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Micropathology > Packet 4 (pages 1- 11.5, Exam 2) > Flashcards

Packet 4 (pages 1- 11.5, Exam 2) Flashcards

1
Q

What is necrosis?

A

cell explodes and dies, this leads to tissue death

ex: bed sores, heart attack, TB necrosis

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2
Q

What is apoptosis?

A

cell slowly shrinks and dies

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3
Q

Which disease has the caudate nucleus undergo apoptosis around 30-50 y/o?

A

huntingtons disease

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4
Q

If a cell is unable to adapt then it will result in….

A

cell injury

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5
Q

If a cell has irreversible injury then what happens?

A

cell death with either necrosis or apoptosis

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6
Q

Reversible cell injury results in cellular and morphological changes that can be reversed if the stress is removed. What are the hallmark signs of this?

short response test q

A

1) mitochondrial changes (decreased ATP resulting in failure of the sodium potassium pump)
2) hydropic cellular swelling (change in ion conc. and water influx)
3) altered cell organelles
-mitochondria and ER swelling (ribosomes detach and decrease protein synthesis and cisternae fill with water)
-cell membrane blebbing (protrusions or bulges allow more water in bc sodium potassium pump isn’t working)
-small, clear vacuoles from within the cytoplasm
-loss of microvilli
-nuclear chromatin clumping
-the number of vacuoles to pick up the damage increases (eventually become autophagic vacuoles)

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7
Q

What are the 9 causes of reversible and irreversible cell injury?

A

1) oxygen deficiency
2) physical agents (traumas, extreme heat or cold, radiation, electrical energy, ionization, free radicals)
3) infectious agents (intracellular parasites, viral fungal, bacterial, protozoan infections, ex of parasitic infection= beaver fever)
4) nutritional deficiencies and imbalances
5) genetic diseases with clotting factors or lysosomal storage diseases
6) cell workload imbalance
7) chemicals, drugs, toxins (can block or stimulate cell membrane receptors, alter enzyme systems, produce free radicals, alter cell permeability, damage chromosomes, modify metabolic pathways, and damage structural cell components)
8) immunologic dysfunction or congenital defects (DiGeorge syndrome (thymus deficiency), thymic aplasia or hypoplasia, autoimmune diseases, hypersensitivities
9) aging (damage to DNA, accumulation of cellular debris)

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8
Q

most strokes are caused by what?

A

ischemia

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9
Q

What is ischemia?

A

lack of blood and oxygen

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10
Q

What is hypoxia?

A

loss of oxygen

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11
Q

ROS/ free radicals happen naturally but can also be from UV exposure, smoking, chemicals, drinking, etc and they will hook up with anything to cause cellular damage. What is this called?

A

nonselective binding

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12
Q

What nutritional deficiencies/imbalances would result in cellular injury?

A

-kwashiorkor
-marasmus
-excess calories
-hyper-supplementation

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13
Q

What are 3 lysosomal storage diseases?

A

1) gaucher’s disease (go-SHAY)
2) neimann-pick disease
3) tay-sachs disease

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14
Q

What does “hydropic” mean?

A

-cell containing water or watery fluid
-characterized by swelling and taking up fluid

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15
Q

What are the 2 features that indicate a cell is undergoing reversible cell injury?

A

cellular swelling and fatty changes (steatosis)

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16
Q

What are the other names for cellular swelling?

A

-hydropic cellular swelling
-hydropic change
-vacuolar degeneration

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17
Q

What is cellular swelling?

A

enlargement of an acutely injured cell is caused by changes in ion conc. and water influx
-sodium potassium pump is impaired due to decreased ATP
-increase in cell membrane permeability
-sodium accumulates inside the cell
-osmotic pressure increases inside of the cell
-water passively moves into cell leading to increase in swelling

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18
Q

What is the #1 change to occur during cell injury?

A

cellular swelling

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19
Q

What happens if too many cells of an organ are affected with cellular swelling?

A

-pallor
-increase turgor (rigidity due to increase pressure)
-increase weight in the organ

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20
Q

T/F: a little fat in the liver is normal

A

true

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21
Q

What is Nonalcoholic steatohepatitis (NASH)?

A

-liver increases in size and weight
-usually due to poor diet
-fat builds up and causes inflammation of the liver

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22
Q

Cellular swelling is easy to observe in parenchymal organs and may be local or affect the whole organ. What are the 3 organs we discussed in class?

A

1) liver (due to hepatitis or hypoxia)
2) kidney (due to shock)
3) myocardium (due to hypoxia or phosphate intoxication)

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23
Q

Organs are made up of parenchymal cells and stromal cells. The functionality of the organ is due to what cells?

A

parenchymal cells

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24
Q

What is the fancy word for fatty changes in cells?

A

steatosis

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25
Q

Fatty changes most commonly affects what organ? What other organ can also get fatty changes?

A

liver is most common

heart is 2nd most common

can also happen in CNS, spleen, pancreas, kidneys, skeletal m.

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26
Q

What are the other names for fatty changes (steatosis)?

A

-fatty degeneration
-fatty metamorphosis
-fatty steatosis

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27
Q

What is steatorrhea?

A

fatty diarrhea

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28
Q

What are fatty changes (steatosis)?

A

-abnormal retention of fat (lipids) within a cell or organ
-cells that have been damaged are unable to adequately metabolize fat (lipids)
-small vacuoles of fat accumulate and become dispersed in the cytoplasm
-usually occurs in parenchymal cells
-mild fatty changes may not affect cell function
-more severe fatty change can cause hypoxic, toxic, and metabolic injury to the cell- IMPAIR CELL FUNCTION
-depending on the cause and severity of lipid accumulation, it is generally reversible

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29
Q

Steatosis most often affects the LIVER- the primary organ of lipid metabolism- where the condition is commonly referred to as:

A

fatty liver disease

(fatty liver develops when your body produces too much fat or doesn’t metabolize fat efficiently enough)

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30
Q

What are the side effects of steroids?

A

-makes you hungrier
-bloating, retain water
-decrease in immune function (same when theres an increase in cortisol)

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31
Q

What is the progression of fatty liver disease?

A

1) steatohepatitis (liver becomes inflamed and tissue is damaged)
2) fibrosis (scar tissue forms in damaged areas)
3) cirrhosis (excessive scar tissue replaces healthy tissue)

liver cirrhosis can lead to liver failure and liver cancer

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32
Q

Is nonalcoholic fatty liver disease (NAFLD) reversible or irreversible?

A

reversible

33
Q

When does the liver become pale?

A

starts to become pale in nonalcoholic fatty liver disease (NAFLD) but will become really pale in nonalcoholic steatohepatitis (NASH)

34
Q

What is the difference between nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH)?

A

NASH has more fat and collagen fibers will appear

35
Q

Is nonalcoholic steatohepatitis (NASH) reversible or irreversible?

A

reversible

36
Q

Is liver cirrhosis reversible or irreversible?

A

irreversible

37
Q

What is liver cirrhosis?

A

-excess fat leads to collagen deposits and scar tissue formation
-often will require liver transplant bc of the damage

38
Q

What is the #1 cause of fatty liver disease?

A

alcoholic liver disease (heavy drinking, alcoholics)

39
Q

What is the 2nd cause of fatty liver disease? Other causes?

A

2nd- nonalcoholic steatohepatitis (NASH)

other risks/causes:
-obesity
-type 2 DM
-metabolic syndrome
-some prescription meds

40
Q

What is metabolic syndrome?

A

combination of:
-insulin resistence
-high BP of 140/90+
-high cholesterol
-high TGs

41
Q

what is cholestasis?

A

-slow or stopped bile flow

42
Q

True/False: the enlargement of hepatocytes due to fatty changes has no effect on bile

test q

A

FALSE
-the enlarged cells may compress adjacent bile canaliculi –> leading to cholestasis

43
Q

what are the symptoms of cholestasis?
test q

A

-intense itching (aka pruritus)
-dark urine
-pale stool

44
Q

where does fatty degeneration of the heart occur?

A

the myocardial sarcoplasm (cytoplasm of striated muscle cells)

45
Q

what are the 2 patterns of fatty changes in the heart?

A

-prolonged moderate hypoxia
-severe hypoxia or diptheritic myocarditis

46
Q

what is prolonged moderate hypoxia?

A

-decrease in oxygen
-causes grossly apparent bands on yellowed myocardium w/ bands of darker/normal colored myocardium
*happens over a long period of time

47
Q

what is severe hypoxia/diptheritic myocarditis

A

-fat infiltrating damaged myocardium
-appears as diffuse yellow myocardium -> uniform changes

48
Q

how does the diptheritic toxin affect the myocardium

A

it interferes with protein and fatty acid metabolism

49
Q

are fatty changes in the heart primary or secondary conditions

A

Secondary! side effect of big list of issues that we don’t need to know until boards:
-myocarditis
-pericarditis
-coronary arteriosclerosis
-myocardial insufficiency
-starvation
-anemia
-fever
-phosphorus or arsenic poisoning
-diphtheria
-scarlet fever
-typhoid fever

50
Q

What is diphtheria?

A

-infection of the nose and throat
-caused by Corynebacterium diphtheria
*exotoxin
*PSEUDOMEMBRANE covering the back of the throat - necrosis of the respiratory tissue

51
Q

What are the 3 types of metabolic disorders of fat metabolism?

A

-lysosomal storage diseases
-steatorrhea
-hyaline degeneration

52
Q

what is hyaline degeneration?

A

tissue (connective) degeneration in which structural elements of affected cells are replaced by homogenous translucent material
-stains intensely w/ acid stains-
-deposition of abnormal materials w/in a tissue

53
Q

what are the 6 types of hyaline degeneration that we need to know?

A

-Zenker’s (waxy) degeneration
-Mallory Bodies
-Councilman bodies
-crooke’s hyaline changes
-Russel bodies and mott cells
-hyaline casts

54
Q

what is zenker’s (waxy) degeneration?

A

a severe glassy or waxy hyaline degeneration or necrosis of skeletal muscles in acute infectious disease
typhoid

55
Q

what are mallory bodies

A

-cytoplasmic hyaline inclusions of hepatocytes (hyaline deposit in cells)
-associated with alcoholic hepatitis but can also occur with other liver diseases

56
Q

what are councilman bodies

A

-aka apoptotic body
-a dying hepatocyte surrounded by normal parenchyma
-acidophilic (stains pink w/ H&E)
-most commonly seen w/ acute viral hepatitis, yellow fever, and other viral syndromes

57
Q

what are crooke’s hyaline changes

A

-accumulation of glassy, hyaline material in the cytoplasm of basophilic cells of the ANT PITUITARY GLAND
-often seen in cushing’s disease (increase cortisol)

58
Q

what is cushing’s disease/syndrome

A

long list of symptoms due to increased cortisol:
-enlarged supraclavicular fat pads
-moon face
-osteoporosis
-hypertension
-muscle wasting in the extremities
-poor wound healing
-dark facial hair (hirsutism)
-cardiac hypertrophy
-obesity
-abdominal striae
-amenorrhea

59
Q

what are mott cells

A

hyaline inside of plasma cells
AKA plasma cells that contain Russell bodies

60
Q

what are Russell bodies

A

-multiple, round cytoplasmic hyaline inclusions filled w/ immunoglobulins inside plasma cells
-general response of secretory cells to synthesis from a mutant ig which can neither exit or be degraded

61
Q

when are Russell bodies and Mott cells seen?

A

in the bone marrow of individuals w/ multiple myeloma or with chronic (autoimmune) infections

62
Q

what are hyaline casts

A

-simplest and most common type of urinary cast
-non-specific –> seen in healthy and unhealthy individuals
-indicated slow or sluggish urine flow
-often seen in nephrotic syndrome

63
Q

what is nephrotic syndrome

A

a kidney disorder which causes the body to excrete too much protein in the urine

64
Q

what are urinary casts

A

-microscopic clusters of urinary particles such as cells, fat bodies, or microorganisms wrapped in a protein matrix in the urine
-clinical indicators of kidney conditions/used to assess kidney function

65
Q

what is hyalinization of connective tissue?

A

a condition in which normal tissue deteriorates into a homogeneous translucent material

66
Q

what are the 3 types of hyalinization of connective tissue

A
  1. old scars
  2. fibrinoid degeneration
  3. hyaline arteriosclerosis (vascular hyaline)
67
Q

what is fibrinoid degeneration

A

when collagen fibers begin to break down

68
Q

what is hyaline arteriosclerosis (vascular hyaline)

A

-thickening of the vessel walls and narrowed lumen
-arteriosclerosis = hardening of the arteries
*leads to decreased blood flow (ischemia)
-most typically occurs in the kidney as a result of hypertension and diabetes

69
Q

what is hyperplastic arteriosclerosis?

A

-an advanced form of hyaline arteriosclerosis caused by severe hypertension (BP ~ 250/140)
-necrosis of the arterial wall
-ONION SKIN APPEARANCE
-severe reduction of lumen

70
Q

what are the four organelles typically affected by injury

A

-cytoskeleton
-mitochondria
-smooth ER
-heat shock proteins

71
Q

what is chemotaxis?

A

the ability of WBC’s to move toward or response to inflammation or injury

72
Q

what are cytoskeleton abnormalities (general)

A

-defects in cell function especially locomotion and translocation –> myofilaments and microtubles

73
Q

what are the 4 abnormalities associated with cytoskeleton injury? (that we need to know lol)

A
  1. impaired sperm motility
  2. decreased function of respiratory epithelium cells
  3. decreased chemotaxis
  4. alzheimer’s disease –> neurofibrillary tangles
74
Q

what happens to the mitochondria after injury

A

-changes involve sizes, shape, number, and function
-> hypertrophy = increased #
-> atrophy = decreased #

75
Q

what are megamitochondria

A

large and abnormally shaped mitochondria
–> occur in nutritional deficiencies and alcoholic liver disease

76
Q

what are oncocytomas

A

tumors made of oncocytes (aka epithelial cells characterized by an excessive amount of mitochondria)
-usually benign
-found in kidney, thyroid, parathyroid, and salivary glands
-appear in early childhood and increase with age

77
Q

why is the smooth endoplasmic reticulum so important?
(enzyme functions)

A

-prevalent in hepatocytes
-contains enzymes responsible for DEGRADING INORGANIC TOXINS –> alcohol/drugs
-cycochrome P450 is essential for the metabolism of many medications –> metabolize 90% of drugs

78
Q

what happens when the sER is damaged

A

all the important enzymes don’t work so the liver can’t process drugs and alcohol

Micropathology (9 decks)

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