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Patho 523 > Patho Exam 1 > Flashcards

Patho Exam 1 Flashcards

1
Q

Macule

A

small in size (<10mm), circumscribed. Round fairly regular border. Flat, not elevated. Similar to a freckle

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2
Q

Patch

A

Large macule. Greater than 6 or 11mm

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3
Q

Papule

A

Small elevations on the surface of the skin. Can vary in shape. Can be flat topped or dome shaped. Not normally fluid filled. Should be full of tissue not fluid. (<5mm)

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4
Q

Nodule

A

Large round papules. Round or dome like shaped. Not flat topped. (>5mm)

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5
Q

Plaque

A

Large, flat top surface (>5mm)

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6
Q

Blister

A

(not official terminology) “seam” separate the layers of skin, have fluid in them. Examples include: vesicle and bulla

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7
Q

Vesicle

A

Type of blister. Small, fluid filled lesions

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8
Q

Bulla

A

Type of blister. Large fluid filled lesions

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9
Q

Pustule

A

Pus filled vesicle. Pus has interstitial fluid, neutrophils, dead cells. Can get very large and lyse.

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10
Q

Wheal

A

Rapidly forming skin lesions. They are elevated. Can form within minutes unlike the previous definitions; which take days, weeks or months. Usually caused by edema. Can be associated with erythema or blanching.

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11
Q

Scale

A

Excessive cornification. Horny like growths protruding from the skin, a few mm in size.

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12
Q

Lichenification

A

Thick tough skin, caused by constant rubbing. Usually not problematic.

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13
Q

Excoriation

A

Linear lesion, possibly a deep scratch. Commonly get a break in the epidermis. Skin is NOT sterile. The break in the epidermis sets you up for a pathology, bacteria can get in. (Left the gate open in the back yard and the dog can get out)

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14
Q

Hyperkeratosis

A

Abnormal thickening of your most superficial layer, stratum corneum (cells that fall off, it is constantly replacing itself). Abnormal keratin (it is a protein, water-retarding protein. Slows down evaporation of the skin, really keeps us from drying out. It is also a structural protein as well).

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15
Q

Parakeratosis

A

abnormal appearance at the cell biology level d/t retention of nuclei. If cells start rising to the surface and don’t dissolve their organelles that is “abnormal”. Important exceptions= mucous membranes

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16
Q

Hypergranulosis

A

Abnormal growth of the stratum granulosum ( where you lose organelles and pack the cells with keratin.) Associated with rubbing.

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17
Q

Why do the stratum granulosum cells start losing their organelles?

A

To fixate on a certain job. In this case to load up on keratin to prevent water from escaping the body.

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18
Q

Why does rubbing cause hypergranulosis?

A

Irritation which is a regulator of mitosis.

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19
Q

Acanthosis

A

Diffuse epidermal hyperplasia. Vague definition. Excessive growth somewhere in the epidermis.

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20
Q

Papillomatosis

A

Surface elevation caused by hyperplasia and enlargement of dermal papilla. (papilla= nipple) clinically problematic.

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21
Q

Dyskeratosis

A

accelerated granulation that is too deep in the skin. Loading up on keratin is occurring in the wrong layer of skin. Poorly functional. Occurs below the stratum granulosum

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22
Q

What are the five layers of the epidermis from bottom to top?

A
  1. Stratum Basale
  2. Stratum Spinosum
  3. Stratum Granulosum
  4. Stratum Lucidum
  5. Stratum Corneum
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23
Q

Stratum Spinosum

A

looks spiny & dendritic-like cells; involved in first line of defense of skin; communicates w/immune cells; if becomes keratinized → compromised

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24
Q

Stratum Basale

A

Often one layer thick

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25
Q

Spongiosus

A

Intracellular edema of the epidermis

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26
Q

Ballooning

A

edema that is intracellular of the keratinocytes. Cells take on too much water, pressure may be to high.

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27
Q

Exocytosis

A

the presence of blood cells in the epidermis. Infiltration of inflammatory cells in the epidermis

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28
Q

Why is the epidermis acellular?

A

The epidermis cells are dead and falling off, don’t want cells that are alive to fall off.

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29
Q

Erosion

A

Partial loss of epidermis. Usually not a big deal.

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30
Q

Ulceration

A

Complete loss of epidermis and maybe the dermis and subcutaneous fat. Example is bed ulcers.

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31
Q

Vacuolization

A

Formation of vacuoles within or adjacent to cells, often refers to basal cell- basement membrane zone area

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32
Q

Lentiginous

A

A linear pattern of melanocyte proliferation within the epidermal basal cell layer

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33
Q

Vitiligo (7)

A
  • Smooth, white patterns on the skin.
  • Most common in people with darker skin pigments.
  • Show up in areas like the wrists and hands.
  • In terms of cancer–> It is benign and asymptomatic.
  • Verify that there is a loss of melanoctyes.
  • NOT albino. Albino has non-functional melanocytes and it is usually systemic
  • Pathogenesis, many people say it is autimmune. Another possibility is neurohumoral
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34
Q

Freckles (7)

A
  • Small in size, “universal” in location
  • Light exposure sensitive
  • Common in the young
  • Should get brighter in the summer and fainter in the winter. Good sign! Means it is a freckle
  • Normal colors are tan to brown range
  • Cause→ localized increase in melanin
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35
Q

Melasma (7)

A
  • “mask like” pigmentation of the face.
  • Often hormonally driven
  • Common in pregnancy
  • Can get it from oral contraceptives, if you stop taking them, they will go away
  • If it is epidermal in origin→ take a black light and figure out how deep it is. If it is not deep you can bleach the skin. Increase in melanin deposition
  • Dermal type→ macrophages phagocytize melanin from the epidermis and accumulate it with the dermis. The problem is you cannot bleach it and get rid of it
  • Can have a mixed type
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36
Q

Lentigo

A

Does not change color through the seasons like freckles do. Stay the same year round.

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37
Q

Melanocytic Nevus (8)

A
  • diverse group of lesions, depends on the specific cause to characterize them.
  • They are usually brown or tan in color.
  • Usually less than 6mm in diameter.
  • Can be a macule to a papule.
  • Melanocytes have a change in activity. They become hyperactive to create this localized lesion.
  • They grow in aggregates. Often exist at the interface of the dermis and the epidermis.
  • Cells do mature, meaning they differentiate correctly. Still make melanin, just a little over zealously
  • Type of mole
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38
Q

Dysplastic Nevi (7)

A
  • Wasn’t until the 70s, through genetics, that the correlation between BK moles and cancer really become popular.
  • Larger than other nevi, larger than 5mm in diameter.
  • Changes in pigmentation! Striking variability in coloration! Blue, red, brown, and likely to change over time.
  • May or may not be on areas of sun exposure.
  • Often exist as dozens to hundreds over the body. Can look like macules or plaques or bull’s eyes.
  • Not all of them become melanomas but they have a decent chance of doing so
  • AKA “BK moles”
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39
Q

Why is the skin more prone to cancer than other organs?

A
  • always exposed to carcinogens/harmful substances d/t wide surface area,
  • high mitotic rate, & inevitable susceptibility
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40
Q

Malignant Melanoma (7)

A
  • Cancerous neoplasms from the cells that can produce melanin
  • UV radiation, light skin color (apt to this)
  • Usually asymptomatic, can be itchy
  • Most lesions are greater than 1cm
  • Borders of these are irregular, jagged edge on the surface of the lesion
  • Clinically you will look for change in size, shape, color
  • Rate of occurrence is increasing exponentially, not the most common skin cancer but it may be on its way
41
Q

Malignant Melanoma Radial Growth

A

Cells spread longitudinal within a layer of skin, sometimes the basement membrane is a decent barrier for metastasis (sometimes can keep things from going deeper into the dermis)

42
Q

Malignant Melanoma Vertical Growth

A

Bigger concern than radial growth. Cells spread into the dermis and hypodermis. There is a positive correlation between depth of growth and how bad the melanoma is

43
Q

Benign Epithelial Tumors (6)

A

These could be confused with something more serious, these are usually not brought to the attention of a provider but if they are you may want to get a biopsy to rule out cancer. Includes:
Seborrheic Keratosis, Acanthosis Nigricans, Fibroepithelial Polyps, Epidermal Cyst, Adnexal Tumors, and Keratoacanthoma

44
Q

Seborrheic Keratosis (2)

A
  • Common on the trunk and limbs of older individuals
  • Round, waxy plaques. They are unique because they often peel right off. Sandwiched between layers of the skin. No a/w discomfort or bleeding
45
Q

Acanthosis Nigricans (5)

A
  • Stratum spinosum→ hyperplasia (this layer has dendritic cells or immune cells that facilitate adhesions)
  • Attracted towards skin folds, hyperpigmentation of S. spinosum with a “velvety” look and texture
  • Can be a marker of both benign and malignant conditions
  • Linear component that is unique
  • Usually benign three quarters of the time in young people and is more cancerous when it is found in older individuals
46
Q

Fibroepithelial Polyps (4)

A
  • AKA acrochordon
  • Skin tag
  • Could be grape size (very big)
  • Dangles as a little appendage
47
Q

Adnexal Tumors

A
  • involve appendages of the skin

- Example would be a sweat gland apocrine, eccrine or a follicle

48
Q

Keratoachanthoma (8)

A
  • Fast growing tumor
  • More common in men, especially white old guys older than 50
  • Growth is bigger than 1 cm
  • Flesh color and dome shaped
  • Usually in sun exposed areas
  • Often cures itself
  • May mimic SCC BUT these are NOT malignant, if you don’t know biopsy
  • Cells should look uniform and differentiated “normal cells”
49
Q

Malignant Epidermal Tumors

A
  • Actinic Keratosis
  • SCC
  • BCC
50
Q

Actinic Keratosis

A
  • Cutaneous horn, size of the tip of your pen
  • Many do lead to malignancy
  • Usually small, less than 1 cm
  • Huge keratin explosion, basically heavy duty nails
  • Positive correlation with sun exposure, can lead to SCC
51
Q

SCC (8)

A
  • Second to BCC, SCC is a little rarer
  • Positive correlation with sun exposure
  • Abnormal development, problems with differentiation
  • Enlarged, hyperchromatic nuclei, round/pea shaped nuclei. Cells are poorly specialized so the cells should start looking odd.
  • Main barrier for keeping metastasis under control is the basement membrane
  • Most of the time these are going to be caught early and are excised
  • Less than 5% of these metastasize
  • Most of the time you get a good prognosis
52
Q

SCC Mutations

A
  • DNA repair mechanisms (mutations in the body are common, but our bodies can most of the time fix them, the problem here is that DNA cannot repair itself correctly and the mutation continues)
  • Increase in mutations
53
Q

What does SCC start as?

A

Begin as in situ carcinomas→ in its normal location, contained at the junction between the dermis and the epidermis. Sharply defined, red scaly plaques (raised). As this progresses it will spread and the plaques become nodules which can ulcerate.

54
Q

BCC (9)

A
  • The most common invasive cancer in the US right now
  • Difference between SCC and BCC is the layer of skin
  • Slow growing tumors that usually don’t metastasize
  • Stimulated by sun exposure, light skin color, immunosuppression ( malfunctioning killer T cells)
  • Very unique appearance, papule with a prominent surface and you can see tiny blood vessels (Looks like a blister but its not clear, you will see the blood vessels) A little on the bloody side
  • May or may not be pigmented, depends on the melanocytes involved
  • It can ulcerate
  • Likes to metastasize to the bone especially the skull and sinuses
  • Can get nodular formations that can create islands that will grow deeper into the body. Surrounded by fibroblasts (for supporting structures) and lymphocytes
55
Q

What is the cell morphology of BCC?

A
  • Early on the basal cells will have normal cell morphology but over time you will get growths and you can get multifocal growths (cells start in the epidermis and then extend over the skin). Multiple locations that grow toward each other.
56
Q

Epidermal Cyst

A
  • AKA wen
  • Tumor contains keratin
  • Epithelium is a pocket or shell for other skin like structures
  • If you palpate this it should be moveable
  • Could be in the dermis, could be subcutaneous
  • Likely to be annoying and have no consequence
57
Q

Urticaria (hives)

A
  • Incredibly itchy
  • Most common in 20-40 year olds
  • Variety of causes
  • Lesions develop and dissipate in hours. Very acute
  • Episodic condition in many cases, you are not necessarily cured if it goes away. You may or may not be exposed again the second time, could just have another reaction
  • Hives can form small papules and can form plaques which are usually temporary and will resolve on its own. Antigen induced.
  • IgE is important with hives antibodies to IgE that are overly sensitive to the antigen
58
Q

What is the mechanism of action for urticaria?

A

Mechanism of action= degranulation of mast cells, histamine release, increased permeability through the microcirculation which creates skin inflammation→ does create the stage for wheals

59
Q

Eczema

A
  • Multifactorial skin disease
  • Greek for “boiling over” fluid accumulates and oozes over
  • Acute condition
  • Multifactorial
  • Red papulovesicular lesions
  • Ooze and crust over
  • Raised, scaling plaques
60
Q

Classification of Scheme

A
  1. Allergic contact dermatitis, example: poison ivy
  2. Atrophic dermatitis- cause unknown
  3. Drug related dermatitis
  4. Photo-induced- UV light
  5. Primary irritant eczema- environmental chemical
61
Q

Hypersensitivity

A

Antigen Presentation= dendritic cells present antigen→ CD4 T cells in a lymph node, memory cells→ inflammation at site of exposure

62
Q

Psoriasis (7)

A
  • Location includes: elbows, knees, glans of the penis, lumbar/sacral regions
  • 1-2% of the population
  • Associated with arthritis
  • A third of the time it is associated with nail problems. Yellow brown discoloration
  • Pink, plaques→scales
  • Decreased function of the stratum granulosum (main function is keratinization)
  • Associated with inflammation and angiogenesis
63
Q

Seborrheic Dermatoses (4)

A
  • In an area of skin with a large number of sebaceous glands, but it is not the causative agent
  • Usually on the scalp and glabella
  • Macules, papules, greasy dandruff
  • Etiology: yeast- induced (not proven)
64
Q

Acne Vulgaris (3)

A
  • Almost universal in teenagers
  • Usually worse in boys than girls due to hormonal changes (follicular developmental changes)
  • One population that does not get acne eunuchs (castration) Shows that testosterone is a key player
65
Q

Inflammatory Acne

A

“white heads” pustule formation. Follicle of the hair. No keratin plugs.

66
Q

Non-Inflammatory Acne

A

Open comedomes (black heads). Follicular plug of keratin that is oxidized.

67
Q

Warts (Verruca Vulgaris) (4)

A
  • Papillomaviruses, there are greater than 150 DNA viruses
  • Most likely to occur on the hands
  • Spread by contact
  • Takes half a year to two years to disappear if you do not treat
68
Q

Cerebral Edema (5)

A
  • Secondary to many conditions, associated with many disorders
  • Gyri are flattened/widened
  • Sulci are narrowed
  • Ventricular cavities compressed
  • Herniation may occur
69
Q

Cytotoxic Edema (4)

A
  • Another type of cerebral edema
  • Increase in the intracellular fluid of the CNS.
  • Secondary to neuronal, glial, or endothelial cell membrane injury.
  • Common causes of this would be hypoxia or intoxication.
70
Q

Increase in Intracranial Pressure/ Herniation (5)

A
  • When the volume of the brain increases beyond the limit permitted by compression of veins and displacement of CSF, the pressure within the skull will increase
  • Pressure gets greater than 20 cmH2O in recumbent patient (csf P) NOT much water
  • Can be diffuse/generalized (generalized brain edema)
  • Can be focal/localized (tumor, abscesses, or hemorrhages)
  • If expansion is severe, herniation may occur
71
Q

Hydrocephalus (6)

A
  • Water on the brain
  • Increase CSF in the CNS, more specifically accumulation of excessive CSF within the ventricular system
  • Usually occurs from impaired flow and resorption of CSF
  • Can also be from tumors of the choroid plexus or problems with the arachnoid granulations (rare)
  • If this happens prior to suture closure (in babies/infants), enlargement of the head and circumference will occur
  • If this happens after sutures are closed, then the ventricles enlarge and intracranial pressure increases without a change in head circumference.
72
Q

Neural Tube Defects (5)

A
  • Failure of a portion of the neural tube to close OR reopening of a region of the tube after successful closure
  • Most common type of CNS malformation. Usually happens around day 28 of gestation
  • Every 1-5/1000 births.
  • Gross changes (decreases) in the calvaria (skull cap).
  • F>M, therefore roles of sex steroids/genetics is a distinct possibility but it still needs to be deciphered
73
Q

Anencephaly (2)

A
  • Malformation of the anterior end of the neural tube, with absence of the brain and calvarium (skull)
  • Failure of forebrain to develop
74
Q

Spina Bifida (5)

A
  • Failure of closure/ reopening of the caudal portions of the neural tube
  • Most common neural tube defect in posterior/ distal end of the spine
  • Can be an asymptomatic bony defect or a severe malformation with flattened, disorganized segment of the spinal cord, a/w an overlying meningeal out pouch
  • Disease represents as out growths of tissue from the vertebral canal. May or may not have meningeal coverings.
  • Can be genetic causes or from folate deficiency
75
Q

Myelomeningocele (5)

A
  • Extensions of CNS tissue through a defect in the vertebral column.
  • Meningocele applies only when there is a meningeal extrusion
  • Usually occurs in the lumber/sacral region
  • Problems with bladder/bowel control
  • Deficits in motor/sensory function in the lower extremities
76
Q

Cerebral Palsy (3)

A
  • Non progressive, motor deficit condition; but with a strong neurologic component
  • S/S May not be recognized at birth, but will present very during development
  • Problems include: ataxia (lack of coordination, herkey jerky type movements), dystonia, spasticity, parietal paralysis/paresis or momentary bouts of muscle weakness
77
Q

Cause of Cerebral Palsy (2)

A
  • Cause: some kind of insult during prenatal or perinatal period, some exogenous factor (may never know what that cause is)
  • Hemorrhage, infarct→ something of that nature (necrosis) that causes a lesion in a specific region of the brain→ where it occurs will determine specific symptoms
78
Q

Generalized Trauma of the CNS (3)

A
  • A blow to the head can be blunt or penetrating and it may cause an open or closed injury
  • Manifest as wedge shaped lesions, immediate point of impact will have damage but if you go deeper into the brain, the color will be more of a brownish color
  • Physical forces associated with head injury may result in: skull fx, parenchymal injury, and vascular injury (which can all coexist)
79
Q

Severity of Trauma (5)

A

Severity: depends on where the trauma occurs:

  • Small lesions→ mm3-cm3
  • In cortex→ may be silent
  • In brainstem→ Lethal
  • Spinal cord→ severe impairments in mobility, sensations of trunk and limbs
  • Magnitude and distribution of lesion depend on the shape of the object used to cause the trauma, the force of impact and whether or not the head was in motion at the time of injury
80
Q

Concussion (5)

A
  • Transient alteration in level of consciousness
  • Usually initiated by force, can be an abrupt shift in momentum
  • Amnesia of causative agent
  • Temporary respiratory arrest, somewhat like “getting the wind knocked out of you”
  • Loss of reflexes: Check for these!
81
Q

Mechanism of a Concussion (3)

A

Mechanism:

  • Change in resting membrane potential→ looks like it is caused by excitatory amino acids
  • Mitochondrial issues→ drop in ATP production (electron transport chain, krebs cycle)
  • Change in vascular permeability
82
Q

Contusion/ Bruising the Brain (5)

A
  • Blood clot→ fibroblasts invade→ fibroblasts secrete large amounts of collagen and other protein fibers→ create a network around the blood clot
  • Laceration→ cut in brain/ surrounding tissue→ parenchyma is a common site of injury
  • Hemorrhage leads to edema in the area, and activates inflammatory response/WBC invasion
  • Usually in one day there will be damage to soma of neurons (neurons do not regenerate well but it does not mean they cant, olfactory neurons do regenerate well). Soma occupy much greater space, so if the trauma happens here, damage occurs here first and the axons are later down the line
  • Elevation in eosinophils→ axonal swelling→ neutrophils and macrophages
83
Q

Coup Injury

A

At the site of impact

84
Q

Contrecoup Injury

A

On the opposite side of the brain, knock your head so hard that your brain actually hits the opposite side of the head and injury occurs there as well

85
Q

Epidural Hematoma (5)

A
  • Hematoma→ pocket of blood, somewhere in the body
  • The space between dura mater and periosteum
  • Increase in space between skull and brain, the skull will not move so the brain has to compensate
  • *If this is severe you will go to surgery, life-threatening situation
  • Something is causing blood to leak out of meningeal arteries
  • Arterial bleed
86
Q

Subdural Hematoma (5)

A
  • Bleeding in the arachnoid space
  • Veins called “bridge veins” in this space→ may be fixed in space, therefore if the brain shifts, the veins may tear and bleed (not proven). Fairly thin walled
  • High rate of reoccurrence
  • How will these people react? Depends on where the hematoma occurs. For example→ if it occurs in the pre-central gyrus, there will be problems with motor function
  • Venous bleed
87
Q

Cerebral Vascular Disease (4)

A
  • Any neurologic disease caused by vascular pathology, brain is bearing the brunt of the blood vessels fault
  • # 3 killer on morbidity list
  • Can be global or focal. It is better to be focal in a small region of the brain. Global ischemia→ life threatening
  • Problems:
    1. Neurons are most susceptible because they have a higher rate of metabolism than glial cells
    2. Oligodendrocytes and astrocytes are sensitive too
88
Q

3 Causes of a Stroke

A
  1. Thrombosis→ blood clot
  2. Hemorrhage→ bleeding
  3. Embolism→ plug in vasculature (fat, tumor, air)
89
Q

Mechanisms of the 3 Causes of Stroke

A
  1. Hypoxia→ decreased oxygen, brain gets 15% of CO, impaired metabolism of the cells
  2. Ischemia→ reduced blood flow to the area, reduce metabolism, decreased cell function
  3. Infarction→ specific area of damage, usually not fixable, but it can be in some cases
90
Q

Meningitis

A

Inflammation of the Meninges

91
Q

Bacterial Meningitis (6)

A
  • Common causative agents: E. coli, Strep. Pneumonia
  • “Pocket of pus” white exudate in cranial floor, inferior view of the brain
  • Neurologic impairments
  • Stiff neck→ common symptom, also problems with basic reflex testing and some cognition issues.
  • Other symptoms→ photophobia, increase in irritability
  • Need to get a sample of CSF→ may be white or cloudy in color, see an increase in protein content and a decrease in glucose, not much of a change in lymphocyte number (which is different from the viral cause which will have a big jump in lymphocyte count)
92
Q

Viral Meningitis

A
  • Misnomer→ cannot see a microorganism as a causative agent
  • Vast majority of the time caused by enterovirus
  • Slow onset progression, run its course and manage symptoms
  • Big increase in lymphocyte count, probably no change in glucose in the CSF
93
Q

Vasogenic Edema

A
  • Type of cerebral edema
  • D/t BBB disruption and increased vascular permeability causing a shift of fluid from intravascular to intercellular spaces of the brain
  • Poor lymphatic drainage in the CNS which does not allow for excess fluid to be resorbed
  • Localized or generalized
94
Q

What is the BBB made of?

A
  • Endothelial cells

- Astrocytes were thought to make up the BBB but they do not, they are just located in that general area

95
Q

Subfalcine (cingulate) Herniation

A

Occurs when unilateral or asymmetric expansion of a cerebral hemisphere displaces the cingulate gyrus under the flax cerebri. Can lead to compression of the anterior cerebral artery.

96
Q

Transtentorial Herniation

A

Occurs when the medial aspect of the temporal lobe is compressed against the free margin of the tentorium.
This can lead to compression of the 3rd cranial nerve and the posterior cerebral artery.
Progression can also lead to hemorrhagic lesions in the midbrain and pons.

97
Q

Tonsillar Herniation

A

Displacement of the cerebellar tonsils through the foramen magnum. This is life-threatening d/t brainstem compression and compromise of the respiratory and cardiac centers in the medulla oblongata.

98
Q

Non-communicating Hydrocephalus

A

Occurs when only a portion (for example, the third ventricle only) of the ventricular system is enlarged d/t excess CSF

99
Q

Communicating Hydrocephalus

A

Enlargement of the entire ventricular system

Patho 523 (2 decks)

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