Midterm 1 Flashcards

1
Q

Define pathology

A

Study of nature and causes of disease which includes changes to structure and function

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2
Q

What is known as the study of abnormal functioning of diseased organs

A

Pathophysiology

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3
Q

Etiology = ?

A

The cause of a disease

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4
Q

Acute cystitis was what aetiology?

A

E.coli infection

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5
Q

Idiopathic = ?

A

etiology unknown

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6
Q

What is the aetiology of Ankylosing Spondylitis?

A

Idiopathic

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7
Q

What is another name for DISH (diffuse idiopathic skeletal hyperostosis)

A

Forestier’s

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8
Q

This idiopathic condition results from the ossification of all the ligaments of the spine

A

Ankylosing Spondylitis

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9
Q

DISH affects what part of the spine?

A

Ossification of the ALL

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10
Q

What is meant by a Congenital Etiology?

A

When the genetic info is fine, but other factors in the embryo’s intrauterine environment interfere with normal development

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11
Q

T or F

Thalidomide has a genetic aetiology

A

False

Congenital

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12
Q

What is meant by a teratogenic effect?

A

This is when some agent can disturb the development of an embryo or fetus.

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13
Q

Give two examples of Teratogenic effects discussed in class

A

Fetal Alcohol Syndrom

Thalidomide

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14
Q

T or F

Huntington’s disease is an example of an acquired aetiology

A

False!

Genetic

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15
Q

An aka for Down’s Syndrome

A

Trisomy 21

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16
Q

What is a genetic etiology?

A

When genes are responsible for some structural or functional defect.

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17
Q

Describe the etiology of Huntington’s disease

A

Can be called Chorea

genetic damage of motor nuclei (basal ganglia) and cerebral cortex of the brain.

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18
Q

What are the symptoms of Chorea

A

Bizarre, involuntary dancelike movements

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19
Q

Give examples of subjective feelings

A

pain, headache, dizziness, heartburn

SYMPTOMS

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20
Q

What is a syndrome?

A

Characteristic combination of signs and symptoms associated with a particular disease

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21
Q

Shingles effects what ganglia in the brain?

A

Nodose

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22
Q

T or F

Shingles can occur on both sides of the body

A

False

Unilateral

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23
Q

Describe the order of skin colour change in a person with Raynaud’s Syndrome

A

White -> blue -> red

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24
Q

What is the etiology of Raynaud’s

A

Vasoconstriction/vasospastic rxn of peripheral arteries of the fingers.

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25
Q

This condition results from autoimmune damage to exocrine glands which results in dryness of mucous membranes

A

Sjogren’s Syndrome

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26
Q

Sjogren’s Syndrome is usually a manifestation of?

A

Rheumatoid arthritis or systemic lupus erythematosus

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27
Q

Name the 3 signs of Sjogren’s Syndrome

A

Xerostomia - dry mouth
Xerophthalmis - dry eyes
Bilateral Parotitis - enlargement of parotid gland

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28
Q

What is the major concern surround Xerophthalmia and Sjogren’s Syndrome?

A

Can damage cornea and cause a corneal ulceration which is very painful and can lead to blindness

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29
Q

T or F

Joint pain is associated also with Sjogren’s Syndrome

A

False!!!!

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30
Q

T or F

Sjogren’s Syndrome is usually associated with middle aged men

A

False

Women

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31
Q

What is known as the pattern of development of a disease?

A

Pathogenesis

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32
Q

What is an acute disease?

A

Short duration 5-10 days, quick onset, severe symptoms

- common cold, acute appendicitis

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33
Q

What is a chronic disease?

A

A disease that last more than 6 weeks and could have insidious onset such as TB or cancer

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34
Q

This type of disease classification is confined to one region of the body

A

Local

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35
Q

What is meant by focal damage

A

Damage that is LIMITED to DISTINCT SITES within a disease organ

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36
Q

How is diffuse damage different from focal?

A

Diffuse is distributed uniformly within the organ and focal is limited to distinct sites

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37
Q

When is a disease considered systemic?

A

When it involves other organs and systems

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38
Q

T or F

Local disease can become systemic

A

True

Cancer metastasizing
TB in the lungs that could spread to other organs if immune system can’t contain it

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39
Q

What is known as the identification of the patients specific disease

A

Diagnosis

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40
Q

Name the different classifications of cell injury

A

Deficiency
Intoxication
Trauma

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41
Q

Give examples of primary deficiency

A

Lack of Vit B3 (niacin) = pellagra (inflammation of the skin)
Lack of Vit C = scurvy
Lack of B1 (thiamine) = beriberi

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42
Q

What is the difference between a primary nutrient deficiency and secondary?

A
Primary = lack of specific components in the food 
Secondary = component is in food but cannot be absorbed
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43
Q

Pernicious anemia is a primary or secondary deficiency?

A

Secondary

- caused by lack of RBC in the blood and Vit B12 cannot be absorbed without the intrinsic factor.

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44
Q

What is the definition of intoxication?

A

Poisoning, toxins, or the presence of a substance that interferes with cell FUNCTION!

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45
Q

What is the difference between intoxication and trauma?

A
Intoxication = interferes with function
Trauma = interferes with structure
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46
Q

Toxins can be classified in what 2 categories?

A

Exogenous

Endogenous

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47
Q

What are the sources of Exogenous toxins?

A
  1. From infection (food contamination -> botulism, salmonellosis)
  2. Chemicals or poisons (alcohol, CC14)
  3. Overdose of some medications or artificial vitamins
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48
Q

Name the different sources of Endogenous toxins

A
  1. Genetic: Accumulation of metabolites or the activation of an alternative pathway
  2. Ionizing radiation
  3. Accumulation of metabolic by-products
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49
Q

Alkaptonuria is an example of what source of endogenous toxin

A

Genetic!

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50
Q

Describe the pathogenicity of Alkaptonuria

A

Caused by the accumulation of homogentisic acid an intermediate of phenylalanine metabolism that builds up due to a lack of the oxidase enzyme for the homogentisic acid.

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51
Q

When homogentisic acid builds up in the IVD cartilage what is it called?

A

Ochronosis

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52
Q

What does Ochronosis cause?

A

Degenerative disc disease or secondary osteoarthritis because of too much alkapton in the cartilage.

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53
Q

What is a typical manifestation of Alkapeonuria?

A

Urine will turn black after being exposed to air for a certain period of time.

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54
Q

Give an example of the activation of an alternative pathway and endogenous toxins

A

Phenylketonuria

- an enzyme is missing to change phenylalanine into tyrosine.

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55
Q

What happens to an individual who does not have the enzyme to convert phenylalanine into tyrosine

A

The phenylalanine is converted into Ketones which build up in the blood as phenylpyruvic acid and this causes brain damage. Children can’t talk until about 15yo

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56
Q

Give an example of an accumulation of metabolic byproducts forming an endogenous toxin

A

Gout

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57
Q

Pathogenesis of Gout

A
  • increase in uric acid concentration from overproduction or decreased excretion from the kidneys.
  • problem with purine metabolism
  • Hyperurecemia! Too much uric acid in blood
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58
Q

What are 3 manifestations of Gout

A
  1. Gouty arthritis
  2. Tophi/Tophus (skin)
  3. Kidney problems
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59
Q

What part of the body is the most susceptible to Gouty Arthritis?

A

Usually the great toe (1st metatarsalphalangeal joint)

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60
Q

When uric acid crystals build up in the skin what is it called? Where does it usually occur?

A

Tophi/Tophus

Ears

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61
Q

List the different types of cell trauma

A
Direct Contact
Hypothermia
Hyperthermia
Mechanical Pressure
Microorganism
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62
Q

What happens physiologically that makes Frost Bite so dangerous?

A

Due to hypothermia the long exposure to really low temperatures causes the water in the body to freeze and therefore expand. The expansion can rupture the cell membrane and kill the tissue.

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63
Q

Give an example of something causing trauma and being an endogenous toxin

A

Ionizing radiation

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64
Q

Give examples of mechanical pressure type traumas

A

Tumor
Stones
Anuerysm
High intensity sound

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65
Q

How does Malaria effect the body?

A

Grows inside the RBC and causes them to rupture

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66
Q

What is the name of the microorganism that can cause distention and rupture of tissue from growth of the worm

A

Echinococcus Cyst

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67
Q

Name the change in cell process that results from accumulation

A

Hydropic Changes

Fatty Changes - Steatosis

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68
Q

Give the akas for Hydropic Changes

A

Hydropic Degeneration

Cloudy Swelling

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69
Q

Pathogenesis of Cloudy Swelling

A
  • Cell injury causes functional inability to produce enough ATP
  • Decrease in ATP = inability to remove Na+
  • Na+ attracks fluid& creates the cloudy swelling which causes narrowing of the lumen.
  • Narrowing of lumen causes increase pressure and when chronic can results in tissue atrophy
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70
Q

What are the causes of Steatosis

A
  • intoxication
  • protein malnutrition
  • anoxia
  • obesity
  • diabetes mellitus
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71
Q

Steatosis refers to accumulation of triacylglycerides in what type of cells?

A

Parenchymal Cells

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72
Q

Give an example of Steatosis

A

Alcoholism results in “Fatty Liver”
- lipoprotein produced in liver, hepatocytes use FFA to make them, if you drink alcohol and damage hepatocytes the FFA will just start to accumulate and make the hepatocytes swell.

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73
Q

Fragments of bacteria or cellular organelles found in an injured cell that the cell failed to digest is known as?

A

Residual Bodies

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74
Q

T or F

Residual bodies can kill the cell

A

False

Cell is alive and functioning

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75
Q

Are these matched correctly in regards to Hyalinization

INTRAcellular = non-reversible
INTERcellular = reversible
A

False

Opposite is true

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76
Q

What is Mallory Alcoholic Hyaline

A
  • Type of Hyalinization

- Deposition of proteins in hepatocytes

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77
Q

T or F

Russell bodies are a type of hyalinization involving inclusions in the nucleus of a cell

A

False

Cytoplasm

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78
Q

What is the name of the hyalinization where inclusions build up in the nucleus?

A

Dutcher Bodies

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79
Q

Russell Bodies and Dutcher Bodies are examples of what type of accumulation?

A

Plasma Cell Dyscrasias

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80
Q

What is the name of the Plasma cell dycrasias that involves the IGG class of antibodies?

A

Multiple Myeloma

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81
Q

What is another name for Multiple Myeloma

A

Plasma Cell Myeloma

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82
Q

This condition results in Hyperviscosity Syndrome

A

Lymphoplasmacytic Lymphoma

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83
Q

What immune antibody is being produced by Lymphoplasmacytic Lymphoma?

A

IGM

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84
Q

T or F

Multiple Myeloma DOES NOT cause Hyperviscosity Syndrome

A

False

It does just not as significant as with the Lymphoplasmacytic Lymphoma because the IGG class of antibodies are much smaller than the IGM and therefore do not affect the thickness of the blood as much but it can still happen.

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85
Q

aka for Hyperviscosity Syndrome

A

Waldenstrom Macroglobulinemia

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86
Q

The monoclonal tumors occur because of problems with what type of cells in the body

A

B-Cells or plasma cells.

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87
Q

Hyaline Arteriolosclerosis can cause what usually fatal event?

A

Hemorrhagic Stroke

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88
Q

What is the pathogenesis of Hyaline Arteriolosclerosis?

A

Deposition of hyaline substances causes dramatic increase in vascular wall hardening. The arterioles can become so hard that the vessel can rupture causing damage or death

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89
Q

Is Hyalinization in arterioles and example of intracellular or extracellular?

A

Extracellular

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90
Q

What is Amyloidosis?

A

Deposits of amyloid in organs and tissue.

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91
Q

What are Amyloids?

A

It is a general term for a variety of proteinaceous materials that are abnormally deposited in tissue interstitium. These are PATHOLOGICAL proteins.

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92
Q

Why does Amyloidosis usually occur?

A

Because of chronic infection or autoimmune problems.

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93
Q

Name the common sites of the body for Amyloid deposition

A

Kidney
Liver
Brain
Skin

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94
Q

This is known as cell/organ enlargement in response to increase in demands

A

Hypertrophy

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95
Q

Name the different Adaptive responses of the cell.

A

Alternative Metabolism

Altered Size - atrophy, and hypertrophy or pressure atrophy

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96
Q

T or F

Hashimoto’s is a hyperthyroid condition

A

False!

Autoimmune that leads to HYPOTHYROIDISM

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97
Q

What hormone binding site is blocked by an antibody in Hashimotos?

A

TSH

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98
Q

Describe the pathogenesis of Grave’s Disease

A

Hyperplasia!
Antibodies permanantley bind to TSH receptors and continuously stimulate the Thyroid
Leads to a huge production of Thyroid Hormone

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99
Q

What is a classical presentation of Grave’s Disease

A

Exophithalmos = bulging eyes

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100
Q

T or F

Hashimoto’s and Grave’s are examples of Hypothyroid conditions

A

False

Grave’s = hyperthyroid

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101
Q

A pouching of the cell membrane is called?

A

Blebs

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102
Q

How many blebs can you see on a cell membrane WITHOUT it causing irreversible changes?

A

2 maybe 3

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103
Q

T or F

Grave’s Disease is more common in women then men

A

True

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104
Q

Are these matched right:

Karyolysis = condensation of nucleus
Pyknosis = dissolution of nucleus 
Karyorrhexis = fragmentation of nucleus
A

No!

Karyolysis = dissolution 
Pyknosis = condensation
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105
Q

Myocardial infarction falls under what category of tissue necrosis?

A

Coagulative Necrosis

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106
Q

Why is coagulative necrosis important?

A

It allows the tissue not to be damaged while cartilaginous material is played down to replace the dead tissue.

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107
Q

T or F

An infarction is a zone of necrosis caused by oxygen deficiency

A

False

This is describing an Infarct!

Infarction is the PROCESS resulting in an infarct

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108
Q

T or F

A red infarct occurs in tissue with dual blood supply

A

True

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109
Q

What is a White Infarct

A

Occurs with single blood vessel supply like the heart

110
Q

This type of infarct results in the complete digestion of dead cells, resulting in transformation of the tissue into a liquid viscous mass.

A

Liquefactive Necrosis

111
Q

In what type of tissue is Liquefactive Necrosis common? Why?

A

Nervous Tissue because there is little or no collagen fibres here.

112
Q

TB and Leprosy are examples of what type of tissue necrosis?

A

Casseous Necrosis

113
Q

Casseous Necrosis appears as?

A

Amorphous granular debris seemingly composed of fragmented, coagulated cells
AND
amorphous granular debris enclosed within a distinct inflammatory border known as a granulomatous reaction.

114
Q

T or F

gummatous necrosis looks like severe glassy or waxy necrosis of smooth muscles in acute infectious diseases

A

False!!

1stly because it is SKELETAL MUSCLES
This is describing Zenker’s Necrosis

115
Q

T or F

Gummatous necrosis develops with primary symphillis

A

False

Tertiary period

116
Q

Some texts say that syphillis will cause a different type of necrosis.. what kind?

A

Liquefaction

117
Q

What is Tabes Dorsalis?

A

Gummatous Necrosis of the Posterior Column of the Spinal cord resulting in a loss of sensory function with symptoms such as numbness and tingling.

118
Q

What is another condition that results from tertiary Syphilis and Gummatous Necrosis

A

General Paresis of Insane

119
Q

Why type of necrosis is seen with Typhoid?

A

Zenker’s Necrosis

120
Q

Aschoff’s Node is a symptom of what condition?

A

Rheumatic Fever

121
Q

In what organ do we find Aschoff’s Nodes?

A

Heart

122
Q

Pancreonecrosis results from what type of tissue necrosis?

A

Fat Necrosis

123
Q

This type of necrosis occurs in the walls of blood vessels when endothelial and smooth muscle cells are injured and dying.

A

Fibrinoid Necrosis

124
Q

T or F

Thromboangitis Obliterates is a type of Wet Gangrene

A

False

Dry Gangrene

125
Q

Diabetic angiopathy is classified as wet or dry gangrene?

A

Dry

126
Q

Systemic sclerosis aka _________

A

Scleroderma

127
Q

Burger’s Disease is common among what population of people?

A

Smokers

128
Q

What is an aka for Buerger’s Disease?

A

Thromboangitis Obliterans

129
Q

T or F

Thromboangitis Obliterates is an example of Wet Gangrene

A

False

Dry

130
Q

When does Wet Gangrene occur?

A

Occurs if the enzyme of invading phagocytic cells break down the necrotic debris and produces some liquefaction

131
Q

What bacteria is often associated with Wet Gangrene

A

Clostridium Prefingens

132
Q

Where is Gas Gangrene commonly seen?

A

With military from bullet wounds.

133
Q

T or F

Gas Gangrene is associated with aerobic bacterial infections

A

False

Anaerobic

134
Q

T or F

Apoptosis is NOT due to cell injury

A

True

135
Q

What is Apoptosis?

A

Programmed Cell Death

136
Q

What are the normal conditions of apoptosis?

A
  1. Programmed destruction of embryogenesis (decidual layer)

2. Hormone dependent involution in adults (gonads)

137
Q

Pigments can either be _________ or __________

A

Exogenous

Endogenous

138
Q

What is Anthracosis

A

Deposition and accumulation of carbon in the tissues, especially lungs

139
Q

What is the name of the disease that is common among coal workers.

A

Coal-worker pneumoconiosis

140
Q

Name the different types of endogenous pigments

A
Lipofuscin 
Melanin 
Homogentisic Acid 
Hemosiderin 
Copper
Calcium
141
Q

Akas for Lipofuscin

A

Lipochrome
Wear & Tear pigment
Brown atrophy

142
Q

What are Lipofuscins?

A

Complexes of protein and lipid derives from free-radical preoccupation of polyunsaturated lipids of sub cellular membranes.

143
Q

T or F

Lipofuscins are dangerous

A

False

Don’t cause problems

144
Q

What is the name of a black abnormal pigment

A

Homogentisic acid

145
Q

T or F

Hemosiderin is an excessive accumulation of iron that can be harmful

A

False

This is the definition of Hemochromatosis

146
Q

an aka for Hemochromatosis

A

Bantu Siderosis

147
Q

What is Hemosiderin?

A

Accumulates in tissues where there is local or system excess of iron and represents large aggregates of ferritin micelles, which are not harmful.

148
Q

Where do we commonly find Hemosiderin micelles?

A

Spleen, liver, and lymph nodes

149
Q

Deposition of hemosidering in many organs and tissues in the cases of systemic overload of iron is describing?

A

Hemosiderosis

150
Q

T or F

Secondary Hemochromatosis is a systemic overload of iron

A

True

151
Q

This type of Hemochromatosis involves increased absorption of iron in the GI tract

A

Primary Hemochromatosis

152
Q

T or F

Females are affected by Hemochromatosis 7:1 compared to males

A

False

153
Q

What is an aka for Secondary Hemochromatosis

A

Transfusion reaction

154
Q

With individuals suffering from Primary Hemochromatosis up to how much iron can be absorbed by the GI? What is a normal amount?

A

50 g

5-6 g

155
Q

Why is Secondary Hemochromatosis so dangerous? What other conditions can it lead to?

A

Liver - hepatoma (increased chance of cancer 20X)
Hepatomegaly
Liver Cirrhosis
Pancreas - diabetes mellitus
Cardiomyopathies - arrythymias, cardiac failure
Skin hyper pigmentation
Abd pain, joint pain

156
Q

Hepatolenticular degeneration aka _________________

A

Wilson’s Disease

157
Q

T or F

Wilson’s Disease is more common in females than males

A

False

158
Q

What is the name of the molecule when Copper binds to alpha globulin?

A

Ceruloplasmin

159
Q

What happens in Wilson’s Disease that leads to an accumulation of copper in the body

A

Ceruloplasmin is not made and copper is not released from the liver.

160
Q

What are some common manifestation/presentation of Wilson’s disease

A
  1. Copper ring at the periphery of the cornea = Kayser-Fleischer ring
  2. Brain damage of midbrain ganglia - motor function impaired with Parkinson’s-like Syndrome
161
Q

What is the only tx for excessive copper in the body

A

D-penicillamine - this compound has chelating properties and removes copper from circulation

162
Q

What is a negative effect of D-Penicillamine?

A

It has cytolytic effects that inhibit cell replication

163
Q

an aka for Primary Tuberculosis Complex

A

Ghon’s Focus

164
Q

What type of calcification involves deposition of calcium salts into necrotic or atrophic tissues?

A

Dystrophic

165
Q

What type of calcification is immunopathological?

A

Systemic

166
Q

Pathogenesis for Systemic Calcification

A

Overactive fibroblasts leads to an overproduction of connective tissue.
Scar tissues begin to replace normal soft tissue which causes contracture.

167
Q

When systemic calcification occurs in the heart what develops?

A

Stenosis of the heart valves

Rheumatic Heart Disease

168
Q

What is Sclerodactyly

A

Claw-like hand - the hardening of the skin in the hands can lead to the hands being in a semi flexed position and the skin is all tight and taught

169
Q

What is the kind of calcification that involves the deposition of Calcium into tissues that are NOT necrotic or atrophic

A

Metastatic Calcification

170
Q

What are some causes of Metastatic Calcification

A
  1. Increase secretion of PTH
  2. Destruction of bone like in Paget’s Disease, immobilization, or Tumors.
  3. Vitamin D disorders
  4. Sarcodosis
  5. Renal Failure in secondary hyperparathyroidism
171
Q

Name the classic signs of inflammation

A
Rubor
Calor
Tumor
Dolor
Functio Laesa
172
Q

What vessel has a spinster to regulate blood flow

A

Arterioles

173
Q

In what vessel does exchange of nutrients occur?

A

Capillaries

174
Q

T or F

Endothelial cells line the inner surface of empty organs.

A

False this is describing Epithelial cells.

Endothelial cells line the vessels

175
Q

Where do pathologist say inflammation actually occurs

A

Post Capillary Venules

176
Q

T or F

Hydrostatic forces are pushing and osmotic are pulling

A

True

177
Q

What are the 2 components of inflammation?

A
  1. Vascular

2. Cellular

178
Q

What does stasis mean in terms of blood flow and why is it important?

A

Stasis is slowing of the blood so that its movement in the capillaries and venues stops.

179
Q

What does hyperaemia mean?

A

Increased blood flow

  • inflammation has about a 20 fold increase in blood flow to the injured area.
180
Q

T or F

Epithelial cells are able to contract and increase the gapping which allows for albumins to be drawn into tissue and water follows the higher concentration of solutes.

A

False

All of this was true only it is not epithelial cells it is endothelial cells

181
Q

What is exudate?

A

Inflammatory fluid
Leakage of fluid portion of blood into tissues at site of injury that is protein rich, has blood cells and sometimes microorganism both dead and alive.

182
Q

What is the specific gravity of exudate?

A

more than 1.020

183
Q

What is Transudate

A

This is a fluid that is not a result of tissue injury. Could be result of normal muscle function
Not protein rich like exudate
Specific gravity less than 1.012

184
Q

What is serous inflammation?

A

A response to a mild injury in which only fluid is allowed to escape. Ex: common cold

185
Q

T or F

Fibrinous inflammation is NOT dangerous

A

False

Fibrinous inflammation is the appearance of Fibrinogen in the exudate. Can lead to conditions such as Rheumatic Pericarditis

186
Q

Are these matched correctly in terms of Suppurative Inflammation:

Localized = Cellulitis 
Diffuse = Abscess
A

No

Localized = Abscess 
Diffuse = Cellulitis
187
Q

Pleural Empyema

Subdural Empyema fall under what type of inflammation

A

Suppurative

188
Q

T or F

RBC play NO role in inflammation

A

True

189
Q

What is Hemorrhagic Inflammation?

A

Accumulation of RBC at site of injury.

190
Q

What is Leukocyte Emigration?

A

Outpouring of large amounts of WBC from the blood

191
Q

In what disease are Lung Abscess a concern?

A

TB & cancer

192
Q

In what vessels does Leukocyte Emigration occur?

A

Postcapillary venules

193
Q

Normal blood flow = ________________

A

Axial blood flow

194
Q

Describe how the blood cells travel together with axial blood flow.

A

Larger blood cells (leukocytes) are in the centre, surrounded by RBCs which are surrounded by platelets.

195
Q

How does injury disrupt axial blood flow?

A

RBCs will become sticky from chemicals released that causes them to stick together and become bigger than the WBC and start to flow down the middle.

196
Q

Describe what Margination is

A

WBC’s become positioned in the periphery of the column as a result of the redistribution that occurs when RBCs move to the centre of the column.
WBC are now close to the vascular endothelium

197
Q

What is pavementing?

A
  • This happens to the leukocytes and is their adherence to the endothelial cell surfaces.
  • Endothelial cells become sticky and project receptors into the lumen
  • WBCS get caught in the receptors.
198
Q

T or F

Margination and Pavementing are a preparation step for Leukocyte Emigration

A

True

199
Q

What does Dr.B define Diapedesis as?

A

The PASSIVE escape of RBC from vessels into site of inflammation.

200
Q

T or F

Leukocyte emigration is a passive process where WBC’s move outside the vessels at the site of inflammation

A

False

ACTIVE process

201
Q

T or F

Polymorphonuclear cells are agranulocytes

A

False

Granulocytes mother truckerrrrrr

202
Q

Name the polymorphonuclear cells

A

Neutrophils
Eosinophils
Basophils

203
Q

Name the agranulocytes

A

Lymphocytes

Monocytes

204
Q
Eosinophils represent what % of granulocytes in the blood:
2 - 4 %
55-60%
0.5-1%
20-25%
A

2 - 4 %

205
Q

What percentage of granulocytes are Basophils?

A

0.5-1%

206
Q

What mononuclear cells represent the least %

A

Monocytes = 4 - 8%

207
Q

T or F

Eosinophils have pink granules

A

False

Red

208
Q

What is the lifespan of Neutrophils

A

8hr - 3 days

209
Q

What WBC are the first to arrive at the site of inflammation?

A

Neutrophils

210
Q

T or F

Neutrophils have a bilobed nucleus

A

False! 3-4 lobes

Bilobed = basophils & eosinophils

211
Q

What are the second WBCs to arrive at the site of inflammation?

A

Monocytes

212
Q

T or F

Macrophages will remain at site of inflammation longer than Neutrophils

A

True

213
Q

What WBCs escape the vessel into site of inflammation?

A

Neutrophils & Monocytes

214
Q

Name the major Phagocytic cells

A
  1. Neutrophils
  2. Monocyte/Macrophage
  3. Eosinophils
215
Q

Name the 4 stages of the Phagocytic process

A
  1. Recognition
  2. Engulfing
  3. Indigestion
  4. Exocytosis
216
Q

What is the name of the antibody like substance in neutrophils?

A

Defensin

217
Q

What stage of Phagocytosis involves the use of pseudopods and the formation of a vesicle surrounding foreign microbe/antigen

A

Engulfing

218
Q

Provide examples of oxygen independent mechanisms of Phagocytosis

A

Lysozyme
Elastase
Collagenase
Defensin

219
Q

What are anions?

A

Found in granules of phagocytic cells that kill bacteria by releasing oxygen.

220
Q

Name the anion’s discussed in lecture

A

Superoxide Anion
Hypochlorite Anion
Hydrogen Peroxide H2O2

221
Q

T or F

Chediak-Higashi Syndrome is a rare genetic disease in children where the child’s phagocytic cells (all of them) are not able to produce free radicals.

A

False

This is describing Chronic Granulomatous Disease of Children

Chediak = impairment of phagocytic cell MOTILITY and therefore cannot go to the site at a proper time.

222
Q

T or F

WBC’s in Chediak-Higashi Syndrome are not able to degranulate and these children often die early

A

True

223
Q

All of the following are initiators of the inflammatory response except:

  1. Complement activation
  2. Histamine
  3. Microbial products
  4. Direct stimulus to mast cells
A
  1. Histamine - this is a mediator of the inflammatory process and is released in response to a physical injury.
224
Q

Name the functions of Histamine

A

Vasodilation
Increase permeability of vessels
Bronchospasm - narrowing of bronchiole lumen
Increase mucous production

225
Q

Name the causes of Degranulation

A
Physical injury
Type 1 hypersensitivity rxn 
Anaphylotoxins CSa, C5a
Neuropeptides like substance P
Cytokines
226
Q

T or F

Neuropeptides stimulate the release of Histamine

A

Fals!!

Anaphylotoxins C3a & C5a do this!

227
Q

What cells produce Serotonin

A

Platelets

228
Q

What is known as the hormone of pleasure?

A

Serotonin

229
Q

Where is substance P produced

A

Nervous fibers - peripheral and central NS

Lungs & GI nervous tissue

230
Q

All of the following are functions of Substance P except:

  • promote production of pain
  • increase vasoconstriction
  • regulate blood pressure
  • increase permeability of blood vessels
A

Increase vasoconstriction

231
Q

Nitric oxide’s axa

A

Endothelial-derived releasing hormone.

232
Q

What mediator of inflammation’s role is to cause Bronchospasm?

A

Histaime

233
Q

what anaphylotoxins stimulate the release of Histamine?

A

C3a and C5a

234
Q

What cytokines will cause the degranulation of the mast cells to release histamine?

A

Cytokines IL-1 and IL-8

235
Q

Where is serotonin located in regards to inflammation?

A

Platelets

236
Q

What inflammation mediator is a product of arachidonic acid?

A

Eicosanoids

237
Q

What Eicosandoid is involved with the inhibition of hair growth?
PGE2
PGD2
PGF2alpha

A

PGD2

238
Q

T or F

PGD2 is associated with bronchospasm and type 1 hypersensitivity reactions

A

True

239
Q

What blood cells are the major produced of prostaglandins?

A

Neutrophils and Macrophages

240
Q

T or F

Prostacyclin = PGI2

A

True

241
Q

What prostaglandin is produced in the platelets?

A

Thromboxane A2 (TXA2)

242
Q

What prostaglandin’s function is opposite to PGI2?

A

TXA2 (Thromboxane A2)

243
Q

What prostaglandin causes Hyperalgesia (increases perception of pn at site of inflammation)?

A

PGE2

244
Q

What prostaglandin is associated with the corpus luteum and induces labour?

A

PGF2alpha

245
Q

T or F

Prostaglandins in excess can cause irritation to the wall of the stomach and cause Peptic ulcers.

A

False

They actually protect against Peptic ulcers and it is common to see individuals who use NSAIDS in excess suffering from ulcers.

246
Q

T or F

COX 1 inhibitors will suppress the immune response more than COX 2

A

True

247
Q

Tumor necrosis factor = ?

A

Interleukins-1 & 6

- produced predominantly by activated macrophages

248
Q

What are the physiological effects of Interleukins?

A
Fever
Decrease appetite 
Increase sleep
Increase acute-phase proteins
Hemodynamic effects (shock)
Neutrophilia
249
Q

What inflammatory mediator is responsible for the perception of pain and causing vasodilation. (hint - not substance P)

A

Bradykinin

250
Q

T or F

Lymph vessels are valveless

A

False

  • contain valves that keep it flowing in one direction -> towards the venous system
251
Q

What one of these enzymes is responsible for Leukotriene production:

  1. 5-lipoxygenase
  2. 12-lipoxygenase
A

5-lipoxygenase

252
Q

What inflammation mediator stimulates monocyte adhesion?

A

Lipoxins

253
Q

Steroids inhibit the production of Eicosanoids by inhibiting what class of enzymes?

A

Phospholipases

254
Q

T or F

IL-1 and IL-6 are produced predominantly by B helper cells

A

False

T-Helper

255
Q

T or F

Antibodies are part of the inflammatory cascade

A

False

But they do promote inflammation

256
Q

Clotting Factor XII aka ?

A

Hageman Factor

257
Q

Lymphangitis = ?

A

inflammation of lymph vessels

258
Q

T or F

When lymph glands are painful it usually indicates metastases of lymph nodes

A

False

They will be painless - painful is a normal response

259
Q

What is an infection of the blood called?

A

Bacteremia

260
Q

T or F

Lymphocytosis is usually seen with a bacterial infection

A

False

Viral

261
Q

What does Leukocytosis mean?

A

Increased leukocytes in the blood >9000 leukocytes per 1 cubic mm

262
Q

Lymphadenopathy of neck and upper thoracic lymph nodes is commonly called?

A

Infectious mononucleosis

263
Q

T or F

Chronic inflammation is associated with an increase in exudate production of the body

A

False

264
Q

How long does inflammation need to last to be considered chronic?

A

6-8 weeks

265
Q

How high can the Neutrophil content(%) increase with a bacterial infection?

A

Greater than 60-70%

266
Q

What happens to bone when there is chronic inflammation in soft tissue?

A

Cytokines will enter the area and they promote osteoclasts and therefore we see a loss of bone density in that area

267
Q

Loss of bone density is referred to as?

A

Osteopenia

268
Q

What is aseptic osteonecrosis?

A

Caused by compressed blood vessels -> infarct -> dissolution of bone without infection -> joint and bone loss

269
Q

Describe what can happen to the tissues the kidneys with chronic kidney inflammation

A
  • tissue replaced by connective tissue
  • the CT will shrink over time (more than half) and pull the other tissue with it causing a tautness or granular appearance.
  • leads to Chronic Granulomatous Nephritis
270
Q

Acute inflammation lasts how many days?

A

7-10 days

271
Q

T or F

It is important to ice injured tissue for at least 3 days following injury or trauma.

A

False

  • 1st day only!
272
Q

T or F

Neutrophils are present in chronic inflammation

A

False

Only macrophages and lymphocytes