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DMD 5243 > Information Needed to answer Bikmans test questions > Flashcards

Information Needed to answer Bikmans test questions Flashcards

1
Q

What disorder is associated with dry, crusty, black sores on toes and feet

A

Dry gangrenous necrosis

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2
Q

what causes gangrenous necrosis

A

hypoxia

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3
Q

why does hypoxia lead to a damaged cell

A
  1. a lack of Oxygen means that ATP can’t be produced from the ETC chain.
  2. Low ATP means that the sodium-potassium pump and calcium pumps can’t work.
  3. cell will swell, and if not corrected the cell will lyse
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4
Q

what happens to the mitochondria in a hypoxia condition

A

the mitochondria swell as well

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5
Q

What are the three main changes that take place in necrosis

A
  1. nuclear changes
  2. cytoplasmic changes
  3. calcification
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6
Q

What are the nuclear changes that take place in necrosis

A

Pyknosis
Karyorrhexis
Karyolysis

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7
Q

what is pyknosis

A

the clumping of chromatin in the nucleus

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8
Q

what is karyorrhexis

A

fragmentation of the nucleus

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9
Q

what is karyolysis

A

nuclear dissolution and chromatin lysis

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10
Q

What is the main cytoplasmic change associated with necrosis

A

increased eosinophilia (seen as red stains)

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11
Q

What causes the calcification associated with necrosis

A

dead cells that are converted into fatty acids (instead of being phagocytosed) those fatty acids attract a lot of calcium and calcification results

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12
Q

What are the two types of calcification

A

dystrophic calcification

metabolic calcification

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13
Q

what is the difference between dystrophic and metabolic calcification

A

metabolic can occur in any tissue and is a result of hypercalcemia
dystrophic occurs with necrosis, often in atheroma. not related to hypercalcemia

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14
Q

What are the different types of necrosis

A 
coagulative necrosis
liquefactive necrosis
caseous necrosis
fat necrosis
fibrinoid necrosis
gangrenous necrosis
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15
Q

what is coagulative necrosis and what tissues does it affect

A

it is protein denaturation (albumin becomes opaque)

it affects the kidneys, spleen, heart, and adrenal glands

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16
Q

what is liquefactive necrosis and what tissues does it affect

A

it affects the hydrolytic enzymes

it affects the neurons and glial cells of the brain

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17
Q

What is caseous necrosis and what tissues does it affect

A

it is a combination of coagulative and liquefactive necrosis, it often forms a granuloma

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18
Q

What is fat necrosis, and what tissues does it affect

A

it affects the action of lipases

it affects the pancreas, breast, and abdominal organs

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19
Q

What is fibrinoid necrosis, and what tissues does it affect

A

it is complexes of antigens and antibodies that are deposited in the walls of arteries

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20
Q

What are the two types of gangrenous necrosis

A

wet and dry

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21
Q

what tissues does gangrenous necrosis affect

A

the limbs, not organs

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22
Q

what is typical of dry gangrenous necrosis

A

insufficient blood
coagulative
dry, crusty, and black skin

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23
Q

What is typical of wet gangrenous necrosis

A

infection
liquefactive
cold, swollen, black
Foul odor (pus)

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24
Q

what are the two types of inflammation

A

chronic and acute

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25
Q

what kind of cells will you see in the tissues in acute inflammation

A

mostly neutrophils

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26
Q

what kind of cells will you see in the tissues in chronic inflammation

A

monocytes/macrophages and lymphocytes

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27
Q

What do monocytes look like

A
  1. Large
  2. oddly shaped
  3. nucleus doesn’t fill the entire space and isn’t segmented
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28
Q

what do lymphocytes look like

A
  1. the nucleus almost fills the entire space and isn’t segmented
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29
Q

what do neutrophils look like

A
  1. has a polymorphuous (PMN or segmented) nucleus

2. few neutral granulocytes

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30
Q

What do eosinophils look like

A
  1. a PMN cell

2. many red granulocytes

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31
Q

what do basophils look like

A
  1. a PMN cell

2. many blue granulocytes

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32
Q

what is the first leukocyte to arrive at the site of infection

A

neutrophils

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33
Q

What role does arachadonic acid play in inflammation

A

it is broken down into 4 different molecules that affect inflammation

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34
Q

what 4 metabolites is arachadonic acid broken down into that affect inflammation

A

Via cyclooxygenase:
prostaglandins
prostacyclins
thromboxanes

Via lipoxygenase:
leukotrienes

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35
Q

From where does a cell get the arachadonic acid that is broken down into prostaglandins, prostacyclins, thromboxanes, and leukotrienes

A

the phospholipids of the cell membrane

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36
Q

what enzyme converts the phospholipids of the cell membrane into arachadonic acid

A

phospholipase A2

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37
Q

What are the products when COX (cyclooxygenase) reacts with arachadonic acid

A

prostaglandins
prostacyclins
thromboxanes

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38
Q

how do prostaglandins affect inflammation

A

they increase inflammation
they increase clotting
and thermoregulation

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39
Q

how do prostacyclins affect inflammation?

A

cause vasodilation
inhibit platelet activation
reduce clotting

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40
Q

how do thromboxanes affect inflammation

A

activate platelets and make them sticky

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41
Q

what are the products of lipoxygenase reacting with arachadonic acid

A

leukotrienes

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42
Q

how do leukotrienes affect inflammation

A

cause smooth muscle contraction in the trachea (they cause most of the inflammation in asthma and allergic rhinitis)

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43
Q

which of the metabolites of arachadonic acid causes the inflammation in asthma and allergic rhinitis

A

leukotrienes

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44
Q

on what enzymes to anti-inflammatory steroids act, what does that cause

A

they act on phospholipase A2 and cyclooxygenase
this stops arachadonic acid from being made from phospholipases, and stop arachadonic acid from being metabolized into prostaglandins, prostacyclins, and thromboxanes

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45
Q

Where does aspirin act

A

On COX (cyclooxygenase) stopping arachadonic acid from being metabolized into prostacyclines, prostaglandins, and thromboxanes

46
Q

What is the affect of Omega 3 fatty acids (n-3 PUFA) on inflammation

A

it inhibits COX and produces resolvins (anti-inflammatory things)
So it reduces inflammation

47
Q

How can one get n-3 PUFAs

A

eating fish, eggs, milk, many meats (grass fed animals)

48
Q

What is the relationship between omega 3 fatty acids and periodontitis

A

intake of omega 3 fatty acids (DHA and EPA) are inversely associated with periodontitis. dietary therapy with more omega 3 fatty acids could help prevent and treat periodontitis

49
Q

what is periodontitis

A

inflammation of the periodontium

50
Q

how is periodontitis associated with insulin

A

periodontitis is associated with insulin resistance

51
Q

how is inflammation associated with insulin resistance

A

inflammation leads to insulin resistance

52
Q

What is a nevus

A

a benign proliferation of melanocytes (a mole)

53
Q

What are the three types of moles (locations in which they are)

A

Junctional (dermal epidermal junction)
Compound (partially into the dermis)
Intradermal (completely in the dermis)

54
Q

which of the three types of nevi (moles) is most likely to become malignant

A

compound nevus

55
Q

What is a melanoma

A

a malignant tumor of melanocytes

56
Q

What are the ABCDE’s you look for in a nevus to determine if it may be malignant

A 
A - Asymmetry
B - Border
C - Color
D - Diameter
E - Elevation
57
Q

can melanoma arise from a benign nevus

A

yes

58
Q

what affect can sun exposure have on our risk of developing melanoma

A

more sun exposure = more risk of melanoma

59
Q

What determines the prognosis of someone diagnosed with melanoma

A

how deep the melanoma has invaded the skin

60
Q

What are the four types of melanoma

A
  1. superficial spreading
  2. nodular
  3. lentigo maligna
  4. acral lentiginous
61
Q

What is a superficial spreading melanoma

A

a melanoma that spreads but stays in the epidermis

62
Q

what is a nodular melanoma

A

the most agressive form of melanoma, it tends to grow deep as opposed to broad

63
Q

what is a lentigo maligna melanoma

A

a melanoma that evolves from a lentigo maligna on the skin

64
Q

what is acral lentiginous melanoma

A

a melanoma that is found on a non-hair bearing surface

65
Q

which type of melanoma is most likely found on the roof of her mouth

A

acral lentiginous

66
Q

what is the % chance of 5 years survival for melanomas that are
1. less than 1mm deep
2. between 1 and 2 mm deep
3 between 2 and 4 mm deep

A
  1. 80-95% 5 year survival
  2. 30-60% 5 year survival
  3. 35% 5 year survival
67
Q

What is the most common type of anemia

A

iron-deficient anemia

68
Q

What kind of anemia is iron-deficient anemia

A

microcytic, hypochromic anemia

small RBCs with Low hemoglobin

69
Q

What are two telling symptoms of iron-deficient anemia

A 
Atrophic glossitis (smooth tongue)
Koilonychia (indented finger nails)
70
Q

What are potential causes of iron-deficient anemia

A
  1. Decreased Iron intake
    a. poor diet
    b. poor absorption
  2. Increased iron loss
    a. GI bleeding
    b. menses
    c. hemorrhage
  3. Increased Iron requirement
    a. pregnancy
71
Q

What is anemia

A

a reduction below the normal in hemoglobin or red blood cell number

72
Q

What are the symptoms of anemia

A 
Pale skin
jaundice (if hemolytic)
breathless ness
tachycardia
dizziness
fatigue
73
Q

what kind of anemia is related to low G6PDH levels

A

G6PDH deficient anemia

74
Q

how does low G6PDH levels cause anemia

A

G6PDH assists glutathione in getting rid of reactive oxygen species. if you have low G6PDH levels, then glutathione wont be able to get rid of them, and you will have high reactive oxygen species. Those kill RBCs

75
Q

is G6PDH deficient anemia intra or extracorpuscular

A

it is intracorpuscular

76
Q

What kind of cells are associated with G6PDH deficiency

A

RBCs with heinz bodies

AKA bite cells

77
Q

is G6PDH a hemolytic anemia

A

yes, it causes the destruction of RBCs

78
Q

the heinz bodies are piles of _____

A

globin

79
Q

Fava beans (and some drugs) can set off what kind of anemia

A

G6PDH deficient anemia

80
Q

can G6PDH deficient anemia cause jaundice

A

yes, because it is a hemolytic anemia

81
Q

in diagnosing jaundice a doctor will look at stool and urin color to figure out where the jaundice is coming from. When the urine and stool are both Dark, what is that indicative of

A

hemolytic anemia

82
Q

what are the signs of hemolytic anemia

A 
increased bilirubin
increased LDH
reduced haptoglobin
increased reticulocytes
nucleated RBCs in blood
83
Q

What are the different types of hemolytic anemias

A 
Microangiopathic hemolytic anemia
autoimmune hemolytic anemia
sickle cell anemia
thalassemia
hereditary spherocytosis
G6PDH deficiency
84
Q

What type of anemia is associated with prominent cheek bones

A

thalassemia

85
Q

is thalassemia intra or extracorpuscular

A

intracorpuscular

86
Q

What are the RBCs like in thalassemia

A

hypochromic and microcytic

87
Q

What is actually the problem in thalassemia

A

inability to make sufficient alpha or Beta chain of hemoglobin

88
Q

What happens to EPO levels in thalassemia

A

they are increased to increase RBC production

89
Q

What can determine whether thalassemia is a problem with the alpha or beta chain of hemoglobin

A

ethnicity
South east Asians = alpha chain problems
Mediterranians = beta chain problems

90
Q

What causes the prominent cheek bones in thalassemia

A

high levels of erythropoesis

91
Q

can thalassemia lead to jaundice

A

yes

92
Q

What is marfan syndrome

A

a disorder of connective tissues, manifested by changes in the skeleton, eyes, and cardiovascular system

93
Q

what is the actual problem in marfan syndrome

A

an abnormality of fibrillin 1 (elastic fibers)

94
Q

What are the features of someone with marfan syndrome

A
  1. unusually tall with long extermities
  2. bilateral subluxination of the eye lens (ectopica lentis)
  3. cardiovascular legions: mitral valve prolapse
  4. increased risk of cleft palate and caries
95
Q

is marfan syndrome a heritable disorder

A

yes

96
Q

is marfan syndrome a sex linked disorder

A

no. it is an autosomal dominant disorder

97
Q

What disorder is most associated with

  • shortness
  • webbing of the neck
  • edema
  • wide chest
  • reduced carrying angle
  • low hairline
A

Turner syndrome

98
Q

what is the actual problem in turner syndrome

A

a female with only one X

99
Q

is turner sydrome autosomal or sex chromosome aneuploidy

A

sex chromosome aneuploidy

100
Q

how could someone get turner syndrome

A

one parent did nondisjunction of the sex chromosomes. so from one parent you get X (normal) from the other you do not get a sex chromosome

101
Q

What are the three ways a tumor will metastasize

A

seeding
lymphatic spread
hematogenous spread

102
Q

What is seeding (metastasize)

A

tumor invades the body cavity
a bit breaks off of something in the body cavity and attaches to something else
ovarian cancer spreads this way

103
Q

What way do carninomas generally metastisize

A

lymphatic spread (tumor spreads through the lymph)

104
Q

what ways do sarcomas generally metastasize

A

hematogenous spread (through the blood)

105
Q

can carcinomas spread through hematogenous spread

A

yes

106
Q

where to sarcomas end up most commonly

A

the liver and lungs

107
Q

What is dysplasia

A

disorderly changes in non-neoplastic epithelial cells

108
Q

what is anaplasia

A

a complete lack of differentiation

109
Q

is a benign tumor highly or poorly differentiated tissue

A

highly

110
Q

is a malignant tumor highly or poorly differentiated tissue

A

poorly

111
Q

What is a benign fat tumor

A

lipoma

112
Q

what is a malignant fat tumor

A

liposarcoma

DMD 5243 (17 decks)

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