Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SBL Final > Path > Flashcards

Path Flashcards

1
Q

Hematoxylin stains _____ _____, calcium salts, and bacteria a purply-blue.

Eosin stains _______ and ______ pink-red.

A

nucleic acid

arginine and lysine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

_______ _____-_____: cis-diols are flaming pink. Any insoluble sugar is a cis-diol including glycogen**, epithelial mucin, cartilage, fungus wall, basement membrane, reticulin, a1-antitrypsin

A

Periodic acid-Schiff (PAS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  • obtained easily by anyone in saliva
  • used to remove glycogen from slides to be PAS-stained
  • PAS+, dPAS- indicates glycogen
  • Seen on liver biopsy reports.
A

Diastase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Oil-red O stain demonstrates what along a vessel?

A

fat cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  • stains epithelial mucins brilliant pink and everything else brown-to-green.
  • It also lights up cryptococcus yeasts.
A

Mucicarmine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What shows up on a trichrome stain?

A

Trichrome gives a blue stain to dense type I collagen (connective tissue, scar, etc.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What stain is used for mycobacteria?

A

acid-fast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What do argentaffin and argyrophil stain using silver?

A

serotonin-rich granules of carcinoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

TQ:

What is the best way to light up fungi, especially pneumocystis?

A

Methenamine silver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  • Stains various cell components different colors due to the way they stack dye molecules
  • Almost all blood smears use this principle for staining.
A

Metachromasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What stain do we use for pap smears?

-Contains some light green (RNA) and orange G (cysteine disulfide bonds)

A

Papanicolaou’s stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Nucleic acid stains _____ brown

A

HPV36

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

-An expensive way to spot viruses such as this CMV when they do not show the classic histopath yet.

A

Gene probes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

TQ:

  • extra neutral fat in vacuoles in non-adipocytes
  • Occurs MC in liver and heart
A

fatty change

6 mechanisms for liver:

  1. Too much free fat coming to the liver
  2. Too much fatty acid synthesis by the liver
  3. Impaired fatty acid oxidation by the liver
  4. Excess esterification of fatty acid to triglycerides by the liver
  5. Too little apoprotein synthesis by the liver
  6. Failure of lipoprotein secretion by the liver.

Non-alcoholic fatty liver is even more common nowadays as a component of the metabolic syndrome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Fatty liver: lipid drops have sharp edges

Causes?

A
  • Alcoholic hep (neuts, mallory hyaline)
  • Metabolic syndrome
  • Reye’s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are two reasons for fatty change in the heart?

A
  • Tiger-stripe / thrush-breast heart of anemia. The muscle away from vessels is hypoxic and can’t burn its lipid fuel.
  • Diptheria: microbes produce poison that interferes with burning of lipid regardless of O2 levels (uniformly flabby and fatty heart)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When do we see cholesterol needles?

A

atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

-Clusters of lipid-laden macrophages seen around the eyes

A

Xanthelasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

-Lipid in quasineoplastic macrophages

A

Xanthoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are 3 examples of xanthomas?

A
  • Strawberry gallbladder
  • Tendon xanthomas (familial hypercholesterolemia)
  • Palmar xanthomas (primary biliary cirrhosis…yellow lines on palms)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
  • Abetalipoproteinemia results from lack of apolipoproteins B48 and B100
  • Patient can’t absorb fat, which accumulates in the intestinal lining cells

What is seen on a smear?

A

acanthocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

“Fatty ingrowth”, in contrast to true fatty change, is simply the appearance of mature fat cells, in excess, in an unusual place

Where do we see it normally? (2)

A
  • pancreas

- lymph node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Glycogen in hepatic nuclei suggests…

A

pre-mortem hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

TQ

  • Mucopolysaccharosis I
  • Lack of a critical enzyme causes accumulation of heparan sulfate and dermatan sulfate in lysosomes
  • Zebra bodies
  • This leads to progressive brain damage / mental and motor deterioration, enlarged liver and spleen, short stature and the characteristic “gargoyle” appearance.
A

Hurler’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
  • Mucopolysaccharosis II (similar to type I)
  • X-linked
  • Accumulations of heparan sulfate and dermatan sulfate
  • Gargoyle appearance
  • Tx: Idursulfase injection
A

Hunter’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q
  • Several of the __________ feature disease of the aortic and mitral valve from accumulation
  • swollen cusps, swollen lysosomes on electron microscopy, some with zebra bodies.
  • mitral stenosis cases are caused by rheumatic fever; much less often, lupus; storage disease a distant third.
A

mucopolysaccharidoses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q
  • Mucopolysaccharidosis III
  • Accumulation primarily of heparan sulfate.
  • The problems mostly involve the brain, with progressive mental deterioration.
A

Sanfilippo

Remember: only heparan sulfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q
  • Mucopolysaccharidosis IV
  • Storage product is keratan sulfate
  • Keratan sulfate is mostly found in bone, cartilage, and cornea.
  • Mentally normal, but are short
  • Develop corneal clouding.
A

Morquio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

TQ

  • Pt presents with intractable burning pain in palms and soles
  • Deficiency of alpha-galactosidase.
  • Ceramide trihexoside accumulates in lysosomes
  • X-linked (lyonization=female carriers of Fabry’s are never altogether healthy)

What is the tip off to the diagnosis?

A

Angiokeratomas
(Fabry’s dz)

The artery deposits show purple metachromasia, pale zebra bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What heart issues are seen with fabry’s?

A
  • cardiomyopathy with rhythm problems

- the septum may be thick (hypertrophic cardiomyopathy) or there may simply be rhythm problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the only storage dz that affects the glomeruli?

A

Fabry’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

TQ

  • Glucocerebrosidase deficiency
  • Glucocerebroside accumulates inside cells, especially the fixed monocyte-derived phagocytes
  • Crumbled tissue paper/kleenex
  • Hepatosplenomegaly!
  • H shaped vertebra
  • Mild–>severe (liver/spleen/bone/brain)
A

Gaucher’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q
  • Lysosomal storage disease resulting from a mutations
  • Accumulation of sphingomyelin
  • Storage cells look spotty more than crinkly
  • Severe brain involvement
  • “childhood alzheimer’s”
A

Niemann-Pick Dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q
  • GM2 gangliosidosis
  • Lack of hexosaminidase A (gene HEXA) with accumulation of ganglioside, mostly in the brain.
  • Enlargement of individual neurons–>enlargement of the entire head.
  • Cherry red macula
A

Tay-Sach’s Dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q
  • Lack of the normal acid lipase in lysosomes so cant break down cholesterol esters
  • Affects the liver and leads to precocious atherosclerosis.
A

Cholesterol Ester Storage Dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q
  • Glucose-6-phosphatase deficiency
  • Patients have difficulty breaking down glycogen, especially in the liver, which becomes overloaded over time (splenomegaly)
  • Glycogen is in the cytoplasm, not the lysosomes
  • Babies have kewpie doll faces

What is the tx?

A

-Continuous ingestion of carbohydrate (often as cornstarch). The key is to avoid “the fasting state” and thus dangerous hypoglycemia.

(Von-Gierke’s Glycogen Storage Dz Type I)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

-Deficiency of acid alpha-glycosidase
-Only glycogen storage disease with glycogen actually within lysosomes (glycogen pellets)
-Heart, skeletal muscle, and liver
are involved (brain spared)
-Babies have enlarged, weak hearts and may present as floppy baby

A

Pompe’s dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q
  • Deficiency of any of the three enzymes that govern the metabolism of galactose, from milk. If it’s missed, the results are catastrophic.
  • Galactose that cannot be metabolized becomes galactitol (dulcitol) and/or galactose-1-phosphate, which causes edema of cells
A

Galactosemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Assoc s/s of galactosemia?

A

-Cataracts: galacitol absorbing fluid into lens
-Severely-affected children
can still suffer brain damage – most famously, a tendency to swap consonants (verbal dyspraxia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q
  • “mucolipidosis II” features a lack of N-acetylglucosamine-1-phosphate transferase so can’t tag proteins to be discarded via the Golgi.
  • Striking accumulations appear in macrophages.
A

I-cell disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q
  • reappeared due to colloidal silver health fraud

- Blue skin

A

Argyria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

-Eosinophilic intranuclear inclusion made of lead complexed with nuclear proteins

A

Lead poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q
  • On polarized light, it looks like hot cross buns (“maltese crosses”)
  • Uremic frost
A

Kidney failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q
  • Carbon enters our body as smoke, soot, or pigment (tattoo)
  • Tattoos: macrophages with carbon
  • Carbon in the tissues such as lung and LN is called what?
A

anthracosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q
  • Brown “wear and tear” pigment… but babies already have plenty in their little heart cells.
  • Strained myocardium has more and it regresses over time on healing.
A

Lipofuscin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q
  • Macrophages of colon are black

- Caused by cascara laxatives, eating rhubarb, or any mass-apoptosis of colon cells

A

Melanosis coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the two types of melanin in mammals?

A

Eumelanin (black)-most common

Pheomelanin (red)-red heads

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q
  • no melanin produced
  • Eye problems make it a “real disease.”
  • Melanin in the choroid is required for normal growth of the fovea.
A

True albinism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is mutated in rufous albinism

  • Binds melanocyte-stimulating hormone for pigment
  • Red hair
A

Mutant MC1R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

TQ

  • Leftover phenylalanine is usually hydroxylated into tyrosine. If this doesn’t happen, the extra phenylalanine becomes phenylketones, which are neurotoxins.
  • Tx: diet low in phenylalanine.
  • Microcephaly from the profound brain damage.
  • Patients tend to be blond(e) since there’s little tyrosine to make into melanin polymer

Lack of what enzyme is responsible?

A

Lack of phenylalanine hydroxylase

Phenylketonuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Mutated kit leads to a distinctive pattern of skin or hair where there is a white patch on the head and stomach. What is this called?

A

piebaldism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

When do you see hemosiderin?

A
  • Hemosiderin-laden macrophages in lung (“heart failure cells”)
  • Areas of repeated injury and bleeding
  • Brain macrophages after encephalitis
  • Scars when high body iron
  • Skin when capillaries break frequently because of venous stasis or frequent irritation / rubbing
  • Asbestos in lung (“ferruginous bodies”)
  • Ringed sideroblasts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q
  • Iron in small bile ducts

- Prussian blue stain

A

Hemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q
  • Copper deposits in liver or basal ganglia
  • Kayser-Fleischer rings
  • Rhodanine stain
A

Wilsons dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q
  • Blackens the thyroid first, then elsewhere

- Teeth also blackened

A

Long-term minocycline use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q
  • Results from lack of homogentisate oxidase, which breaks the aromatic ring of tyrosine
  • Homogentisic acid accumulates
  • Fragile cartilage
  • Low back pain
  • Urine turns black if left exposed to open air.
  • “ochronosis” blackening of the cartilages (ear)
A

Alkaptonuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

TQ
In malaria, the plasmodium protect themselves from free iron-heme complex by converting it into _______, which accumulates as cytoplasmic granules
-Looks like hemosiderin but no prussian blue rxn
-Kupffer cells

A

hemozoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

TQ:

  • __________: All indirect (unconjugated) bilirubin
  • Biliary obstruction: All direct (conjugated) bilirubin at first
  • Hepatocellular disease: Plenty of both
A

Hemolysis

may see bile plugs in obstructive jaundice or primary cancer of hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

-Something calcifies because it is already abnormal.

Ex:

  • Uterine fibroid, scar, aortic valve, atherosclerosis
  • Psammoma bodies: tumors BM
  • Schaumann bodies, Langhans giant cells
  • Monckeberg’s: media of large arteries
A

Dystrophic calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

-Something calcifies because the serum calcium and/or serum phosphate is too high.
-The lungs and kidneys are most likely to be seriously involved (calcify)
Ex:
-Parathyroid hyperfunction (Ca)
-Kidney failure (P)

A

Metastatic calcification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Any mass composed of a single protein will look “hyaline” – it’s an adjective.

A

hyaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Hyaline

  • Eosinophilic droplets in proximal tubular epithelial cells
  • Protein resorption in renal tubular lysosomes in a patient with what?
A

heavy glomerular proteinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Hyaline

  • Round accumulations of monoclonal protein (IgG) that are inside the ER, usually Ig in plasma cells
  • Grape/mott cells
A

Russel bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q
  • Hyaline globule
  • Remnant of apoptotic cells found at sites of ongoing apoptosis
  • Also seen in tumors that have forgotten how to remove apoptotic fragments
A

Thanatosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Viral inclusions, such as in CMV and herpes are made of what?

A

hyaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

-The usual problem is that a1-antitrypsin can be made but not exported from the rough endoplasmic reticulum of the liver -Liver damage from the deposits, and/or pulmonary emphysema in non-smokers (from lack of elastase inhibition) results

What do you see and stain with?

A

Antitrypsin hyaline globules (gumballs) stained with PAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q
  • Scrambled keratin-ubiquitin typically in liver cells
  • Aggresomes
  • Pink cottage cheese
A

Mallory’s alcoholic hyaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are yokoo bodies?

A

giant mitochondria due to drinking (hyaline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Collagen can be hyalinized in scars and other abnormal proliferations. What are these called?

A

Keloid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Thick BM in glomeruli (hyaline)

A

Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Amyloid is _-pleated anything. What stain do we use?

A

B (beta)

  • Congo red
  • apple green when polarized
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Fibrinoid is seen in the walls of blood vessels that are dead but still have flowing blood. What does this result from?

A
  • Type III immune injury
  • High physical pressure (malignant HTN)
  • Radiation
  • Pregnancy or Infx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Greatly increased ground substance is called what? What is it seen in?

A

Myxoid change

  • hypothryoidism
  • colloid cancers–>large mucin lake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Swollen mitochondria

A

Reye’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q
  • Caused by lack of a protein that mobilizes iron from in & around mitochondria, which then sustain free-radical damage.
  • Progressive dz
  • Cerebellum affected, dilated cardiomyopathy, high arched feet

What is the gene?

A

Gene=FXN: Frataxin

Friedreich’s ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Parking lot crystals and ragged red fibers=?

A

mitochondrial myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What cells are packed with mitochondria?

A

Hurthle cell & oncocyte tumor cells, and apocrine sweat glands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

TQ

Giant mitochondria in an alcoholic’s liver

A

Yokoo bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

A ______ is a mutated clone of melanocytes which lost their way

A ______ is a mutated clone of melanocytes which over produces melanin. No changes in the dermis

A

nevus

freckle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q
  • Extra pigment production under eyes/cheeks; no one knows why. -
  • See “raccoon eyes” appearance, and is known as the “mask of pregnancy,” because it is sometimes seen in pregnant patients that are taking oral contraceptives.
A

Melasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q
  • Extra pigment & elongated rete pegs.
  • Your stable “moles”
  • As you grow older, you may see a set on your back and upper shoulder.
  • Another variant is the familiar large, single one on an older person’s face.
A

Lentigo

solar lentigo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

-melanotic macules

A

Café au lait spots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Dx?

  • melanotic macules are giant melanosomes. They are called “Coast of California café au lait spots.”
  • Also see armpit freckles.
A

Neurofibromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Nevi genetics:

-Acquired mutations in what leads to a nevi?

A

NRAS or BRAF downstream of RAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q 
TQ
Which nevi?
-small, relatively flat lesions
-symmetric and uniform
-Nests of odd melanocytes at the dermal-epidermal junction (@ ridges)
A

Junctional nevus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q 
TQ
Which nevi?
-Symmetric and well circumscribed 
-Regular arrangement of nests
-Both junctional and intraepidermal components
A

Compound nevus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

TQ
Which nevi?
-The nervus cells are primarily in the dermis and don’t reach the junction.
-The odd melanocytes stay a short distance from the epidermis

A

Intradermal nevus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

TQ
Which nevi?
-present at birth but may not pigment until later
-malignant melanomas may arise
-Cells are deep in the dermis and may involve hair!
-occur on a dermatome, so no matter how much you excise it, it will grow back. Something in the spinal nerves causes this change. One example is the “Faun’s tail.”

A

Congenital nevus

Ex: Hairy congenital nevus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

TQ
Which nevi?
-Flat, blue, or blue-gray skin markings near the buttocks that commonly appear at birth or shortly thereafter.
-They typically fade by the age of 5.
-DON’T call it “child abuse that was so severe that the bruise never went away!!”
-histo: dendritic melanocytes deep in dermis

A

Mongolian Spot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

TQ
Which nevi?
-Black-blue nodule
-The odd, spindle-shaped melanocytes are deep in the dermis and resemble dendrites
-Use a Melan-A stain: the deep dermis is what gives it a blue appearance.

A

Blue nevus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

TQ
Which nevi?
-Reddish-pink, brown red
-Nasty looking cells that mature as they go deeper→nests of cells that look like rain
-Epitheliod-and-spindle cell nevi seen in kids
-May be compound and may see kamino bodies at dermoepidermal jx
-Often on the face
-Looks like malignant melanoma
-Must biopsy

A

Spitz nevus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

TQ
Which nevi?
-melanocytic nevi that are under attack by the immune system
-Local depigmented area around the nevus.

A

Halo nervus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

TQ
Which nevi?
-A dark blue-brown birthmark that sometimes appears on the eye
-Due to dendritic melanocytes in the dermis
-Asians, forehead, temple, cheeks, and nose

A

Ota’s nervus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q 
TQ
Which nevi?
-Super-androgen-sensitive
-A big, dark, extra-hairy patch that usually appears on a man’s upper back or shoulder at puberty. 
-Extra arrector pili muscles=firm area
A

Becker’s nevus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

TQ
Which nevi?
-These are “premalignant moles”
-Can often see fused rete pegs, large nests, and layered fibrosis in the upper dermis near the lesion
-Loss of fx in CDKN2A gene for melanoma
-Notch-1 positive when stained.
-Typically >5mm across, flat or slightly raised, multicolored and irregular borders
-Can occur on sun exposed and non-sun exposed skin

A

Dysplastic nevi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q
  • Lentigo composed of malignant melanocytes on sun damaged skin but without invasive features
  • Bump formation with fine dusty melanocytes (bizarre), and epidermal atrophy
  • It looks like a normal lentigo, but there are ugly cells (Anaplastic cells at dermal-epidermal junction). -Use a Melan-A stain (stains nasty melanocytes brown)
A

Lentigo maligna

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q
  • Due to sun exposure or autosomal dominant inherited defect
  • UV damage–>mut of CDKN2A cell cycle control genes–>incr melanocyte prolif
  • Incr RAS, PI3K/AKT signaling for growth and survival
  • Preservation of telomeres–>uncrontrolled growth (TERT gene)
A

Melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q
  • Big nucleoli are usual—stain with S100 or HMB-45 (and then it does NOT light up with keratin stain)
  • Mitotic figures, fine dusty appearance, fibrosis, regression
  • The “vertical growth phase”: begin to invade deeper..assoc with a nodule
  • Look for irregular borders and variegated pigmentation
  • Rapid growth and bleeding are signs
  • Satellite lesions (little black patches just beyond the main lesion, are extremely suggestive of this→ if seen microscopically, more likely to be aggressive

How do we measure the clinical outcome of this dz?

A

Melanoma outcome measured by Breslow thickness (histo)

Breslow depth corresponds to clarks levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q
  • occurs on the palm/sole, mouth, or black-white junction of a darkly-pigmented person’s hands and feet (non hair-bearing places)
  • Common in black folks especially in the tropics
  • Often involves fingernail!!
  • atypical melanocytes assoc with desmoplasia (scarring) and dermal invasion
A

Acral-lentiginous Melanoma

“Bob Marley’s cancer”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q
  • malignant cells dont make melanin
  • skin may be pink, purple, red, normal
  • asymmetrical and irregular with a faint border
  • very poor prognosis
A

Amelanotic melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

TQ

  • a congenital hamartoma usually on the hairline on the temple
  • often present at birth
  • **epidermal hyperplasia with incr sebaceus glands and hair follices
  • Assoc with neurocutaneous syndrome
  • Looks like a patch of flies eggs.
A

Nevus sebaceus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q
  • See benign basal-type cells (benign pearls) and horn cysts.
  • These keratosis often contain clear cells and pigment that are foolers for melanoma, however all the cells are keratinized
  • The lesions are pigmented, usually are crusty, and can be scraped off with a butter knife.
  • P63 stain will show uniform nuclei
  • S100 stain is negative
A

Seborrheic keratosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

“The sign of Leser-Trelat” is a sudden eruption of seborrheic keratoses. Why is this impt?

A

This is a warning of internal malignancy (probably colon cancer or other malignancy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q
  • multiple black facial spots seen on many people of African ancestry
  • histo looks like seborrheic keratosis
A

Dermatosis papulosa nigra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q
  • seborrheic-style hyperplasia covering each armput and/or the groin.
  • Warning of internal adenocarcinoma and / or syndrome insulin resistance OR a result of nicotinamide administration
A

Acanthosis nigricans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q
  • mysterious little bumps of soft tissue covered with epidermis.
  • Just tie them off at the base with a thread. Favorite spot is the neck
A

Fibroepithelial polyps / skin tags / achrocordons

107
Q
  • hemangiomas with an overlying hyperkeratotic epidermis

- If you see these all over…think Fabry’s.

A

Angiokeratomas

108
Q
  • Spheres of epithelium turned inside-out
  • Skin products (sebum, keratin) accumulate and cause the mass to grow.
  • You DO NOT want to puncture these→ they are full of debris
A

Epithelial (inclusion) cysts / wens

109
Q
  • Seen in Gardner’s syndrome
  • These inclusions are the least of someone’s worry though—send them in for a colonoscopy! The cysts are covered in stratified squamous epithelium, and have keratin on the inside.
A

Multiple epidermoid inclusions

110
Q

-a true “sebaceous cyst”

A

Pilar / tricholemmal cyst

111
Q
  • little epidermoid inclusion cysts that are usually multiple—appear in groups.
  • Usually around eyes or behind ears.
A

Milia

112
Q
  • A hideous looking, volcano-shaped lesion that is likely to vanish as suddenly as it appears
  • Often seen in sun damaged skin, unbilicated lesion filled with keratin
  • Looks like SCC
  • Well differentiated glassy cells
A

Keratoacanthoma

113
Q
  • Also called “turban turmor”
  • They are all over one’s head
  • Benign adnexal tumor with nest of cells surrounded by collagen like eosinophilic material, hyperchromatic nuclei, and lymphocytes are DECREASED
  • This is an anti-oncogene deletion syndrome
A

Eccrine cylindoma

114
Q
  • the cell of origin is the eccrine sweat gland
  • yellow bumps on eyelids, vulvua, armpits, etc
  • tadpole morphology to the cells embedded in a fibrous stroma with numerous small ducts
A

Syringomas

115
Q
  • a benign tumor that makes little hair follicles
  • See little bumps all over face esp in nasal folds, upper lip, nose, and forehead
  • Horn cysts surrounded by basophilic cells, which form islands in the stroma
A

Trichoepitheliomas

116
Q
  • see “ghost cells”=cells leaving cytoplasm behind
  • calcifying epithelioma of malherbe, usually on face and upper extrem.
  • Firm blue-red nodule
  • Multinucleated giant cells, basaloid cells surrounding ghost cells
A

Pilomatrixoma

117
Q

TQ

  • This is squamous cell carcinoma in situ (premalignant)
  • It occasionally turns to real SCC.
  • Sometimes see “Skin horns” when keratin is not shed
  • Sun damages areas with bands of parakeratosis and orthokeratosis with atypia
A

Actinic keratosis

118
Q
  • type of squamous carcinoma in situ but intraepidermal→very anaplastic
  • Appears as red plaque on sun-exposed skin, oral mucosa, or genital skin.
  • On the penis, it’s called erythropasia of queyrat (erythematous plaque)
  • Arsenic exposure is a risk factor, so is viral infx
  • Does not penetrate basement membrane
A

Bowen’s dz

119
Q
  • This is an intra-epithelial adenocarcinoma.
  • Mammary and extramammary paget’s
  • Slow noninvasive
  • often on vulva or penis
A

Paget’s disease of the skin

FYI Histo: mucin seen and then when stained with keratin 7, you see “Christmas tree” pattern

120
Q

-Old radiation dermatitis is a breeding ground for what type of cancer?

A

squamous!

121
Q
  • cancer of small, cuboidal-like cells.
  • Grossly you will see the familiar central ulcer (rodent ulcer) and a pearly border, and it is vascular
  • Well demarcated edges with pink to red borders and monochromic pigment
A

Basal cell carcinoma

  • On histology, look for the “picket-fence” edges.
  • Rule: most skin CAs on or above the lower eyelid are basal cell carcinomas. Most skin tumors below the lower eyelid are squamous cell carcinomas
122
Q

TQ

  • autosomal dominant that can cause unusual facial appearances and predis for basal cell
  • PTCH gene chr 9 mut
  • announces itself as jaw cysts
  • rib and vertebrae abnormalities
  • can treat with Vismodegib to regress.
A

Gorlin’s basal cell nevus syndrome

123
Q

“oat cell of the skin”

A

Merkel cell carcinoma

124
Q
  • Tumor of macrophages and fibroblasts.
  • Cells are usually spindle shaped
  • Edges are sharply circumscribed and does extend to top of dermis.
  • It doesn’t quite connect to the epidermis. If you pinch it, the overlying skin will dimple. These usually follow a minor, injury or bug bite.
A

Dermatofibroma

125
Q
  • dermatofibroma variant seen on sun exposed skin (tops of ears is favorite site)
  • also in radiation and younger pts
  • solitary or multiple red juicy lesions often dome shaped, ulcerated, or crusted
  • mitotic figures, hypercellular
A

Atypical fibroxanthoma

126
Q
  • These are cholesterol-rich macrophage clusters that appear around the eyes.
  • These occur when LDL is elevated.
  • You see “foam cells” on histology
A

Xanthelesma (xanthomas)

127
Q
  • Round nodules that pop up especially on the heads and trunks of babies.
  • See flower giant cells wih infiltrate
  • stains vimentin CD68, HAM56, Factor IIIa
A

Juvenile xanthogranuloma

128
Q
  • These occur at birth and soon after
  • Self-limited tumor of endothelial cells that line blood vessels
  • See thrombosis and scarring of the little vessels that cause the lesion to fade and contract
  • May ulcerate or bleed
A

Hemangiomas

129
Q

_____ hemangiomas: these start popping up in some adults around the age of 20.

A

Cherry

130
Q
  • Chunk of granulation tissue that never heals itself
  • Red cells get lost in the spindles
  • Form of lobular capillary and is usually lobulated or smooth, can be red, pink, or purple
A

Pyogenic granuloma

even though not pyogenic or granuloma

131
Q
  • It’s a pseudotumor caused by Herpes 8.
  • It makes vessels proliferate.
  • In the lung / guts, it’s deadly anyway.
A

Kaposi’s sarcoma

132
Q

Cutaneous lymphoma is of which origin?

-Biopsy to confirm

A

Most are of T-cell origin

133
Q

Mycosis fungoides: A type of T-cell lymphoma

  • See T-cells with convoluted nuclei=sezary cell
  • See _____ ________=masses of sezary cells inside epidermis
A

pautrier microabscesses

FYI
It is not an easy diagnosis. The CD3 pan-T-ell stain makes it much easier to diagnose (stains T cells black)

134
Q
  • Generalized hyperplasia of mast cells. There are 5 subtypes.
  • One type is urticarial pigmentosum

What is extremely impt?!

A

It is important to “not rub the spot on the baby’s head,” because the baby can go into shock!

135
Q

Patient gets the flu and a rash—maybe petechial

  • Usually in the winter and spring, children and teens get this
  • There may or may not be N/V and signs of meningitis
  • The rash is petechial and evolves to palpable purpura with central necrosis. It only takes a few hours for DIC to set in.
A

Meningococcemia

136
Q

The patient gets the flu and a rash after going to the woods

  • Rash begins on day 4 and usually begins on wrists and ankles and spreads centripetally
  • Treat with doxycycline
A

Rocky Mountain Spotted Fever

137
Q

Person complaining of pain out of proportion to findings

  • There are likely to be systemic symptoms (malaise, fever, diarrhea)
  • If you don’t treat with the appropriate antibiotic, your patient will have massive necrosis of the involved area, and then death.
A

Necrotizing fasciitis

138
Q

Patient gets the flu and a sunburn

  • Look for red eyes and a “strawberry tongue”
  • The staph may be hiding in a tampon, a nasal pack, a surgical dressing, or just a skin boil
A

Staph toxic shock

139
Q

It’s just a trivial strep infection

  • The patient may have a cellulitis, strep throat, or deep strep infection
  • There may be a generalized red rash
  • Call a surgeon and begin antibiotics immediately
A

Strep toxic shock

140
Q

A macular / popular generalized rash, that normally appears on the palms and soles.

A

Syphilis

141
Q

A patient complains of a mild rash and is taking a common medication

A

Toxic epidermal necrolysis and/or Stevens-Johnson

142
Q

A patient you know is already seriously sick, and you see multiple necrotizing skin lesions that are caused by pseudomonas sepsis.

A

Ecthyma gangrenosum

143
Q

Tiny blisters in the epidermis where swet got trapped in a sweat duct outlet. “Prickly heat.”

A

Miliaria

144
Q

Increased filaggrin production (“keratohyaline granules”) result in a thicker, more durable outer keratin layer

A

Skin callus

145
Q

Physical shearing force has detached the epidermis from its basement membrane

A

Friction blister

146
Q
  • The male keratin is thick, and men sweat a lot
  • The water denatures the keratin
  • The denatured keratin and dirt plug the sweat gland ducts
  • Fungi like it there
A

Jock itch

147
Q

A group of genetic dz’s with very abnormal skin plus some other ectodermal structures (e.g., teeth)

A

Ectodermal dysplasia

148
Q
  • Results from microbleeds in legs where the blood has trouble returning to the heart.
  • Iron pigmentation, swelling and scarring can occur.
A

Stasis dermatitis

149
Q
  • Cells that recognize themselves to be radiation-damaged undergo apoptosis
  • Apoptosis of endothelial cells causes vasodilation and “delayed-prolonged leakage”
  • This causes the peeling or “desquamation”
A

Sunburn

150
Q
  • See “blue” fibers in high dermis
  • This occurs in skin exposed to heavy sunlight for long periods of time
  • Upper layer of the dermis exhibits a poorly-understood change in its fibers and ground-substance
  • Pale basophilic material that stains like elastin is deposited
  • Rhomboid-shaped wrinkles on back on neck
A

Solar elastosis

151
Q
  • Cells of the keratin layer stay attached
  • “Alligator-like” pattern of scales mostly on the extremities.
  • Desmosomes stay intact longer than they should, delaying the shedding of the dead epidermal cells
  • Defective synthesis of filaggrin (autosomal dominant)
A

Common ichthyosis

152
Q
  • A mix of genetic diseases
  • Defective K1 or K10 keratins
  • Defective transglutaminase.
  • “Gator kids”
  • Autosomal recessive
A

Lamellar ichthyosis

153
Q
  • Autoimmunity attacks the melanocytes
  • Genetic forms tends also to produce autoimmune adrenal insufficiency and/or immune gastritis
  • Most cases are idiopathic
  • Check all these pts for hidden melanoma
A

Vitiligo

154
Q
  • Mutated kit tyrosine kinase

- White streak of hair extending down the middle of forehead

A

Piebaldism

155
Q

A patch of always-light hair

A

Poliosis

156
Q
  • Common especially in older folks
  • Minor, harmless mystery of medicine
  • “Rain drops”
A

Guttate hypomelanosis

157
Q

The familiar wheal (dermal edema) and flare -(dilated vessels)
-Result of mast cells degranulating in the skin

A

Urticaria

158
Q
  • Acute injury to the epidermis, with edema and loss

- Red, oozy, crusty, flat/vesicular

A

Eczema (“atopic dermatitis”)

159
Q

“Spongiosis” (in eczema) is:

A

Edema and separation of skin cells

160
Q

Lichenified skin…

A

Chronic dermatitis

161
Q
  • Thickened (“acanthotic”) spiny layer
  • Elongated rete pegs
  • Abundant keratohyaline granules (“hypergranulosis”) accompanying extra keratin
A

Lichen simplex chronicus

162
Q

Allergy, direct physical/chemical damage, or often a mix…

A

Contact dermatitis
(Type IV hypersensitivity)

e.g., nickel, poison ivy, neomycin

163
Q

4 stages of poison ivy:

A

1) Contact
2) Cell Swelling: Damaged cells become more permeable to sodium, causing them to fill with water
3) Cell Death: The lesions turn red because the little arteries in the dermis dilate, a non-specific response to local injury
4) Cell Dissolution

164
Q
  • Secondary infection of an area of contact dermatitis
  • Honey-crusts
  • S aureus or S pyogenes
A

Impetigo

165
Q
  • Often produces a palpable purpura
  • It’s a drug eruption until proved otherwise
  • Under microscope: dead/dying neuts around the blood vessels of the skin (“leukocytoclastic vasculitis”)
A

Vasculitis

166
Q

TQ

  • CD8+ T-killer cells attack the epidermis
  • “Target” lesions (CD8’s in center, CD4’s at the edge)
  • Assoc with infections, drugs, cancers, autoimmune dz
A

Erythema multiforme

167
Q

TQ

  • Characterized by fever, bulla formation and necrosis, sloughing of skin, and a high mortality rate
  • Typically 2 mucous membranes are involved (e.g., lips and eyes)
  • Skin lesions may appear as targets as seen in erythema multiforme
  • Usually assoc with adverse drug rxn
A

Stevens-Johnson syndrome

168
Q

TQ

  • A more severe form of Stevens-Johnson syndrome with > 30% of the body surface area involved
  • T-cells are NOT involved
A

Toxic epidermal necrolysis

169
Q

TQ

  • Painful inflammatory lesions of subcutaneous fat, usually on anterior shins
  • Often idiopathic, but can be assoc with sarcoidosis, coccidioides (famous), histoplasmosis, TB, strep, leprosy, and Crohn dz
A

Erythema nodosum

170
Q
  • Common in Hawaii
  • Granuloma around dead collagen with a mix of mucin
  • Goes away in a few years
A

Granuloma annulare

171
Q
  • Uncommon but devastating inflammatory disorder
  • Neuts fill base of the lesion – a growing ulcer with purply, undermined edges
  • Many pts have ulcerative colitis
  • Neuts in the dermis
  • Rx: dapsone (slows neuts)
A

Pyoderma gangrenosum

172
Q

TQ

  • Papules and plaques with silvery scaling, especially on knees and elbows
  • Acanthosis with parakeratotic scaling (nuclei still in stratum corneum
  • Thick stratum spinosum, thin stratum granulosum
  • Kogoj spongiform pustules (spiny layer)
  • Munro microabscesses (scale)
  • Auspitz sign – pinpoint bleeds (exposure of dermal papillae) when scales scraped off
  • Assoc with nail pitting and arthritis
  • Link to HLA-Cw*0602
  • CD4, CD8, CD1 cells
A

Psoriasis

173
Q

TQ

  • Pruritic, purple, polygonal planar papules and plaques (“6 P’s”)
  • CD8 T-cells at the dermal-epidermal interface (basal cells)
  • Sawtooth appearance
  • Assoc with hepatitis C
A

Lichen planus

174
Q
  • Flaky and depigmented lesions
  • Keratin plugs (hyperkeratosis)
  • Basal cell hydropic vacuoles
  • Granules of immunoglobulin and complement at the dermal-epidermal junction
A

Discoid lupus

175
Q
  • Sebaceous glands undergo hyperplasia in response to androgens when puberty hits
  • Keratin plugs follicles
  • Propionibacteria in buried plugs generate free fatty acids&raquo_space; attracts neuts&raquo_space; dissolve the area, leaving pus
A

Acne vulgaris

176
Q

The one undeniable effect of dioxin / “Agent Orange”:

A

Chloracne

177
Q
  • Central face (cheeks)
  • Flushing, then…
  • Persistent erythema / telangiectasias, then…
  • Pustules and papules, then…
  • Rhinophyma
A

Rosacea

178
Q
  • Marked hypertrophy and hyperplasia of the sebaceous glands of the nose, with fibrosis and deformity
  • Believed to be a result of rosacea
  • Exacerbated by alcohol
A

Rhinophyma

179
Q
  • Very common, trivial

- Pregnant women and babies may have it appear suddenly

A

Sebaceous hyperplasia

180
Q

Antigens seen in pemphigus:

A

Desmoglein

181
Q

Antigens seen in paraneoplastic pemphigus:

A

Desmoplakin

182
Q

Antigens seen in bullous pemphigoid:

A

BPAG2 / Collagen XVII

183
Q

Antigens seen in dermatitis herpetiformis:

A

Anchor filaments / reticulin

184
Q
  • Potentially fatal autoimmune skin disorder with IgG against desmoglein (component of desmosomes) – “tombstone layer”
  • Flaccid intraepidermal bullae caused by acantholysis; oral mucosa also involved
  • Immunofluorescence: Abs around epidermal cells in a reticular (net-like) pattern
  • Nikolsky sign (separation of epidermis upon manual stroking of skin)
A

Pemphigus vulgaris

185
Q
  • Major problem in the warmer areas of Latin America

- Molecular mimicry from sandfly salive

A

Pemphigus foliaceus

186
Q
  • Results from mutant ATP2C1, a Ca2+ channel
  • Groin most involved
  • Fragile desmosomes, not autoimmunity
A

Benign familial pemphigus

“Hailey-Hailey dz”

187
Q
  • Less severe than pemphigus vulgaris
  • IgG against hemidesmosomes (epidermal basement membrane; Abs are “bullow” to epidermis)
  • Tense blisters containing eosinophils affect skin but spare oral mucosa
  • Immunofluorescence: Linear pattern at epidermal-dermal junction
A

Bullous pemphigoid

188
Q
  • Little blisters form on the palms and soles in hot weather… develop into sore cracks
  • Topical glucocorticoids
  • Low-zinc diet supposed to be effective
A

Pompholyx

“Dyshidrotic eczema”

189
Q
  • Pruritic papules, vesicles, and bullae (often found on elbows)
  • Deposits of IgA and eosinophils at the tips of dermal papillae
  • Assoc with celiac dz (gluten-free helps!)
A

Dermatitis herpetiformis

190
Q

TQ

  • Non-Ab-mediated detachment of the basal layer
  • “Simplex” – keratin 14 or keratin 5 in the basal layer
  • “Junctional” – BPAG2 / collagen XVII of the basement membrane
  • Acquired form – Type VII collagen of the basement membrane
  • Similar to bullous pemphigoid, but there are NO Abs against the dermal-epidermal junction
A

Epidermolysis bollusa

191
Q
  • Viruses take over a patch of skin for their own purposes
  • HPV family is responsible
  • Huge poxvirus inclusions, NOT giant cells
A

Molluscum

“Dimple warts”

192
Q

TQ

  • “Herald patch” (on arm) followed days later by “Christmas tree” distribution
  • Multiple plaques with collarette scale
  • Self-resolving in 6-8 weeks
A

Pityriasis rosea

193
Q

TQ

  • Very superficial skin infection
  • Usually from S aureus or S pyogenes
  • Highly contagious
  • Honey-colored crusting (neuts beneath stratum corneum)
A

Impetigo

194
Q

-Caused by exfoliative toxins (results in bullae) produced by staph in the area of the infection

A

Bullous impetigo

195
Q

5 subcorneal blistering diseases:

A
  • Staph scalded skin
  • Miliaria
  • Bullous impetigo
  • Pemphigus foliaceus
  • Some epidermolysis bullosa
196
Q

3 suprabasal blistering diseases:

A
  • Pemphigus vulgaris
  • Bullous eczema
  • Some epidermolysis bullosa
197
Q

6 subepidermal blistering diseases:

A
  • Bullous pemphigoid
  • Dermatitis herpetiformis
  • Erythema multiforme
  • Friction blisters
  • Toxic epidermal necrolysis
  • Some epidermolysis bullosa
198
Q
  • Exfoliative toxins travel by bloodstream and produce subcorneal (only in stratum granulosum) blisters which can involve much of the body
  • Seen in newborns and children
A

Staphylococcal scalded skin syndrome

199
Q
  • Presents as obvious systemic illness
  • Initially, skin change suggests sunburn
  • Later, skin may desquamate on palms and soles
A

Toxic shock syndrome

200
Q
  • Deeper tissue injury, usually from anaerobic bacteria or S pyogenes
  • Results in crepitus from methane and CO2 production
  • “Flesh-eating bacteria”
  • Causes bullae and a purple color to the skin
A

Necrotizing fasciitis

201
Q
  • Pitted keratolysis on bottom of toes and soles
  • Horribly smelling

What bacterium is responsible?

A

Corynebacterium

202
Q
  • Neuts rampaging in dermis +/– epidermis, not chasing bacteria
  • Think of some underlying leukemia / preleukemia
A

Sweet’s syndrome

203
Q
  • Mysterious process involving follicular plugging, altered immunity, and formation of nodules that often become necrotic, usually where there are apocrine glands
  • Abundant neuts and debris among and within the adnexal structures
A

Hidradenitis suppurativa

204
Q
  • Flat, greasy, pigmented squamous epithelial proliferation with keratin-filled cysts (horn cysts)
  • Looks “stuck on”
  • Lesions occur on head, trunk, and extremities
  • Common benign neoplasm of older persons
  • Leser-Trelat sign – sudden appearance of multiple seborrheic keratoses, indicating an underlying malignancy (e.g., GI, lymphoid)
A

Seborrheic keratoses

205
Q
  • Greasy scales and redness occur, with exacerbations and remissions
  • On areas rich in sebaceous glands
  • Mild form = common dandruff
  • Infant form = “cradle cap”
  • Tends to flare in people with Parkinson’s
  • On biopsy, see hyperkeratosis and maybe neuts / spongiosis / fungal elements
A

Seborrheic dermatitis

206
Q

Offending agent of “jock itch” / “crotch rot”:

A

Trichophyton rubrum

207
Q
  • Brown, scaly lesions, usually in the groin

- Corynebacterium responsible

A

Erythrasma

208
Q
  • Fungi in the dead keratin layer
  • Pruritic lesions with central clearing resembling a ring
  • Caused by dermatophytes
A

Ringworm

209
Q

TQ

  • Caused by Malassezia furfur
  • Degradation of lipids produces acids that damage melanocytes and cause hypopigmented and/or hyperpigmented patches
  • Occurs in hot, humid weather
  • “Spaghetti and meatball” fungus in dead keratin
A

Tinea versicolor

210
Q
  • Fungal infection seen in Polynesia

- Thick, fungus-rich keratin

A

Tinea imbricata

211
Q
  • Tiny worms block lymphatic vessels

- Leads to elephantiasis

A

Filariasis

212
Q
  • Causes “mange” in dogs

- “Usual suspect” in rosacea

A

Demodex (mite species)

213
Q

Auto-Abs directed against hair follices

A

Alopecia areata

214
Q
  • A group of hairs all go on the same cycle and are lost at the same time
  • Usually “from stress”
A

Telogen effluvium

215
Q
  • “Slapped cheeks” rash in children
  • Erythema infectiosum (“Fifth disease”)
  • Aplastic crises in sickle cell disease

What virus is responsible?

A

Parvo B19

216
Q
  • Small, painless ulcers on genitals&raquo_space;
  • Swollen, painful inguinal lymph nodes that ulcerate (“buboes”)
  • Rx: doxycycline
A

Lymphogranuloma venereum

Chlamydia trachomatis

217
Q

Palms and soles? Think…

A
  • Secondary syphilis
  • Kawasaki
  • Meningococcemia
  • Reactive arthritis
  • Rocky mountain spotted fever
218
Q

What is an easy office test for herpes 1, 2, and 3?

A

Tzanck test

219
Q
  • Necrosis and acantholysis in the epidermis produces the blisters
  • Nuclear inclusions

Which herpes subtype?

A

Herpes 3 (zoster)

220
Q

What would you see on a Tzanck test?

A

Giant cells with one inclusion in each nucleus

221
Q

Lost pigment and lost sensation…

A

Leprosy

222
Q
  • Prick from a rose / bayberry thorn

- Short “cigar stub” fungi

A

Sporotrichosis

223
Q
  • Excessive fibrosis and collagen deposition throughout body
  • Manifests as puffy and taut skin with absence of wrinkles
  • Thin epidermis, dense dermis, flat pegs, lost hairs
  • 2 major types: Diffuse and Limited (CREST syndrome)
  • Calcinosis
  • Sclerodactyly
A

Scleroderma

224
Q

Keloid… What type of collagen?

A

Type I collagen fibers

225
Q
  • Proliferative disorders of dendritic (Langerhans) cells from monocyte lineage
  • Presents in child as lytic lesions and skin rash or as recurrent otitis media with a mass involving the mastoid bone
  • Cells are functionally immature and do not stimulate primary T-cells via antigen presentation
  • S-100 and CD1a
  • Characteristic Birbeck granules (“tennis rackets”) on EM
A

Langerhans cell histiocytosis

226
Q
  • AD inherited disorder of blood vessel
  • Telangiectasia (lips), recurrent epistaxis, skin discolorations, AV malformations, GI bleeding, hematuria

Also known as:

A

Osler-Weber-Rendu syndrome

“Hereditary hemorrhagic telangiectasia”

227
Q
  • A mass of granulation tissue that does not regress

- “Rotten cherry”

A

Pyogenic granuloma

228
Q

Bone and vessel overgrowth…

A

Klippel-Trenaunay

229
Q
  • Malignant tumor of endothelial origin

- Assoc with exposure to arsenic, vinyl chloride

A

Angiosarcoma

230
Q

All of the following are deaths that the ________ _________ will see:
-No physician willing to complete the death certificate
-Any death not from disease
-Any death in which homicide, suicide, or accident might be the
manner, even if the final means of exit was disease
-Any death with possible public health implications
(i.e., suspected index case in a poison or disease outbreak)
-Any death of someone in apparent good health
-Any death in police custody, jail, prison, detox, halfway house
-Anyone dying under age 18
-Any death from occupational disease (this gets ignored a lot)
-Any death during surgery
-Any death thought to be due perhaps to illegal drugs
-Any death that’s “suspicious or unusual”
-Any death from a therapeutic misadventure (relatively few lately)
-Any death within the first 24 hours after hospital admission
-Anybody dying with a bullet inside (the last isn’t always law)

A

medical examiner

231
Q

You have been appointed medical examiner. Take the CORE temperature when the body is found, so we can get a better estimate of the actual time of death. Maggots help too. Whats the best way to ID the patient?

A

DNA

Tattoo!

232
Q

TQ
-__________: An act by another set in motion the events leading to death. Justifiable (“I had to kill him”) and negligent (“What I was doing was very stupid but I didn’t mean to hurt anyone”) are included.

__________: A person’s intent, more or less, to end life set in motion the events leading to death.

_________: Disease. Your MOST COMMON cause of sudden death will be coronary disease without MI.

________: Mishap. Unfortunate incident that was unexpected and unintended. No need to belabor the paradoxes. Ex: Car accidents

_________: Can’t or don’t want to say.

A

Homicide

Suicide

Natural

Accident

Undetermined

233
Q

What is the manner of death?
-Fatal HIV injection from blood administered for wound

-Penicillin shot–>analphylaxis–>die

A

homocide

234
Q

T/F: The death certificate contains mode of death and mechanism of death.

A

FALSE
only contains the cause of death

Mode of death: Stuff like shock, coma, pulmonary edema, cardiac rhythm disturbance, pneumonia.

Mechanism of death: Stuff like right-to-left shunt,
poor perfusion of the conduction system.

235
Q

TQ
“Chemical asphyxiants” include cyanide and carbon monoxide, which bind to cytochrome oxidase, hemoglobin, and myoglobin. What are some clues a patient may be poisoned by each?

A

cyanide: smell almonds or the cherry-red lividity (pink)

carbon monoxide: headaches, loss of muscle strength, cherry-red lividity (pink), survivors have necrosis of globus pallidus

Note: in the poor nations, cassava consumption causes chronic poisoning. Fires at industrial plants do too!

236
Q

TQ
Pt CC: headaches lately

High index of suspicion for what?

A

Carbon monoxide poisoning!

237
Q

Kid comes in and hasn’t been acting right…also has wrist drop

High index of suspicion for what?

A

Lead poisoning

  • look for “lead line” and basophilic stippling
  • Absorbed in gut
  • Binds sulfides–>neuro issues
  • In moonshine
238
Q
  • inhibits delta-aminolevulinic acid dehydratase and ferrochelatase producing a mixed acquired porphyria and microcytic anemia;
  • it inhibits ribonuclease, producing the basophilic stippling of RBCs, raising RBC protoporphyrin levels & maybe ringed sideroblasts.
  • blocks excretion of uric acid, predisposing folks to gout.
  • Poisoning often causes colic – a very painful acute abdomen.
A

lead

239
Q

Lab tech presents as “crazy”

High index of suspicion for what?

A

Mercury poisoning (the mad hatter)

  • binds to sulfhydryl groups and inhibits selenium enzymes to produce renal tubule toxicity
  • neurotoxic! (mad)
240
Q

TQ
“I just don’t feel well.” “A couple of doctors are sick this week.” “I feel strange.” “Something isn’t right.”

  • glove/stocking neuropathy
  • Garlic breath
  • Muscle weakness
  • pigment in neck, armpits
  • incr keratin on palms
  • numbness in leggs
A

Arsenic poisoning!

  • binds sulfhydryl groups
  • GI, cardiac, CNS S/S
  • chronic poisoning darkens skin and causes peripheral neuropathy and keratoses on palms and soles
241
Q
  • cause of “Itai-Itai” (“Ouch! Ouch!”) disease…Japanese mining pollution
  • batteries
  • desquamative pneumonitis
  • Fanconi syndrom: proximal tubules
A

Cadmium poisoning!

242
Q

TQ

  • hair loss and red skin
  • pain
  • oral prussian blue
  • GI upsets and parathesias
A

thallium poisoning

243
Q

Worlds most popular method of suicide

A

organophosphate poisons such as insecticides

244
Q

-There are around 10 million problem drinkers in the US, and alcohol is a factor in around 100,000 deaths / year

(accidents, homicides, suicides, cirrhosis, and cancers of the oral cavity, larynx, esophagus)

What is the cancer causing molecule in alcoholics?

A

Acetaldehyde

245
Q 
Predictable side effects of ...
Cyclophosphamide
Adriamycin
Penicillin
Amphotericin B
Nitrofurantoin
A
  • Cyclophosphamide: hemorrhagic cystitis
  • Adriamycin: cardiotoxic
  • Penicillin: hemolysis
  • Amphotericin B: fever, chills, necrosis
  • Nitrofurantoin: eos lung kills
246
Q

What is the biggest danger of cocaine?

What are some assoc risks?

A

psychological craving #1

  • cardiomyopathy
  • septal perforation
  • delirium
247
Q

Morphine used for pain relief but cause constipation and seuxal dysfx
-risk of abuse of opiates?

A

sudden death from respiration suppression

248
Q

Pt dies and has froth out of mouth

A

heroin overdose

249
Q
  • wasting of the body tissues
  • oral lesions are due largely to ischemia
  • death due to heart rhythm disturbances
A

methamphetamine

250
Q
  • dementia
  • lungs freeze
  • suppress brain function
  • rhythm disturbances
A

Inhalants (huffing)

251
Q

-metabolized by an alternate pathway into a liver poison (N-acetyl-p-benzoquinoneimine)
that reacts with membranes & protein
-upset stomach
-Liver necrosis

A

Acetaminophen toxicity

252
Q
  • respiratory alkalosis (from hyperventilation) and metabolic acidosis
  • acetylates platelets and at toxic levels uncouples oxidative phosphorylation and inhibits the Krebs cycle= ketoacidosis
  • tinnitus, upset stomachs, and a tendency to ulcers and GI bleeding
A

Aspirin overdose

253
Q

__________: Skin damaged. Scrapes.

  • road rash
  • gag/strangulations
A

Abrasians

254
Q

__________: vessels damaged. Bruises

A

Contusions

255
Q

_________: connective tissue torn. Blunt trauma w/ intact NV bundles
-bruised, rough edges with bridging

A

Lacerations

256
Q

________ _____ ______: severed NV bundles, smooth edges

  • stab wounds: deep
  • incised wounds: wide (self-mutilation)
  • chop wound: heavy (hatchet)
  • dicing injuries: windshield glass
A

Wounds from sharps

257
Q

What are these common findings of?

  • handprint
  • looped cord injury
  • belt
  • torn frenulum
  • callus on CT
  • metacarpals/metatarsal breaks
  • *corner fracture
  • bucket handle
  • thermal trauma
  • Immersion burn
  • cigarette burn
  • bite marks
  • ear contusions
  • blow to head or kick to abdomen
  • shaken baby syndrome (retinal, subdural hem)
A

child abuse

258
Q

What is impt when treating a burn pt?

Superficial / first degree – epidermis only
Partial-thickness / second degree – into the dermis Full-thickness / third degree – into the subcutaneous tissue

A
  • microvasculature becomes hyperpermeable, and myocardial function may be depressed. Fluid resuscitation is of paramount importance
  • Controlling infection! Pseudomonas; Staph is next.
259
Q

Risks of extreme heat?

Heat cramps, exhaustion and.....
Hint:
-Core temp >104
-Red, dry skin
-Brain malfunction from hyperthermia
-Will die / get brain damage if not treated as an emergency
A

Heat stroke

260
Q
  • Frostbite: actual freezing

- immersion foot / pernio / chilblains: ischemia, necrosis, inflammation)

A

Hypothermia

261
Q

Electrical injury by power tool, live wire, or pole runs the risk of what? (2)

A

ventricular fibrillation

asystole

262
Q

How does ionizing radiation injure living tissue?

A
  • The most radiosensitive cells in the body are the reproductive epithelium, the marrow, the lymphoid tissue, and the GI epithelium.
  • Once heavily radiated, the intima of vessels will continue to proliferate and compromise the vasculature. This is slow but never stops
  • late effects of radiation on the skin->atrophy, dense fibrosis, telangiectasias.
263
Q

Quantitate radiation:

  • ____ rads: Hematopoietic syndrome, probably recover
  • ____ rads: Hematopoietic syndrome, probably die
  • > 500 rads: Gastrointestinal syndrome, death in a few days
  • > 5000 rads: Cerebral syndrome, death in ~ an hour
A

200
500

Review:

  • Rad: A dose of energy resulting in absorption of 100 ergs / gram of target tissue. Gray (Gy): 100 rads.
  • Curie: How much isotope. 3.7 x 1010 disintegrations per second.
  • Sievert (Sv): Formerly REM, Roentgen equivalents for a (person). A REM was Rads multipled by the relative biologic effectiveness for the type of radiation.

SBL Final (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions