• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/116

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

116 Cards in this Set

  • Front
  • Back
E(Epidermal) GF
Made in platelets, macrophages

Acts on keratinocytes to migrate, divide
Acts on fibroblasts to produce “granulation” tissue
T(Transforming) GF-alpha
Made in macrophages, T-cells, keratinocytes
Similar to EGF, also effect on hepatocytes
H(Hepatocyte) GF
Made in “mesenchymal” cells
Proliferation of epithelium, endothelium, hepatocytes
Effect on cell “motility”
VE(Vascular Endothelial) GF
Made in mesenchymal cells
Triggered by HYPOXIA
Increases vascular permeability
Mitogenic for endothelial cells
KEY substance in promoting “granulation” tissue
PD(Platelet Derived) GF
Made in platelets, but also MANY other cell types
Chemotactic for MANY cells
Mitogen for fibroblasts
Angiogenesis
Another KEY player in granulation tissue
F(Fibroblast) GF
Made in MANY cells
Chemotactic and mitogenic, for fibroblasts and keratinocytes
Re-epithelialization
Angiogenesis, wound contraction
Hematopoesis
Cardiac/Skeletal (striated) muscle
T(Transforming) GF-beta
Made in MANY CELLS
Chemotactic for PMNs and MANY other types of cells
Inhibits epithelial cells
Fibrogenic
Anti-Inflammatory
K(Keratinocyte) GF
Made in fibroblasts
Stimulates keratinocytes:
Migration
Proliferation
Differentiation
I(Insulin-like) GF-1
Made in macrophages, fibroblasts
Stimulates:
Sulfated proteoglycans
Collagen
Keratinocyte migration
Fibroblast proliferation
Action similar to GH (Pituitary Growth Hormone)
TNF (Tumor Necrosis Factor)
Made in macrophages, mast cells, T-cells
Activates macrophages
KEY influence on other cytokines
Interleukins
Made in macrophages, mast cells, T-cells, but also MANY other cells
MANY functions:
Chemotaxis
Angiogenesis
REGULATION of other cytokines
INTERFERONS
Made by lymphocytes, fibroblasts
Activates MACROPHAGES
Inhibits FIBROBLASTS
REGULATES other cytokines
EDEMA
ONLY 4 POSSIBILITIES!!!
ONLY 4 POSSIBILITIES!!!
Increased Hydrostatic Pressure
Reduced Oncotic Pressure
Lymphatic Obstruction
Sodium/Water Retention
Transudate vs Exudate
Transudate
results from disturbance of Starling forces
specific gravity < 1.012

Exudate
results from damage to the capillary wall
specific gravity > 1.012
HYPEREMIA
Active or passive process?
Active process
CONGESTION

Passive or active process?
Passive process
When does pulmonary edema occur?
Pressure?
Pulmonary edema occurs only when the pulmonary capillary pressure rises to values exceeding the plasma colloid osmotic pressure, which is approximately 28 mm Hg in the human. Because the normal pulmonary capillary pressure is 8 to 12 mm Hg, there is a substantial margin of safety in the development of pulmonary edema.
What is the difference between Pre and post-motrem clot?
Premortem clots have texture and usually ADHERE to a vessel wall. Post mortem clots have a jelly or chicken fat consistency.
PLATELET ADHESION
Primarily to the subendothelial ECM
Regulated by vWF, which bridges platelet surface receptors to ECM collagen
PLATELET AGGREGATION MOLECULES
ADP
TxA2 (Thromboxane A2)
THROMBIN from coagulation cascade also
FIBRIN further strengthens and hardens and contracts the platelet plug
Vit-K dep. factors:
II, VII, IX, X, Prot. S, C, Z
Virchow’s TRIANGLE

(thrombosis)
ENDOTHELIAL INJURY

ABNORMAL FLOW
(NON-LAMINAR)

HYPER-
COAGULATION
Lines of Zahn
Lines of Zahn, gross and microscopic, top, is evidence to prove a clot is PRE-mortem.
Red vs. White infarction?
RED vs. WHITE
END ARTERIES vs. NO END ARTERIES
MHC MOLECULES (Gene Products)
I
I (All nucleated cells and platelets), cell surface glycoproteins, ANTIGENS
MHC MOLECULES (Gene Products)
II
II (APC’s, i.e., macs and dendritics, lymphs), cell surface glycoproteins, ANTIGENS
MHC MOLECULES (Gene Products)
III
III Complement System Proteins
HYPERSENSITIVITYREACTIONS (4)
I (Immediate Hypersensitivity)
II (Antibody Mediated Hypersensitivity)
III (Immune-Complex Mediated Hypersensitivity)
IV (Cell-Mediated Hypersensitivity)
HYPERSENSITIVITYREACTIONS
I
I (Immediate Hypersensitivity)

“Immediate Allergic Reactions”, which may lead to anaphylaxis, shock, edema, dyspnea death
HYPERSENSITIVITYREACTIONS
II (4)
II (Antibody Mediated Hypersensitivity)
HYPERSENSITIVITYREACTIONS
III (4)
III (Immune-Complex Mediated Hypersensitivity)
HYPERSENSITIVITYREACTIONS
IV (4)
IV (Cell-Mediated Hypersensitivity)
TYPE II DISEASES
Autoimmune Hemolytic Anemia, AHA
Idiopathic Thrombocytopenic Purpura, ITP
Goodpasture Syndrome (Nephritis and Lung hemorrhage)
Rheumatic Fever
Myasthenia Gravis
Graves Disease
Pernicious Anemia, PA
TYPE III HYPERSENSITIVITY
IMMUNE COMPLEX MEDIATED
DESIESE
Common Type III Diseases- SLE (Lupus), Poly(Peri)arteritis Nodosa, Poststreptococcal Glomerulonephritis, Arthus reaction (hrs), Serum sickness (days)
TYPE IV HYPERSENSITIVITY
Example
Tuberculin Skin Reaction

DIRECT ANTIGEN to CELL CONTACT
GRANULOMA FORMATION
CONTACT DERMATITIS
LUPUS (SLE)
Etiology
Morphology
Biochem test?
Etiology: Antibodies (ABs) directed against the patient’s own DNA, HISTONES, NON-histone RNA, and NUCLEOLUS


Morphology: “Butterfly” rash, skin deposits, glomerolunephritis (NOT discoid)

Postive A.N.A
CANCERS of AIDS
KAPOSI SARCOMA
B-CELL LYMPHOMAS
CNS LYMPHOMAS
CERVIX CANCER, SQUAMOUS CELL
Misnomers

hepatoma:
hepatoma: malignant liver tumor
Kuru
Kuru is an incurable degenerative neurological disorder (brain disease) that is a type of transmissible spongiform encephalopathy, caused by a prion found in humans. Taken from the Fore word "kuria/guria", 'to shake'. It is also known as the laughing sickness due to the pathologic bursts of laughter people would display when afflicted with the disease. Kuru was probably transmitted among members of the Fore tribe of Papua New Guinea via cannibalism.
ARTERIO-SCLEROSIS
GENERIC term for ANYTHING which HARDENS arteries
Atherosclerosis (99%)
Mönckeberg medial calcific sclerosis (1%)
“Framingham” data
Major riskfactor for atherosclerosis

Hyperlipidemia
Hypertension
Cigarette Smoking
Diabetes Milletus
hypertension is described as two different types of changes in arterioles, usually renal.

HOW?
Benign: Hyalization of arteriole wall
Malignant: Fibrinoid necrosis and “onion skinning” of arteriole wall
THROMBOANGIITIS OBLITERANSBUERGER(‘s) Disease
100% caused by cigarette smoking
MEN>>>F, 30’s, 40’s
Often arteries are 100% obliterated, hence the name “obliterans”
EXTREMITIES most often involved
Raynaud “Phenomenon”
Primary
PRIMARY: (formerly Raynaud “DISEASE”)
Digital PALLORCYANOSISHYPEREMIA
(WHITE) (BLUE) (RED)
Vasoconstriction usually triggered by COLD, emotion
Can be tip of nose, not only digits
Self Limited, Gangrene UN-common
Arteries often do NOT show diagnostic pathology
Raynaud “Phenomenon”
Secondary
SECONDARY: (formerly Raynaud “Phenomen.”)
Atherosclerosos
SLE
Buerger Disease
“BOXCAR” effect.
squaring off of the nuclei, so called “BOXCAR” effect.
(in heart i think)
CONGENITAL HEARTDEFECTS
(critical period?)
Faulty embryogenesis (week 3-8)‏
CHF: Autopsy Findings
Cardiomegaly
Chamber Dilatation
Hypertrophy of myocardial fibers, BOXCAR nuclei
CHD L to R shunt
LR SHUNTS: all “D’s” in their names
NO cyanosis
Pulmonary hypertension
SIGNIFICANT pulmonary hypertension is IRREVERSIBLE
CHD R to L shunt
RL SHUNTS: all “T’s” in their names
CYANOSIS (i,.e., “blue” babies)
VENOUS EMBOLI become SYSTEMIC
Libman-Sacks
Libman-Sacks endocarditis is a form of nonbacterial endocarditis that is seen in systemic lupus erythematosus
Carcinoid Syndrome
Episodic skin flushing
Cramps
Nausea & Vomiting
Diarrhea
↑serotonin, ↑ 5HIAA in urine
FIBROUS INTIMAL THICKENING
RV, Tricuspid valve, Pulmonic valve (all RIGHT side)
Similar to what Fen-Phen does on the LEFT side
“restrictive” cardiomyopathy
A “restrictive” cardiomyopathy is a wall which is NOT thickened or dilated necessarily, but RIGID in diastolic relaxation.


↓ ventricular compliance
Chiefly affects DIASTOLE
NORMAL chamber size and wall thickness
THREE similar diseases affecting predominantly the SUBENDOCARDIAL area:
Endomyocardial Fibrosis (African children)
Loeffler Endomyocarditis (eosinophilic leukemia)
Endocardial Fibroelastosis (infants)
Dilated cardiomyopathy
Impairment of contractility (systolic dysfunction)
Interstitial Fibrosis
50% die in 2 years
Hypertrophic cardiomyopathy
Impairment of compliance (diastolic dysfunction)

INTERSTITIAL fibrosis
CLINICAL: ↓chamber volume, ↓SV, ↓ diastolic filling
MYOCARDITIS
INFLAMMATION of MYOCARDIUM
Chiefly microbial
COXACKIE A & B, CMV, HIV
Trypanosoma cruzi (Chagas dis.), 80%
Trichinosis
Toxoplasmosis
Lyme disease (5%)
Diphtheria
IMMUNE: Post-viral, rheumatic, SLE, drug hypersensitivityalpha-methyl dopa, sulfas


BOTH HYPER-, HYPO- -thyroidism
PERICARDITIS
Serous
Rheum. Fever (RF), SLE, scleroderma, tumors, uremia
PERICARDITIS
Fibrinous
FIBRINOUS: MI (Dressler), uremia, radiation, RF, SLE, s/p open heart surgery
PERICARDITIS
Hemorrhagic assoc. w/
HEMORRHAGIC: Malignancy, TB
PERICARDITIS
Casoeus
CASEOUS: TB
PERICARDITIS
Chronic
CHRONIC: (ADHESIVE, CONSTRICTIVE)
Most common place for metastis in general?
LUNG is the MOST COMMON site for all metastatic tumors, regardless of site of origin
It is the site of FIRST CHOICE for metastatic sarcomas for purely anatomic reasons!
NECROTIZING” Upper Airway Lesions
“WEGENER” Granulomatosis
“Lethal” Midline Granuloma


“Lethal” midline granuloma is thought to be a malignant tumor of NK (Natural Killer) cells.
OLFACTORY`-ESTHESIONEUROBLASTOMA
Has what in micro?
Like any other neuroblastoma, it may have “rosettes”.
“zell-ballen''
Tumors of the carotid body are composed of “balls of cells”, or “zell-ballen” in German
Warthin Tumor
PAPILLARY CYSTADENOMA LYMPHOMATOSUM of salivary gland (beign)
Schiatzki
Schiatzki “Ring” in lower esophagus
“ZENKER” diverticulum
High diverticulum of esophagus
MALLORY-WEISS
LACERATION in lower esophagus
tumor cells are derived from the interstitial cells of Cajal..?
G.I.S.T.
ACUTE APPENDICITIS diagnosis
NEED NEUTROPHILS in the MUSCULARIS to confirm the DIAGNOSIS
JAUNDICE
Hemolytic
Type of bilirubin?
Hemolytic (UN-conjugated)
JAUNDICE
Obstructive
Type of bilirubin?
Obstructive (Conjugated)
BERGER DISEASE
IgA NEPHROPATHY

Mild hematuria
Mild proteinuria
IgA deposits in mesangium
ALPORT SYNDROME
Progressive Renal Failure
Nerve Deafness
VARIOUS eye disorder
DEFECTIVE COLLAGEN TYPE IV
Henoch-Schonlein Purpura
(IgA-NEPH)
Malacoplakia
soft yellow plaques filled with macrophages and calcium
found in the urinary tract

is associated with:
Prolonged therapy with systemic corticosteroids
Organ transplantation
Diabetes mellitus
Lymphoma
Rheumatoid arthritis
Michaelis-Gutmann
Michaelis-Gutmann bodies contain Fe and Ca in macrophages
found in the urinary tract
Is assoc. w/ Malacoplakia
Brunn nests
Brunn nests are clusters of urothelium which usually lie UNDER the surface mucosa. They can undergo glandular (i.e., columnar) metaplasia.
Schiller-Duvall Body
YOLK SAC TUMOR

Most common testicular tumor in male CHILDREN
Compare testicular and ovarian teratomas
Most testicular teratomas are malignant.
Most ovarian teratomas are benign (e.g., dermoid cyst)
Lichen Sclerosus et Atrophicus
Inflammation of vulvular skin
VIN, SCC
Like condylomas, HIGHLY linked to HPV

VIN=changes leading to SCC-in-situ, look like “plaques”
Stein-Leventhal syndrome
POLY-Cystic Ovarian Disease
“Immature” teratomas are regarded as
“Immature” teratomas are regarded as malignant
Call-Exner bodies
Call-Exner bodies are virtually diagnostic of granulosa cell tumors.
Q: Do they remind you of “rosettes”? Ans: YES
Number 1 commandment in pathology:
Number 1 commandment in pathology: NEVER diagnosis a malignant papilloma on a frozen section!!!!! NEVER. :P
“INDIAN” FILE PATTERN assoc w/
INFILTRATING LOBULAR CA.
(breast)
ANTERIOR PITUITARY
ACIDOPHILS
ACIDOPHILS
GROWTH HORMONE
PROLACTIN
ANTERIOR PITUITARY
BASOPHILS
BASOPHILS
TSH
ACTH
LH, FSH
Sheehan’s syndrome
HYPO-pituitarism
Sheehan’s syndrome (Post-partum ischemic necrosis)
Goiter
Exophthalmos
???
HYPER-THYROIDISM
Cretinism

Myxedema (coma)
HYPO-THYROIDISM
GRAVES DISEASE
aka, diffuse toxic goiter

HYPERTHYROIDISM
EXOPHTHALMOS
PRE-TIBIAL MYXEDEMA

Autoimmune, auto-antibodies to TSH
PLUMMER DISEASE
aka, nodular toxic goiter
Hyperthyroidism
HÜRTHLE
oxyphilic adenoma
BIOLOGIC BEHAVIOR of thyroid malignacy:
Papillary CA
Follicular CA
Papillary CA lymph nodes

Follicular CA  blood vessels, bone
PHEOCHROMOCYTOMAS, rule of 10 applies to what?
PHEOCHROMOCYTOMAS, aka, primary tumors of the adrenal medulla
10% arise in an MEN setting
10% are EXTRA-adrenal
10% are bilateral
10% are malignant
10% are in childhood
Wermer Syndrome
Wermer Syndrome = MEN I
Parathyroid, pancreatic, pituitary
cotton wool spots
RETINOPATHY in Dm
PREMALIGNANT/MALIGNANT
Of skin and there character
ACTINIC (Solar) KERATOSIS, i.e. precursor to SCC

SQUAMOUS CELL CARCINOMA, squamous “pearls”, intercellular bridges.

BASAL CELL CARCINOMA, by far, MOST COMMON, BLUE palisading nests. BOTH SCC and BCC related to SUN (i.e., radiation) exposure. (as is MM also)


MERKEL CELL CARCINOMA (TUMOR), VERY MALIGNANT AND LETHAL, LOOK LIKE SMALL CELL CA. OF LUNG
Name the FOUR histopathologic findings in most of the forms of psoriasis: 1,2,3,4
1) Parakeratosis,
2) hyperplasia,
3) rete peg elongation,
4) MUNRO abscesses.
Acanthylosis
Acantholysis: Loss of intercellular connections resulting in loss of cohesion between keratinocytes.
Paget Disease (bone)
OSTEOCLAST DYSFUNCTION
POTTS disease
TB of spine is known as POTTS disease
Guillain-Barré
Guillain-Barré (inflmmatory nephropathy)
Preceded by “influenza”-like illness
NO actual specific etiologic agent isolated, autoimmune disease to myelin gangliosides most likely
Inflammation of a peripheral nerve
DEMYELINATION
“ASCENDING” paralysis
Why are Schwannomas the ONLY tumors of peripheral nerve?
Because SCHWANN cells are the ONLY nucleated cells found IN a nerve
Hassal’s corpuscles
Hassal’s corpuscles are fused epithelial reticular cells in Thymus
Syringomyelia

(Syrinx)
Syringomyelia is damage to the spinal cord due to the formation of a fluid-filled area within the cord
PRION DISEASES:common features
“SPONGIFORM” changes in neurons and glia
TAUOPATHIES
Most cortical dementias are known as TAUOPATHIES
eg. Pick's disease (frontal lobe)
LEUKO”-DYSTROPHIES
abnormal “myelin” synthesis
Eg. Krabbe
Metachromatic-
Adreno-
Pelizaeus-Merzbacher
Canavan
What is a typical histo-finding in Glioblastoma?
Pallisading and necrosis
What is a typical histo-finding in Neuroblastoma?
rosettes
FAMILIAL TUMOR SYNDROMES
NF-1
Neurofibromas
Gliomas
FAMILIAL TUMOR SYNDROMES
NF-2
Schwannomas
Meningiomas