with collaterals such as liver, lungs, and intestines.

Pale infarcts occur in solid tissues with one blood supply such as the heart and kidneys.

31
Q

What is hypoxia and what are the 3 main categories of hypoxia?

A

Hypoxia is low O2 delivery and caused by:
1-Ischemia (decreased blood flow to an organ)
2-Hypoxemia (decreased pressure Po2 in blood)
3-Decreased oxygen carrying capacity.

32
Q

What are three possible causes of ischemia

A

Decreased arterial perfusion: atherosclerosis
Decreased venous drainage: Budd-Chiarri syn.
Shock: hypotension

33
Q

What is hypoxemia & what are 4 causes of hypoxemia?

A

Hypoxemia is decreased pressure oxygen in the blood ( Pao2< 90% & normal Sao2)

  1. High altitude: decreased pressure
  2. Hypoventilation: high pCO2 causes low O2
  3. Diffusion defect: pulmonary fibrosis
  4. V/Q mismatch
34
Q

What causes decreased O2 carry capacity?

A
  1. Anemia (less RBCs): Pao2 & Sao2 normal
  2. CO poison: Pao2 normal & Sao2 decreased
    - - cherry red skin, headache to coma to death.
  3. Methemoglobin: Pao2 normal & Sao2 decreased = ferric (3+)&raquo_space;> ferrous (2+) causes decreased ability to bind O2. Caused by oxidative stress ie sulfa/ nitrite drugs in newborn. Chocolate colored blood treat with IV methylene blue.
35
Q

What organs are susceptible to hypoxia?

A

Watershed areas: splenic flexure, ACA/ MCA.
Heart: subendocardial tissue (not in contact with blood).
Kidneys: PCT/ TAL.
Liver: around central vein.
Neurons

36
Q

What are the steps of leukocyte extravasion?

A

Margination occurs first.

  1. Rolling
  2. Adhesion/tight binding
  3. Diapedesis
  4. Migration
37
Q

During leukocyte extravasion what happens during margination?

A

During margination vasodilation slows blood flow in postcapillary venules and cells marginate from the center of flow to the periphery.

38
Q

During leukocyte extravasion what happens during rolling step?

A

The endothelium is induced by TNFalpha & IL1 to express E-selectin which bind Sialyl Lewis on the leukocytes transiently causing rolling. P-selectin stored in Weibel-Palade Bodies are expressed as a result of histamine.

“Roll selection for Lewis”

39
Q

During leukocyte extravasion what happens during adhesion (tight binding)?

A

ICAM-1 on the endothelium binds LFA-1 (integrin).

40
Q

During leukocyte extravasion what occurs during diapedesis?

A

During diapedesis leukocytes travel between the endothelial cells and exit the blood vessel ( pt of no return). PECAM-1 is expressed on both the endothelium and neutrophils.

41
Q

During leukocyte extravasion what characterizes the migration step?

A

During the migration step, leukocyte travels through interstitium to the site of injury or infection guided by chemotactic signals: must know the “CILK” v8 used to migrate and hone in =
C5a
IL-8
LTB4 & Kallikrein

42
Q

How does free radical injury damage cells?

A

Free radical damage cells via membrane lipid peroxidation, protein modification, and DNA breakage.

43
Q

Where do free radicals that can cause tissue damage come from?

A

Radiation exposure, metabolism of drugs in phase 1, redox reactions, nitric oxide, transition metals, and leukocyte oxidative burst.

44
Q

How are free radicals eliminated?

A

Free radicals are eliminated via enzymes (catalase, SOD, glutathione peroxidase), spontaneous decay, and antioxidants (vitamins A,C,E).

45
Q

What 6 pathologies are associated with free radical damage?

A
  1. Retinopathy of prematurity
  2. Broncho pulmonary dysplasia
  3. CCl4 leading to liver necrosis (fatty change)
  4. Acetaminophen
  5. Iron overload
  6. Reperfusion after anoxia especially after thrombolytic therapy.
46
Q

What is atrophy and 6 examples?

A

Atrophy is reduction in size (ubiquitin proteosome degradation) or number (apoptosis) of cells as a result of decreased stress. Causes include:

  1. Decreased hormones (uterus/vagina)
  2. Decreased innervation (motor neuron damage)
  3. Decreased blood flow
  4. Decreased nutrients
  5. Increased pressure in nephrolithiasis.
  6. Occlusion of secretory ducts (CF)
47
Q

What are the 5 characteristics of inflammation and what are they caused from?

A

Rubor- redness & Calor- heat = due to vasodilation and increased blood flow. Arteriolar smooth muscle relaxation is mediated by histamine, prostaglandins, and bradykinin.

Dolor- pain = bradykinin & prostaglandins sensitize nerve endings.

Tumor- swelling = due to exudate leaking from postcspillary venules into the interstitium and mediated by histamine (endothelial cell contraction increases gaps) & tissue damage (endothelial cell disruption).

Functio laesa- loss of function

48
Q

What are the 3 stages of inflammation and their characteristics?

A
  1. Fluid exudation (increased vascular permeability, vasodilation, endothelial injury).
  2. Fibrosis (fibroblast emigration & proliferation; deposition of extra cellular matrix).
  3. Resolution: restoration of normal structure or granulation tissue (highly vascularized & fibrotic), abscess (fibrosis surrounding pus), fistula (abnormal communication), or scarring (collagen deposition resulting in altered structure & function).
49
Q

Differentiate between Acute & Chronic inflammation.

A

Acute inflammation is immediate (secs-mins) lasts minutes to days with limited specificity. It involves neutrophils, eosinophils, and antibody mediated (complement).

Chronic inflammation is delayed but more specific with mononuclears (lymphocytes & plasma cells). It is characterized by persistent destruction and repair, blood vessel proliferation and fibrosis. Granuloma is prominent (modular collections of epithelioid macrophages & giant cells).

Pathology- Inflammation (2 decks)

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