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Pathology Exam 1 > Intro to Pathology > Flashcards

Intro to Pathology Flashcards

1
Q

What is pathology?

A

study of suffering

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2
Q

What is a pathologist

A

trained in diagnosis of disease on the gross, microscopic and ultrastructural level

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3
Q

what is thanatology?

A

study of death

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4
Q

What does thanatology involve?

A 
1) signs of death
2 agonal and postmortem processes
3) exam of corps/carcasses
4) determination of cause of death
5) determination of manner of death
6) determination of mechanism of death; final common pathways of death
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5
Q

What is agony?

A

1) transition time from life to death

2) loss of fn and coordination of respiratory system, CV and CNS –> generalized organ dysfunction

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6
Q

Describe different time durations of agony

A

1) very short: seconds - gun shot wound to heart
2) short: minutes - exsanguination from liver rupture
3) hrs: neoplastic diseases

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7
Q

Define cause of death

A

disease or injury responsible for the terminal lethal sequence of events

  • may include a root and an immediate cause
  • is as specific as possible
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8
Q

Give an example of a root and an immediate cause

A

root: husbandry
immediate: marked acute fibrinous pleuropneumonia

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9
Q

Define mechanism of death

A

alterations of physiology and biochemistry whereby the cause of death exerts its lethal effect (final terminal events)
-etiologically unspecific

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10
Q

What are the types of “manner of death”

A

natural, non-natural (or violent) or undetermined

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11
Q

What are violent manners of death?

A

accident, homocide, suicide

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12
Q

What are the types of death?

A

somatic and cell death

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13
Q

what are the death marks?

A

rigor mortis, pallor mortis (paleness), algor mortis, livor mortis, decomposition, skeletonization/mummification

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14
Q

What is death defined as?

A

absence of vital signs

  • brain death
  • permanent vegetative state
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15
Q

What are the 4 aspects of the disease process?

A

etiology = why
pathogenesis = how
morphologic changes
clinical significance

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16
Q

Define etiology

A

the science or study of causation (some form of noxious stimulus)
-cause or causative factor

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17
Q

Define pathogenesis

A

mechanisms of disease or sequence fo events in the development of a lesion, clinical signs, from inception/initial stimulus to resolution

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18
Q

What are morph changes?

A

structural alterations in cells or tissues characteristic of disease or diagnostic of etiology

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19
Q

What is clinical significance?

A

functional consequences of morphologic changes

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20
Q

What is pathology essentially?

A

study of lesions

-structural and/or functional changes associated with disease

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21
Q

What is a lesion?

A

any departure from normal; abnormality in the tissue

-postmortem/euthanasia artifacts vs lesion

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22
Q

Define necropsies

A

systematic examination of a corpse or carcass for lesions by a vet or vet pathologist

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23
Q

What are some postmortem artifacts?

A

autolysis, scavenging, postmortem clots, rigor mortis, bloody imbibition, biliary imbibition, pseudomelanosis

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24
Q

define autolysis

A

putrefaction; inc temp, imc autolysis

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25
Q

define bloody imbibition

A

leakage of vessels

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26
Q

define biliary imbibition

A

gallbladder leaks - greenish coloring

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27
Q

define pseudomelanosis

A

hemorrhage under influence of bacterial enzymes: turn red –> black

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28
Q

what are euthanasia artifacts?

A

deposition of crystallized barbiturates

-spleen congestion

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29
Q

What are agonal lesions?

A

pulmonary congestion and edema; hypostasis

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30
Q

what is hypostasis?

A

pooling of blood on dependent side (in lungs or kidneys)

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31
Q

What are incidental lesions?

A

lesions that do not cause any clinical disease - can predispose the animalt o clinical signs under certain circumstances

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32
Q

What are the characteristics of lesions?

A

1) location
2) shape (symmetry)
3) size
4) color
5) consistency
6) appearance of cut surface
7) odor
8) taste

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33
Q

What is a diagnosis?

A

concise statement or conclusion concerning the nature, cause or name of a disease as determined from careful investigation of the signs/symptoms and history (evidence based)

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34
Q

What is the accuracy of a diagnosis limited by?

A

history provided and the evidence (lesions) available for study

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35
Q

What is a clinical diagnosis?

A

based on the data obtained from the case history, clinical signs/symptoms and physical examinations
-may only suggest the system involved and usually supplemented by a list of differential diagnoses

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36
Q

What is a differential diagnosis?

A

the “rule outs” in clinical medicine; a list of diseases that could account for the evidence or lesions of the case

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37
Q

what is the clinico-pathologic or anatomo-pathologic diagnosis?

A

based on changes observed in the chemistry of fluids and the structure and function of cells collected from the living patient (smears, aspirates, biopsies)

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38
Q

What is a morphologic diagnosis?

A

lesion diagnosis - based on predominant lesions in tissues

-addresses the severity, duration, distribution, location, and nature (degenerative, inflammatory, neoplastic)

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39
Q

What are morphologic differential diagnoses?

A

lesion that looks similar or alike

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40
Q

What is an etiologic differential diagnosis?

A

agents/processes that cause same or similar lesions

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41
Q

define etiologic diagnosis

A

even more definitive and names the specific cause of the disease
(only get this by culturing, need fresh tissue)

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42
Q

define disease diagnosis

A

equally specific as etiologic diagnois and states the common name of the disease

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43
Q

What are the two causes of disease?

A

endogenous (intrinsic) = genetic/certain malformation or immunologic factors
exogenous (extrinsic/acquired) = physical or chemical noxes, alimentary causes, infectious organisms

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44
Q

genetic causes of disease

A

heritable = mutation in germline cells –> can be passed on to offspring
inheritable = mutation in somatic cells –> passed on to subsequent generation of cells but NOT to offspring
-spontaneous or caused by env factors

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45
Q

Name the types of mutations

A

1) single gene
2) genome (numeric chromosomal alterations)
3) chromosome (structural chromosomal alterations)
4) complex multigenic disorders

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46
Q

Name the consequences of point mutations

A

1) silent mutation = doesn’t alter AA seq of protein
2) Missense mutation = single AA change seq
3) nonsense mutation = produces stop codon in mRNA –> terminates tln of protein

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47
Q

Consequences of single gene missense or nonsense?

A

1) formation of abnormal protein
2) reduced or increased synthesis of protein
3) modification of postranslational mechanisms, or transport of proteins out of cell

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48
Q

What types of proteins can be affected?

A

1) enzymes –> accumulation in cell or lysozome
2) membrane receptors and transporters –> accumulation
3) non-enzyme proteins –> structural
4) unusual drug reactions –> multi-drug resistant gene

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49
Q

What are the effects of an enzyme defect?

A

1) accumulation of substrate (storage disease)
2) metabolic block (lack/deficiency of substrate for norm cell fn)
3) failure to inactivate tissue damaging factors

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50
Q

give example of autosomal dominant trait

A

PSSM

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51
Q

give ex of autosomal recessive trait

A

LWFS

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52
Q

give ex of x-linked disorder

A

hemophilia

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53
Q

What are chromosomal disorders

A

numeric alteration of set of chromosomes (genome mutation)

  • entire set may be altered (aneuploidy)
  • only the number of inidividual chromosome is altered (down syndrmoe - trisomy 21)
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54
Q

how are chromosomal disorders created?

A

structural alteration of chromosome by deletion, inversion, isochromosome fomration, translocation
-usually sex chromosomes affected –> intersex

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55
Q

What are complex multigenic/polygenic disorders?

A

caused by interactions of multiple genes and environmental factors
-disease only occurs when multiple polymorphisms occur simultaneously and certain env factors are present

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56
Q

What are the contributing factors of disease?

A

disposition, constitution and conition

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57
Q

What are the two types of dispositions?

A

genetic (species, breed, family, gender, individual) and acquired (nutrition, occupation, age)

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58
Q

Define constitution

A

sum of inherited and acquired dispositions of an individual

-marked individual and temporal variations

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59
Q

Define condition

A

sum of acquired dispositions of an individual influenced mainly by external factors (training, nutrition, climate, hygiene)

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60
Q

What are the different physical noxious stimuli?

A

trauma, temperature, actinic,electricity, climate

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61
Q

Describe different types of trauma

A

1) sharp force injury and gun shot wounds (organ perforation, fractures, exsang)
2) blunt force trauma (distorsion, fractures, dislocation, laceration, contusion)
3) local effects (local infections)
4) systemic effects (anemia, woundd shock, hyperkalemia, bone marrow emboli to lungs (after bone fracture), generalized infection)

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62
Q

define wound shock

A

loss of fluid due to histamine release in damaged tissue (aggravates blood loss)

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63
Q

define hyperkalemia

A

release of intracellular potassium from large number of lethally injured cells –> arrhythmias

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64
Q

define crush kidneys

A

reduced blood supply to kidneys plus increased amt of myoglobin (toxic effect on renal tubules) form damaged muscle cells flooding kidney –> insufficient blood supply; degenerative change in kidney

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65
Q

describe different types of temperature physical noxious stimuli

A

hyperthermia (often in combo ith strenuous exercise), combustio, hypothermia, congelatio

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66
Q

describe consequences of hyperthermia

A

1) denaturing of protein because of heat
2) dehydration due to fluid and electrolyte loss (sweating)
3) vasodilation in skin and vasoconstriction in internal organs –> hypovolemia
4) Heat shock –> DIC, disseminated intravascular coagulation (head exposed to direct heat –>brain overheated, BT norm)

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67
Q

describe combustio

A

burn(dry heat)/scold(hot liquid)

  • everything sloughing off because of over exposed sun (reddening of skin)
  • animal may burn to death or after burn
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68
Q

describe hypothermia

A

<95 degrees F - not enough blood supply to brain

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69
Q

describe congelatio

A

freezes, damage to internal structure

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70
Q

describe different types of actinic

A

visible sunlight/UV light and ionizing radiation

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71
Q

describe visible sunlight/UV light as a noxious stimuli

A

damaging after photosensitization occurs = presence of photodynamic comp in skin –> damage to non-haired non-pigmented skin regions
-sun burn –> sq cell carcinoma

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72
Q

describe types of ionizing radition

A
  • local radiation versus full body radiation, oral uptake
  • x-rays, gamma rays
  • mitotic active cells and water containing tissues are highly vulnerable
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73
Q

Describe different types of photosensitization

A

1) primary = uptake of photodynamic compounds with food (plants) –> depositio in skin
2) secondary = inherited defect in porphyrin metabolism; aberrant porphyrin metabolites are photodynamic and deposited in skin
3) hepatogenic = only in ruminants;phylloerythrin persists in circulation in animal with liver disease and is deposited in skin

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74
Q

What are the consequences of acute total body radiation?

A

1) central nervous syndrome - death within minutes to hrs, vomiting, cramping,
2) lymphopenia
3) gastro-intestinal syndrome - death w/in 2 wks
4) hematopoietic syndrome - may need bone marrow transplant
5) subclinical or prodromal sndrome - patient can recover

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75
Q

What are some skin reactions as a result of ionizing radiation?

A

1) Epilation (1deg) = loss of keratin and depigmentation of skin and hair
2) Erythema (2deg) = dermatitis, hair loss, depigmentation of re-growing hair
3) Exudate (3deg) = exudative dermatitis with blisters and crusts and permanent alopecia
4) Necrosis and poorly healing ulcers (radiation dermatitis)

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76
Q

What are some chronic consequences of ionizing radiation?

A

1) cancer - leukemia, thyroid, mammary, pulmonary and salivary gland carcinoma, skin cancer
2) Fibrosis - radiation-assoc vasculopathy (hypoperfusion)
3) Others: lymphopenia, infertility (gonad atrophy), cataracts, impaired wound healing

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77
Q

What are examples of electrical noxious stimuli?

A

1) household current - burns, arrhythmia
2) lightening strike
3) power line collisions in birds

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78
Q

What are examples of climate noxious stimuli?

A

1) slow dec in atm pressure and [oxygen], high altitude disease
2) sudden dec in atm P - diver disease
3) sudden inc in atm P (explosion) - pulm hemorrhages

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79
Q

What are chemical noxes?

A

toxins - intoxications (poisoning; exogenous and endogenous

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80
Q

How do chemical noxes get into your system?

A

oral, percutaneous, inhaled, into blood stream (bite)

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81
Q

What are exogenous toxins?

A

1) environmental toxins (lead, mercury)
2) plant toxins (alkaloids, glycosides)
3) Animal toxins (venom)

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82
Q

What are endogenous toxins?

A

by product of metabolism - ammonia, ketones, urates

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83
Q

What are toxins made up of?

A

antigenic and toxiphoric groups

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84
Q

What factors influence toxic effects

A

1) dependent on concentrations
2) route of up-take
3) frequency of up-take
4) toxins must be soluble to be absorbed by cells or at least adherent to cells

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85
Q

What are some effects of toxins?

A

1) cytolysis, altering enzyme activity and cell metabolism
2) biochemical mechanisms (toxify in liver)
3) acute toxicoses vs chronic toxins (carcinogens)
4) reversible vs irreversible effects (cells affected must die off and be replaced)
5) local irritation on skin, alimentary tract and respiratory tract or systemic effects (cardiotoxic, nephrotoxic, hepatotoxic, neurotoxic)

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86
Q

What are host defense mechanisms against toxin?

A

reflexes, elimination and metabolism in the liver

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87
Q

What are some pathologic anatomic findings of intoxication?

A

some have pathogenomic lesions but most have no or unspecific findings

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88
Q

How do you test for toxins?

A

history, CSI, chemical analysis (gastric content, liver, kidney, urine, blood, brain, adipose tissue) - depends on toxin type and time course

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89
Q

What are two ways of testing nutrition?

A

1) quantitative: emaciation (cachexia - def syndrome) and obesity (def)
2) qualitative (hyper/hypo-vitaminoses): lack of essential factors, reduced enteric absorption or presence of capture mols or antagonistic/competing cmpds in food

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90
Q

What is a common nutrition pathology?

A

mineral element deficiency

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91
Q

What are mineral elements function?

A

serve mainly as co-enzymes, regulation of pH in intra and extracellular milieu, and bone formation

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92
Q

Give some examples of mineral element deficiencies

A

1) rickets (P def)
2) tetany (Mg def)
3) milk fever (Ca def)
4) white muscle disease (selenium/vit E def)
5) milk anemia (Fe def)

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93
Q

What are the two types of vitamin pathologies?

A

1) hypovitaminoses (and avitaminoses) - K, A, B1 - due to primary thiamin def or due to presence of thiaminases
2) Hypervitaminoses (fat soluble vits) - A (due to liver diet in cat) and D (iatrogenic)

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94
Q

What is dehydration?

A

lack of water, loss of water (and Na), loss of Na, loss of water via kidney

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95
Q

What’s the cause of loss of water (and Na)?

A

1) diarrhea and vomiting

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96
Q

What’s the cause of loss of sodium?

A

due to deficient Na reabsorption of renal tubular epithelial cells in acute renal failure (hypotone dehydration)

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97
Q

What’s the cause of loss of water (not Na) via kidney?

A

diabetes insipidus and mellitus –> hypertone dehydration, PD

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98
Q

What is hyperhydration?

A

increased infusion of fluid, often iatrogenic

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99
Q

What are the different types of hyperhydration?

A

1) isotone = rate of hydration with physio soln is higher than renal excretion
2) Hypertone = due to inc Na up-take or dec Na excretion in animals with renal insufficiency (inc water excretion)
3) Hypotone = due to infusion with too much hypotone soln, dec water excretion in animals with renal insufficiency –> pulm edema, ascites (accum of clear fluid in abdominal cavity), hydrothorax, brain edema

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100
Q

What is parasitism? ex?

A

negative effect for host; virus, bacteria, fungi, parasite

101
Q

What is an infection?

A

colonization, attachment, invasion and proliferation of obligate or facultative pathogenic parasite
-infection does NOT equal inflammation

102
Q

What may infection result in?

A
  • local or generalized infection

- disease or clinically inapparent

103
Q

Can local infection become generalized?

A

yes

104
Q

Give examples of generalized infection?

A

1) cyclic course
2) septicemia/sepsis
3) virus induced tumor disease (leukemia)
4) diseases due to infection-assoc immune modulation
5) factor diseases and mixed infections

105
Q

What are some causes of diseases? (immunologic reactions)

A

1) immune response - cells damaged in immune response to infectious agents
2) hypersensitivity (allergic) rxns - anaphylactic rxn to a foreign protein or drug
3) autoimmune diseases - rxn to self-antigen

106
Q

cells encountering physiologic stresses or pathologic stimuli can undergo___ to achieve ________

A

adaptation, homeostasis

107
Q

What happens when cells can’t maintain homeostasis?

A

cell injury (demands exceed adaptive capability)

108
Q

Where are cells embedded in?

A

extracellular matrix

109
Q

Whats the fn of cytoskeleton? describe the different types?

A

transport of substances through the cell

microfilaments, intermediate filaments, microtubules

110
Q

What is reversible cell injury?

A

cell degeneration

111
Q

What does irreversible cell injury lead to?

A

necrosis

112
Q

What are causes of reversible and/or irreversible cell injury?

A

O2 deficiency, physical agents, infectious agents, nutritional deficiencies and imbalances, genetic derangement, workload imbalance, chemical drugs and toxins, immunologic dysfunction, aging

113
Q

What is the progression of pathological changes with cell injury?

A

after 6 hrs - 1st lesions often on ultrastructure
after 12 hrs - changes in cell (cell membrane)
another day or so - gross changes

114
Q

Describe mechanisms of cell injury

A
  • dec ATP –> dec cell function
  • membrane and organelle membrane damage:
  • ->lysosome –> leakage –> self digestion
  • ->mito –> cell death
  • ->plasma membrane –> lose cell contents, influx of other comp
  • inc intracellular Ca+2/ROPs –> DNA damage and protein breakdown
115
Q

What intracellular systems are highly vulnerable to cell injury?

A

1) cell membranes
2) aerobic respiration (mito)
3) protein synthesis (ER)
4) genetic apparatus
5) cytoskeleton

116
Q

Define reversible cell injury (cell degen)

A

cell undergoing functional and morphologic changes as a result of injury –> if stimulus is removed in time, changes resolve (cells can still regenerate)
-once pass certain point, injury becomes irreversible –> cell death

117
Q

name characteristics of irreversible cell injury

A

reduced oxidative phosphorylation –> ATP depletion (Na/K ATPase) –> cellular swelling (Na remain in cell and osmotically active –> inc water into cell –> organelles swell)

118
Q

Whats another name for cellular swelling?

A

cell edema

119
Q

What is cell swelling?

A

disturbance of cellular water balance; increased cell size and volume resulting from an overload of water (hyperhydration)
-most common and fundamental expression of cell injury

120
Q

What causes cell swelling?

A

failure of cell volume regulation –> swelling, modification and degeneration of organelles

121
Q

What is hypoxia?

A

reduced oxygen partial pressure in blood or tissue

122
Q

What is ischemic hypoxia?

A

decreased circulation of tissue in terminal capillary bed

123
Q

What does ischemic hypoxia result in?

A

O2 deficiency, dec delivery of nutrients and decreased removal of cytotoxic metabolites

124
Q

What can happen to cells who experience ischemic hypoxia?

A

cells may adapt to mild ischemia (muscle atrophy) or die with severe and sudden onset ischemia

125
Q

What is infarction?

A

localized area of ischemic necrosis (coagulation)

126
Q

What is anemic hypoxia?

A

decreased oxygen carrying capacity of blood

127
Q

define hypoxemic hypoxia

A

respiratory insufficiency (insufficient O2 to lungs), high altitude, crowding in closed rooms

128
Q

define histiotoxic hypoxia

A

oxidative cellular metabolism is impaired (due to toxic insults such as cyanide toxicity)

129
Q

define hypoglycemic hypoxia

A

lack of glucose/substrate for oxidation

130
Q

when does hypoxia occur?

A

reduced amts of saturation of hemoglobin ( really any defect in O2 transportation)

131
Q

When does ischemia occur?

A

mechanical obstruction in the arterial system (thrombus or embolus)
-catastrophic fall in BP (loss of blood)

132
Q

What is the difference btw hypoxia and ischemia?

A

hypoxic conditions - glycolytic energy production can occur
-in ischemia - even delivery of substrates needed for glycolysis and disposal of toxic/injurious metabolites are compromised

133
Q

What does tissue sensitivity to hypoxia depend on?

A

demand of cells (exercise vs sleeping)

134
Q

What tissues are highly/intermediate/low susceptible to hypoxia?

A 
high = neurons
intermediate = hepatocytes, cardiomyocytes, renal and intestinal epithelium
Low = fibroblasts, keratinocytes, myocytes
135
Q

What are gross lesions?

A

organ swelling and pallor (enzyme leakage into blood stream); organ changes that are caused by degenerative changes end with “osis”

136
Q

What is dystrophy?

A

disease that is caused by degenerative changes due to deranged cellular metabolism

137
Q

What is the morphology of cell swelling?

A

1) cell is enlarged
2) nucleus normal position
3) cytoplasm pale or staining altered
- cloudy; vacuolar degeneration - swollen organelles; hydropic degneration - ballooning degen

138
Q

What are common consequences of hypoxic and toxic injury?

A

depletion ATP, decreased ATP synthesis

139
Q

What results from dec ATP/ATP synthesis?

A

inc AMP –> inc anaerobic glycolysis –> inc lactic acid –> dec intracellular pH –> impaired cell enzyme activity

140
Q

T or F: cells with greater glycolytic capacity have an advantage over cells which are more or exclusively reliant on oxidative phosphorylation

A

True

141
Q

What are cytomorphologic changes of irreversible cell injury?

A

1) plasma membrane damage
2) Ca entry into cell
3) mito swelling and vacuolization
4) lysosomal swelling

142
Q

What’s another name for oxidative stress?

A

Free radical induced injury; common cause of damage to cell membranes

143
Q

Describe different ways to generate free radicals

A

1) Cell metabolism (byproduct) - cell redox rxns
2) Enzymatic metabolism of exogenous chemicals (drugs)
3) ionizing radiation - hydrolysis of water into OH and H free radicals
4) Divalent metals - transition metals, catalyze free radical formation, free radicals

144
Q

What are characteristics of free radicals?

A

extremely unstable, readily react with organic or inorganic cmpds, attack and degrade proteins/nucleic acids and membrane mols

145
Q

define oxidative stress

A

cell injury occurs when the free radical generation overwhelms radical-scavenging defense mechanisms

146
Q

What are main sites of damage for free radicals?

A

membranes (cause instability - lipid peroxidation), proteins (structural damage), DNA (cause breaks)

147
Q

the cell’s response to injurious stimuli depends on?

A

type of injury, duration and severity

148
Q

the consequences of cell injury depends on?

A

type, state and adaptability of injured cell

149
Q

When irreversible ischemic injury persist?

A

if ischemia persists

150
Q

What are two characteristics of irreversible ischemia?

A

1) inability to reverse mito dysfunction

2) profound disturbances of membrane function

151
Q

What is the sequence of events in a cell injury?

A

1) Hypoxia - deficiency of O2
2) decrease of oxidative phosphorylatin and then ATP
3) increased glycolysis, increased intracellular lactate (dec pH) and depletion of glycogen stores
4) failure of Na/K pump due to ATP deficiency
5) Net influx of Na, Ca and water with loss of intracellular K and Mg
6) swelling of mito, the cytocavitary network and nucleus
7) detachment of ribosomes, clumping of nuclear chromatin, loss of microvilli, vesiculation of ER
8) severe disruption of cell membranes, influx of Ca into mito and cytosol, overall cell enlargement, release of lysosomal enzymes and clearing of the cytosol
9) irreversible cell injury, cell death

152
Q

What are types of cell death?

A

1) oncosis - cell death due to a lethal insult
2) apoptosis = programmed/genetically controlled cell death due to a suicide signal
3) autophagia

153
Q

What is oncotic necrosis?

A

severely damaged membranes –> lysosomal enzymes enter cytoplasm –> digest cell –> cellular contents leak out

154
Q

define necrosis

A

distinctive morphologic patterns depending on whether enzyme catabolism or protein denaturation predominates

155
Q

What are morphologic patterns of necrosis?

A

Coagulation, liquefactive, casous, gangrenous and fat necrosis

156
Q

What is coagulation necrosis?

A

most common manifestation of cell death; characteristic of hypoxic/ischemic death of cells in all tissues

  • protein denaturation predominates over enzymatic digestion
  • injury/intracellular acidosis denatures enzymatic proteins –> blocks proteolysis
  • brain has a lot of fat
157
Q

What does coagulative necrosis appear grossly?

A
  • architecture resembles normal tissue
  • lighter in color (coagulation of cytoplasmic proteins and decreased blood flow)
  • usually firm
  • tissue may be swollen or shrunken
  • may see a local vascular/inflammatory rxn to necrotic tissue
158
Q

How does coagulative necrosis appear microscopically?

A
  • original cell shape and tissue architecture preserved
  • increased eosinophilia
  • hyalinized (glassy appearance)
  • vacuolated cytoplasm
  • may be mineralized
  • shrunken basophilic nucleus
  • nuclear fragmentation
159
Q

What are cytoplasmic changes in dead cells?

A
  • loss of differential staining characteristics of nucleus and cytoplasm (eosinophilia)
  • massive swelling of cells and organelles with fragmentation
  • loss of cell to cell contact
  • loss of microvilli and cilia
160
Q

What is liquefactive necrosis?

A

enzymatic digestion of necrotic cell predominates

161
Q

When does liquefactive necrosis occur?

A
  • in bacterial infections (neutrophils contain potent hydrolases)
  • in hypoxic damage of CNS
162
Q

What does liquefactive necrosis appear grossly?

A

affected tissue is liquefied to a soft, viscous fluid mass

163
Q

What does liquefactive necrosis appear microscopically?

A

may see degenerative neutrophils and/or amorphous necrotic material

164
Q

When does caseous necrosis occur?

A

seen with specific bacterial diseases

165
Q

How does caseous necrosis appear grossly?

A

cheesy; grey white dry, friable to pasty necrotic material; freq with dystrophic calcification

166
Q

How does caseous necrosis appear microscopically?

A

dead cells persisting as amorphous, coarsely granular eosinophilic debris

  • necrotic cells do not retain cellular outline
  • necrotic cells do not undergo complete dissolution
  • freq association with granulomatous inflammation and thick outer fibrous capsule
167
Q

What is gangrenous necrosis?

A

ischemic necrosis of extremities; gangrenous inflammation = aspiration penumonia and gangrenous mastitis (very malodorous)

168
Q

What is dry gangrene?

A

coagulation necrosis of an extremity with subsequent mummification

169
Q

What is wet gangrene?

A

when the coagulative necrosis of dry gangrene is modified by the liquefactive action of saprophytic/putrefactive bacteria

170
Q

what is gas gangrene (emphysematous)?

A

clostridial infections with necrosis and gas production

171
Q

How is fat necrosis distinguished?

A

by its location in body fat stores

172
Q

What is the cause of fat necrosis?

A

inflammation, Vit E deficiency, trauma, idiopathic

173
Q

How does fat necrosis appear grossly?

A

firm to hard, white/chalky and gritty areas; can be soft

174
Q

How does fat necrosis appear microscopically?

A

ares of necrosis of fat tissue

-see basophilic calcium deposits and often surrounded by inflammatory cells

175
Q

What is hemorrhagic necrosis?

A

necrosis + hemorrhage;

  • usually when venous outflow to tissue is blocked
  • hemorrhagic infarction of bowel
176
Q

What is fibrinoid necrosis?

A

vasculature affected

  • freq found in auto-immune disease but also in lead toxicosis
  • histo: eosinophilia and hyaline appearance of media of vasculature
177
Q

What are consequences of necrosis?

A
  • biochemical changes: leakage of tissue specific enzymes; detectable in serum
  • Inflammation: beginning at transition of necrotic to healthy tissue
178
Q

What is the outcome of necrosis?

A

1) restitutio ad integrum (regeneration with restoring of normal fn)
2) reparation (scarring, healing without restitution)
3) Demarcation (including sequester formation/sequestration)

179
Q

What factors must be present in order for regeneration to occur?

A
  • if damage was minor
  • if texture of tissue was maintained
  • if affected tissue/individual has good healing capacity
180
Q

What happens with demarcation of necrosis?

A
  • necrotic tissue is surrounded by area of inflammation (reddened)
  • shedding of damaged tissue in skin and mucous membranes (ulcer)
  • sequester in lung and bone (with fistulous tract)
181
Q

What is apoptosis?

A

programmed cell death; nuclear dissolution without loss of membrane integrity; cell dies thru activation of an internally controleld suicide program; may be physiologic or pathologic

182
Q

What are causes of apoptosis?

A

1) cells undergoing programmed cell death during embryogenesis
2) cells undergoing normal turnover (cell deletion in proliferating pop)
3) immune system (deletion of autoreactive T cell clones in thymus)
4) cell death in neoplasms
5) pathogenic stimuli (viruses, immune-mediated processes)

183
Q

What are mechanisms of apoptosis?

A

genetically determined, energy-dep sequence of molecular events of initial cell signaling (initiation phase), regulation by regulatory mols, (execution phase) and dead cell removal (phagocytosis

184
Q

describe the two pathways of apoptosis

A
  • extrinsic pathway = receptor-initiated, ligand-binding, initiator capase
  • intrinsic pathway = mitochondrial pathway; if cytochrome c is released and other members join –> activation of caspases and executioner caspases; pro=Bak mol, anti=Bcl mol –> which side has larger [ ] of mols dictates end result
185
Q

What is the execution phase of apoptosis?

A

proteolytic cascade that ultimately results in activation of the execution caspase 3 or 6

186
Q

What is a caspase?

A

C=cysteine enzyme
aspase=capability to cleave aspartic acid residues
-exist as proenzymes (zymogens) and needs to be cleaved for activation

187
Q

What does a caspase do?

A

cleave proteins of cytoskeleton and nuclear matrix, proteins involved in txn and tln process, proteins of DNA repair machinery

188
Q

Describe the morphology of apoptosis

A

1) cell shrinking
2) chromatin condensation
3) Formation of cytoplasmic blebs than apoptotic bodies
4) phagocytosis of apoptotic cells/bodies

189
Q

Describe main differences btw apoptosis and cell necrosis pathways

A

-both programmed cell death pathways
Apoptosis: cell shrinks –> with budding/blebbing –> clean up by phagocytes
Necrosis –> cell swells –> with blebbing –> elicit inflammatory rxn

190
Q

What are some apoptosis assays?

A

1) nuclear morphology: chromatin condensation and nuclear lobulation/fragmentation) in histo/EM
2) TUNEL and related assays
3) Caspase assays
4) Cyt C release into cytosol (want to see activated caspases)

191
Q

How does a cell adapt to a “workload” imbalance?

A

1) atrophy when cells are no longer stimulated (can become necrotic)
2) hypertrophy/hyperplasia when cells are overstimulated
3) metaplasia: reversible, replacement of one adult cell types by another cell types of the same germ line (more to less specialized)
4) Dysplasia
5) Anaplasia

192
Q

Define atrophy

A

focal or diffuse shrinkage of organ; reduction of cell size and number OR numeric atrophy with lipomatosis (loss of cells but replacement by adipocytes)

193
Q

When does physiologic atrophy occur?

A

fetal development, thymus atrophy/atrophy of lymphoid tissue, senile atrophy (brown atrophy due to intracellular lipofuscin accumulation), age-independent atrophy (involution of uterus/mammary gland post partum)

194
Q

What are pathologic atrophies?

A

1) localized = disuse atrophy, neurogenic atrophy, ischemic atrophy, compression/pressure atrophy, nerve cell atrophy
2) Generalized = inanition atrophy (starvation), systemic atrophy

195
Q

Describe the mechanism of atrophy

A

increased protein degradation through:

1) lysosonal acid hydrolases
2) ubiquitin-proteasome pathway
- often accompanied by increased numbers of autophagic vacuoles
- if not digestible, membrane bound residual bodies remain

196
Q

Define hypertrophy

A

response to increased stimulation of post-mitotic cell (permanent cells - neurons and cardiomyocytes)

197
Q

Define hyperplasia

A

response to increased stimulation of cells with mitotic capacity (quiescent and labile)

198
Q

What is metaplasia due to?

A

chronic damage

199
Q

What are examples of metaplasia?

A

1) chronic irritation/inflammation = squamous metaplasia of respiratory epith
2) Vit A deficiency = squamous metaplasia of respiratory epith and glandular epith in psittacine birds
3) Hyperestrogenism = prostatic squamous metaplasia in ferret with adrenal tumor/ in dogs with testicular sertoli cell tumor

200
Q

What are intracellular accumulations?

A

evidence of chronic sublethal cell injury and cellular adaptation

201
Q

What are different types of intracellular accumulations?

A

1) accumulation of normal cellular comp due to increased production or decreased disposal
2) accumulation of abnormal cellular cop due to production of abnormal mols (endo) or due to up-take of cmpds (exo)
3) Accumulation of pigment

202
Q

Describe characteristics of intracellular accumulations?

A

1) increase of cell size if severe enough
2) usually harmless to cell but occasional toxic
3) intracytoplasmic or intranuclear
4) may be reversible or permanent

203
Q

What are causes of intracellular accumulations?

A

1) too much of a normal cell comp (lipid accumulation)
2) genetic or acquired defect of metabolism resulting in prod of non-functional enzymes (storage disease)
3) inability to degrade phagocytized material

204
Q

What are intracellular lipid accumulations due to?

A

deranged intracellular fat metabolism

-TAGs, cholesterol esthers, phospholipids

205
Q

Where does intracellular lipid accumulations occur?

A

in hepatocytes and cardiomyocytes, myocytes and renal tubular epith cells

206
Q

What is hepatocellular degeneration?

A

fatty liver, hepatic steatosis or lipidosis

207
Q

What are the stages of hepatocellular degeneration?

A

1) early stages = FAs accumulate in small globules in cytoplasm of hepatocytes; cell have sharply delineated round clear cytoplasmic vacuoles
2) severe or long-standing=globules fuse –> large globule, uniformly light yellow, greasy and friable, floats in water or fixative

208
Q

What is the pathogenesis of hepatocellular lipidosis?

A

excessive transport of FAs and carbs to liver; abnormal hepatocyte fn, decreased apoprotein/lipoproteins synthesis, impaired secretion of lipoproteins from the liver

209
Q

What does deranged intracellular carb metabolism result in?

A

intracellular glycogen accumulation –> patho accumulation when glu and gly met is impaired, liver swollen and pale brown in severe cases; histo - cell cytoplasm has irregular clear spaces with indistinct outlines, nucleus central

210
Q

What is characteristic of deranged intracellular protein metabolism?

A

1) hyaline cartilage - eosinophilic to glassy appearance
2) excessive production of normal protein
3) storage of abnormal proteins (degraded in proteosomes –> accumulate in cells)
4) resorption droplets in renal tubular epith cells (PT - inc urine protein conc –> inc resorption of protein)

211
Q

what are other intracellular accumulations?

A

autophagic vacuoles, viral inclusion bodies, lead inclusions

212
Q

define autophagocytosis

A

catabolic mechanism that involves cell degradation of unnecessary or dysfunctional cellular components via lysosomes

213
Q

What mechanisms are involved in autophagocytosis?

A

1) vacuoles/phagolysosomes may be expelled from the cell or may be accumulate within cells in residual bodies containing lipofuscin
2) damaged/misfolded proteins are constantly marked by ubiquitin for disposal in proteasomes

214
Q

What are extracellular accumulations?

A

hyaline substances, fibrinoid change, gout and pseudogout, cholesterol and collagen

215
Q

What is gout?

A

deposition of urates as a result of oversaturation/overfeeding
-uric acids in blood in form of monosodium urate (rel insol in water)

216
Q

How is gout formed?

A

increased concentration in blood or in synovial fluid or pH changes in fluids –> crystallization and formation of insoluble urate salts

217
Q

Define primary and secondary gout

A 
primary = excessive protein intake
secondary = decreased nitrogen excretion (renal disease and dehydration)
218
Q

What are the two types of calcification?

A

dystrophic and metastatic

219
Q

What is dystrophic calcification?

A

calcification in necrotic tissue (Ca accumulates in mito and cytoplasm); focal to multifocal lesion, normal serum Ca levels, rapid process in cardiomyocytes and muscle cells, bacterial and parasite granulomas; HARMLESS

220
Q

What is metastatic calcification?

A

generalized intracellular or extracellular Ca salt deposits in previously undamaged tissue (mito); particular at elastic fibers and basement membranes and in cells iwth acidic cytoplasm (lungs); hypercalcemia; hyperparathyroidism

221
Q

What are the different types of hyperparathyroidism?

A

1) primary = dysfunction
2) secondary renal = retain P, but body wants to maintian P:Ca ratio (PTH activated –> chief cell hyperplasia –> Ca from bones –> become soft –> Ca precipitate in blood
3) secondary nutritional
- mobilize Ca from bone –> hypercalcemia (due to chief cell hyperplasia)

222
Q

What are the two main differences btw dystrophic and metastatic calcification?

A

dystrophic - necrotic tissue, normocalcemic

metastatic - begins in healthy tissue, hypercalcemic (deposited in tissues)

223
Q

What are the two pigment types?

A

exogenous and endogenous pigments

224
Q

What are some exogenous pigments?

A 
carbon - usually inhaled --> lung and lung lymph nodes (smoker or living with smoker); particles bronchiolar/alveolar macrophages
dust
tattoos
carotenoids
tetracyclins
melanin --> melanosis
lipfuscin-ceroid --> contain lipids/proteins
hematogenous pigments
225
Q

What are carotenoids?

A

fat-sol pigments of plant origin includign precursors of vit A (b-carotene);
-not detectable in standard histo (washed out)

226
Q

what are tetracyclins?

A

treatment of pregnant/gravid mother or neonatal animal –> discoloration of bones and teeth of neonate

227
Q

Give examples of hematogenous pigments

A

hemoglobin, hematin, hemosiderin, hematoidin, bilirubin, porphyrin

228
Q

Describe melanin

A

black intracellular pigment, produced by melanoblasts/melanocytes

  • -> hyperpigmentationn of skin, focal - freckles and moles
  • Depigmentation - destruction of melanocytes with release of melanin –> phagocytized and removed; generalized (Cu def); albinism
229
Q

What is albinism

A

inherited defect of enzyme system for melanin production

230
Q

What is lipofuscin?

A

yellow brown intracellular pgiment; contains proteins and lipids;

231
Q

What is the morphology of lipofuscin?

A
  • autofluorescent
  • may cause brownish discoloration of tissues (brown atrophy)
  • accumulates to the degree of visibility at LM (post mitotic cells-neurons and slowly dividing cells-hepatocytes)
  • non-degradable end prdt of autophagocytosis of damaged organelles
  • usually harmless to cell (unless storage disease)
232
Q

What is hemoglobin?

A
  • red pigment
  • degradation in macrophages of liver, spleen and bone marrow
  • broken down to heme and globin –> bile acids and iron bind to proteins
  • acute severe hemolysis leads to hemoglobinemia and hemoglobinuria
233
Q

Describe hemosiderin

A

brown pigment

  • reserve iron: bound to protein, either ferritin or siderin (non-bioavailable iron)
  • siderin is stored in siderosomes (granules)
234
Q

What is generalized hemosiderosis?

A

usually due to hemolysis, first detectable in macrophages (bone marrow, spleen, liver)

235
Q

What is localized hemosiderosis?

A

in areas of hemorrhages including in body cavity after intracavitary hemorrhage

236
Q

What is hemochromatosis?

A

increased enteric iron resorption with massive storage in hepatocytes

237
Q

What is parasite hematin?

A

waste product of certain parasites

238
Q

What is acid hematin?

A

melena (blood exposed to HCl in stomach)

239
Q

What is a formalin pigment?

A

annoying microscopic formalin artifact when pH of fixative < 6
-artifact of processing

240
Q

What is hematoidin?

A

produced from hemoglobin in tissue after hemorrhage

  • detectable 9 days after
  • free of iron
  • birefringement
  • resembles bilirubin
241
Q

What is hyperbilirubinemia a result of?

A

hemolysis

242
Q

What are the 3 different types of icterus?

A

1) prehepatic = hemolysis
2) hepatic = damage of hepatocytes or biliary cells –> impaired uptake , metabolism, secretion and transport of bile pigments within the liver
3) posthepatic = extrahepatic cholestasis (main bile duct)
- bilirubin stains tissue yellowish –> adipose, sclera, arteries, tendons

243
Q

Can you see bilirubin in tissues?

A

no, only in liver

-don’t confuse with carotenoid pigments or localized hemosiderosis

244
Q

What is bilirubin?

A

end product of hemoglobin metabolism during RBC degradation in cells of mononuclear macrophage system

245
Q

What is hemoglobin?

A

heme, iron and globin –> bilirubin –> glucoronide –> bile canaliculi –> urobilinogen –> excretion in feces

246
Q

What are types of disturbances of keratosis/cornification?

A

1) hyperkeratosis - regular but excessive cornification (skin callus)
2) parakeratosis - faulty maturation of the stratum corneum (greasy skin, Zn def)

247
Q

What are concretions?

A

precipitation of organic material and Ca salts or other minerals

  • pathogenesis involves an increased conc of water insoluble cmpds and a crystallization point
  • occurs mainly in alimentary tract and urinary tract
248
Q

Give examples of concretions

A 
salivary gland - sialoliths
biliary system of liver - choleliths
pancreas - pancreatic calculi
teeth - tartar, dental calculus
urinary tract - sediment or calculi
249
Q

What are pseudoconcretions?

A

stony conglomerations of inspissated exudates (calculi in guttural pouches of horses, calculi in vagina, preputial calculi)
-trichobezoars in GI tract or plant material

Pathology Exam 1 (1 decks)

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