Brainscape's Knowledge GenomeTM

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


See full index

Histology Fall 2012 > Histology w Introdcution to Histopathy-Wound Healing 11.15.12 > Flashcards

Histology w Introdcution to Histopathy-Wound Healing 11.15.12 Flashcards

1
Q

What are 3 primary morphological classes of Disease

A

Degenerative

Inflammation

Neoplastic

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

What are 2 Primary morphological classes of inflammation?

A

Acute (neutrophil)

Chronic (lymphs- B & T; monocytes; macrophages)

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

What are 2 primary morphologies for NEOPLASMS

A

Benign (no infiltration into other tissues)

Malignant- Infiltration into other tissue

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

What are 4 primary processes of DEGENERATION

A

Aging

Atrophy

Hyperplasia

Hormonal Involution

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

Cell’s response to Stress

A

Adaptation to environment (i.e. Atrophy)

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

Cell response to Cell INjury

A
  1. Reversible injury, cell recovery, and return to normal function
  2. Apoptosis and programmed cell removal
  3. Cell death and Necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What types of Cell Adaptiations are there to normal chagne it ins enviroment or damaging stimulus

A
  1. Hypertrophy larger cell size (pregnancy-uterus; hypertension in heart; Sport, heart, sk muscles
  2. Atrophy- reduction in cell size Plaster cast (sk muscles)
  3. Hyperplasia (enlargement of organ due to inc. cell number) - Pregnancy (uterus)
  4. METAPLASIA Nromal tissue –> normal tissue

change types of tissue
a. GERD0 acid irritiats esophageal lining –> turns tissue into epithelium with glandular mucus epithe (From squamous)

b. Smoker- noraml ciliatd lining of trachea –> stratified squamous cells

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

What is atrophy?

A

Reduction in size of organ or tissue due to shrinkage of parenchymal cells (cells resp for main fucntion of organ)

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

What is simple atrophy

A

reduction in cell volume

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

What is number atrophy

A

Reduction in cell number (by apoptsis)

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

Is atrophy reversible?

A

Yes, if missing stimulus is replaced

if muscle atrophied due ot decreased load (atrophy of disuse) then re-use of muscles will cause enlargemetn of atrophied fibers

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

What is Endocrine Atrophy

A

Occurs when horone stimulus is reduced or elianted

ie. Estrogen stimulates osteoblasts in somen of reproductive age; after menoapouase, estrogen levels drop – >decrease bone density –> spongy bone weaker and more pourous –> osteoporosis

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

What is brain Atrophy

A

premature abnormal aging of the rain, invovling massive loss fo neurosn and therefore cognitive function

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

What is Cachexia

A

Physical Wasting (atrophy) at organismal level, with loss of weight and muscle mass caused by disease (tumor growth) or starvation (INANITION)

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

What is Compressive Atrophy

A

atrophy may be self-inflicted, or imposed by social mores

Chinese foot-bidning

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

What is Band Atrophy

A

an example of COMPRESSIVE ATROPHY, in whch pressure on an organ or tissue (the optic tract), makes teh nerve and optic disk shrink

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

What is Hypertrophy? What actiates it?

A

Increase in cell or organ size due to INCREASE IN VOLUME of individual organ cells

stimulus that induces increased fucntion activates PROTO-ONCOGENES ; Growth inhibiors prevent MITOSIS, so CELL NUMBER doesn’t incrase

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

Examples of normal hypertrophy

A
  1. long distance runner with increased cardiac muscle cells
  2. Endocrinal Hypertorphy - uterine growth during pregnancy
  3. Compensatory Hypertrophy- with weightlifter and increased sk muscle with increased load
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Examples of Pathological Hypertorphy

A
  1. Muscular Dystrophy (some atrophy, some hypertrophy)

Cardiac muscle increase in size due to HIGH BP

Cardiac muscles increase in sieze due to ABNORMAL MYOSIN (congential hypertrophic cardiomyopathy)

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

What is Hyperplasia

A

enlargement of organ due to Proliferation of Paranchymal Cells

Stmulus that induces increased function activates proto-oncogenes

continued sitimulation activates mitogenes, which cause celsl to divide and multiiply

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

What is Regenerative Hyperplasia

A

Represents re-growth of normal tissue (as when a liver regenerates after protion is removed0)

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

What is Endocrinal Hyperplasia

A

overstimulation of target tisseu by high hormone levels

mammary gland ducts in presence of high esterogen levels

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

What is Compensatory (overload) hyperplasia

A

from chronic loads placed on an organ

HIgh demand for its secretory product can cuase hyperpalsia of an endocrin organ

Chronic kidney disease –> dec in Ca2+ –> increase parathyroid gland activaity –.> inc PTH –> HYEPERPLASIA

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

What is METAPLASIA

A

REVERSIBLE transformation of one normal cell type into antoehr normal cell type

int he esophagus, chronic acid reflux (GERD) irritates the stratified squamous epithelial lining, causing it to transform into a glandular epithelium with goblet cells

SSE –> transofrmed into glandular epithelium with goblet cells

Prevention of acid reflux causes the tissue to rever to SSE

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

What is Dysplasia?

A

Deranged Cell Growth of a specific tissue that results in celsl with abnormal size, shape, and organization

it is potentially reversible, but can develop into cancer

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

Why do cells depend on intact membranes/

A

b/c of their need to maintain an ionic gradient

Calcium gradient is particularly important. Many cellular processes (proteases) are activated when intracellular caclium levels rise, whcih can occur pathologically when the membrane is damaged

27
Q

What does low oxygen (hypoxia, ischemia) lead to?

A

reduced mitochondrial functin, wtha number of negative metabolic consequences

28
Q

What is apoptosis?

A

programmed cell death, ocurs as a result of a killing proces,either initatd by teh cell itself, or triggered by adjacent cells

Apoptosis Results in Shrinkage and Necrosis, int eh ABSENCE OF INFLAMMATION

29
Q

what is the differnce between apoptosis and necrosisW

A

Apoptosis- phagocytosis of apoptotic cells and fragments

Necrosis- enzymatic digestion and leakage of cellular contents

30
Q

What is necrosis?

A

cells may be too seriously damaged to undergo slow, controlled apoptotic process, in which case they lyse and die

Necrosis is the SUM of all morphological phenomena occurring int eh wake of a partial or total cell or tissue death in a living body

31
Q

what are the two types of necrosis ?

A

Coagulative or Liquefactive

32
Q

What is Coagulatie necorsis

A

macroscopic transformation of a completely dead area of tissue into a yellowish, dry, mortar0like mass as a result of PROTEIN PRECIPITATION (coagulation)

33
Q

What is Liquefactive Necrosis

A

Macroscopic soft, mushy transformation of an area of dead tissue due to rapid enzymatic digestion by cellular proteases

THe principal process here is hydroysis rather than precipitaiton

34
Q

What is gangrene?

A

dry coagulatie necrosis

35
Q

What are the five signs of INFLAMMATION

A

calor- local hypohtermia, fever

Rubor- hyperemia (redness)

Tumor (tissue swelling)

Dolor- Burning, pain

Fntiolesa- funcitonal impairment

36
Q

What is the difference between INFLAMMATION and NEOPLATIC TU OR

A

inflammation is always TENDER upon palpation

Neoplastic tumor is not

37
Q

What is the cell for Acute Inflammation

A

Neutrophil

38
Q

What cell type is the 1st to signal that there is a problem by releasing cytokines?

A

Mast Cells

39
Q

What is the first phase of Inflammaton?

A

The vascular phase

  1. Reduction of Blood flow- phase is hsort (minutes) , but causes intiail Pallor (paleness)`
  2. Blood Flow INcreases: into infected area, causing reddenign (Rubor
  3. SM sphincters on the exist BC slose, causing blood to back up
    Vascular endothelium becomes leaky, and fluid (with ions, protins, etc) enters the EC space of damaged tissue, causing swelling (tumor, edema). The leakkage of fluid is called EXUDATION
40
Q

What is EXUDATION

A

the leakage of fluid

41
Q

What is the Second Phase of Inflammation?

A

CELLULAR PHASE

Leukocytes, mainly Neutrophils, gather along the margins of the Endothelial Cells (margination_ then bind to endothlium in response to signal moleucles emanating form teh damaged tissue (Adhesion)

Leukocytes cross the endothelial wall by DIAPEDESIS (transmigration) and enter CT, where they become active

42
Q

What are the types of Acute Inflammation

A

Serous Inflammtion

Seromucous Inflammation

43
Q

What is Serous Inflammation?

A

acute inflammation with exudate of fibrin-free serum

Serous = watery

i.e. serous membranes of the larynx and epiglottis’ when seriously inflamed can cause asphysixa

44
Q

What is Seromucous Inflammation (C)?

A

Seromucous Inflammation- acute inflammation of mucous membranes of respriatory and GI tract (i.e. the ones that normally produce a mucous secreation).

Watery exudate of serum and mucus

i.e. Acute rhinitis (common cold)

Virus infects and kill the epithelial; the body rspons with INFLAMMATIONand ExuDATINO.

The inflammation irritates the epithelium, which udnergoes HYPERPLASIA (D) to rpoduce many mucus-producing cells –> Runny Nose

45
Q

What is Fibrinous Inflammatin

A

form of acute inflammation that produces an exudate of Fibrinogen-containing serum that polymeraized to fibrin outside the BV .

This serves to immoblize and fix pathogens

i.e. Fibrinous Pericarditis- inflammation of the pericardium, with fibrin-rich exudate that forms adhesiosn with teh heart muscle, imeding its movement.

46
Q

What is Fibrinous Mucosal Inflammation?

A

type of Fibrinous Inflammation
Fibrin-rich exudate forms in a mucosa, generally after epithelium has been damaged (eg by a pathogen) and beomes necrotic

47
Q

What is Diptherial Infectino

A

type of fibrinous mucosal inflammation

48
Q

What is Antibiotic-associated enterocolitis

A

Inflammation of the large bowel during antibiotic therapy

ANtibitooic Tx reduces populations normal gut organisms, facilitating growth of Clostritidum difficile, which releases toxic substances (endotoxins) that kill the gut epithelium,.
Small spots are similar to Diptheria-induced lesions

49
Q

What is MUCOPURULENT INFLAMMATION

A

Form of pus-containing (suppurative) inflammation that affects mucosal tissue.

Epithelium is damaged by a pathogen, the resulting tissue debris becomes massively infected, and neutrophils

DAMAGED TISSUE IS DISSOLVED (this has signgiiacnt implications for wound healing)

Acute appendicits shows all the classic features of acute inflamation

50
Q

What is Fibrinous Pericarditis

A

Fibrinous Inflammation

produces exudate of Fibrinogen-containing serum that polymerizes to fibrin outside the BV

serves to immobilixe pathogens

51
Q

Diptherial Infection

A

Fibrinous Mucosal Inflammation

Fibrin-rich exudate forms in a mucosa, generally after epithelium has been damaged and become necrotic

52
Q

Antibiotic-associated Enterocolities

A

FIBRINOUS MUCOSAL INFLAMMATION

Antibiotic treatment reduces populations of normal gut organisms, facilitating growht of Clostiridum difficle, which releases toxic substance (endotoxins) that kil the gut epithelium

53
Q

Fibrinopurulent Appendicitis

A

mucosa has been destroyed and replaced by FIBRINOUS EXUDATE of inflammatory cells (mostly NEUTROPHILS), pathogens, and cellular debris

Acellular pink region is CLOTTED FIBRIN

54
Q

Appendiciitis with Lequefactive Necrosis

A

mucosa has been destoryed and replaced by a fibrin-free PURULENT EXUDATE containing inflammatory cells (mostly NEUTROPHISL), pathogens, and cellular debris

55
Q

Neutrophil Chemotaxis

A

BV in the uscualr wall of the appendix

concentration of WBC marginating against the vessel walls ,preparign to cross into surrounding tissue

In venule, lots of Neutrphils in peripheral

NOT SUPPOSE TO BE IN A LOT IN PERIPHERAL BLOOD!

56
Q

Acute Suppurative (purulent) Inflammation

A

of the meningieso f brain

Can result from middle-ear infectios or BB infections with Neisseira meningitids

Acute Suppurative Inflammtion fo bronchi within the lung (arrows)

57
Q

INFLUENZAL PENUMONIA

A

Hemorrhagic Inflammation

Acute Inflammation involving microvascular injury and massive bleeding, producing an EXUDATE containing many RBCs

Viral destruction of alveolar epithelium damages underlyign capillaries, causing bleeding direlty into alveolar spaces

Smilar process takes place in PNEUMONIC PLAGUE

58
Q

NECROTIZING INFLAMMATION

A

acute inflammation with extensive necrosis

59
Q

Peptic Ulcer

A

Type of NEcrotizing INflammation

Infection with H pylori has caused necrosis through entire depth of mucosa, completely down to the udnerlyign mucular wall of sotmach.

Rim of crater is made of GRANULATION TISSUE

60
Q

What is the rim of the “crater” made in an ulcer called?

A

Granulation Tissue

61
Q

Summary of Steps in Acute Inflammation

A
  1. Mast Cells signal injury –> release Substanve, Histamine, Inflammation markers
  2. Inclrease permeabilty and vasodilation, F inot capillaries
  3. Sweeling, wmaring, reddening, pain (act nociceptors, R of pain) + Granulocyte stim muscle of neutrophils
  4. Four etc, inc WB, result from signal that cells release
62
Q

Chronic Inflammation

A

represents bodys attempt to heal an area that is acutely inflamed

Hallmark of this process is the GRANULMOA, which ahs 3 zones

63
Q

What are the 3 zones of the Granuloma

A
  1. RESORPTION ZONE- bordersthe necrotic area; contains large numbers of phagocytotic cells (neutrophils and macrophages); pathoglics call macrophages histiocytes”
  2. GRANULATION ZONE
    Repair zone, rich in FIBROBLASTS and CAPILLARIES. Capillaries look granular, hence the name “GRANULATION TISSUE”
  3. MATURE CT ZONE
    Fibroblasts and CT; a repaired/rebuilt zone

Histology Fall 2012 (6 decks)

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