Study your flashcards anywhere!

Download the official Cram app for free >

  • 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

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/52

Click to flip

52 Cards in this Set

  • Front
  • Back
Kinds of Pathology
–Surgical pathology –Cytology –Autopsy (includes forensic)
•Clinical pathology –Clinical chemistry –Microbiology –Hematopathology –Transfusion, coagulation –Toxicology –Molecular pathology
•Experimental pathology
What does a pathologist do?
Surgical Pathology (70%) •Cytology (10%) •Autopsy, Administration, Clinical Pathology (~20% combined)
•99+% of specimens are from living patients
•Surgical pathology entails: –Frozen sections –Permanent sections –Diagnosis
Cell Injury & Adaptation
- kinds of adaptations
–Of entire cell –Of specific organelle
•Hyperplasia
•Metaplasia •Dysplasia
Atrophy
Cell shrinkage or loss
•Caused by:
–Lack of hormonal signals
–Loss of innervation
–Lack of use
–Loss of blood supply
-Starvation
–Individual cell death
Hyperplasia
•Increase in number of cells
•Causes are similar to hypertrophy (stress, hormones, etc.)
•Can occur with hypertrophy
•Examples: –BPH –liver, kidney –breast, endometrium
Metaplasia
•Replacement of one cell type by another
•Examples:
–Smoker's airways
–Cervix
–Barrett's esophagus
Dysplasia
•Disordered hyperplasia without maturation
•Preneoplastic
•Examples:
–Uterine cervix
–Bowel in IBD
–Esophagus with Barrett's
Causes of cell injury & death
Trauma - force, heat, cold
•Ischemia - inadequate circulation
•Toxins & radiation
•Infection
•Inflammation
•Genetic diseases
•Nutritional problems (too much or little, vitamin deficiency)
•Tumors
Cells Most Prone to Injury
•High metabolic activity
–Cardiac myocytes
–Renal tubular cells
–Hepatocytes
•Rapidly proliferating
–Testicular germ cells
–Intestinal epithelium
–Hematopoietic cells
Free Radicals
•Unpaired electron in outer orbital (such as •OH)
•Major cause of cellular damage
•Causes:
–radiation
–ischemia (and reperfusion)
–toxins
–inflammatory mediators (NO, HOCl in neutrophil respiratory burst via myeloperoxidase)
–Iron can propagate free radicals
•Degraded by glutathione, catalase, vitamins A, C, & E
Apoptosis
Orderly, energy-requiring cell death
•Often a normal phenomenon
•No inflammation, One cell at a time
•Happens in:
–Normal embryology
–Normal cell turnover (intestine, skin, menses)
–Viral infection
–Damaged cells (DNA, other)
–Immunologically mediated
•Fas or TNF signals
Necrosis
Uncoordinated cell death
•Cell membrane disruption, Ca++ signal, & energy loss (ATP depletion) are EARLY events
•Often happens to cell clusters rather than individual cells
•Incites acute inflammation from leakage of cell contents
•Cells often swollen (loss of ion pumps early in process)
Patterns of Necrosis
•Coagulative - with ischemia - see infarct
•Liquefactive - loss of substance - in brain or abscess
•Fat necrosis - necrosis in fat •Caseous necrosis - necrotizing granulomas - combination of liquefactive & coagulative - Fungal or TB infection
•Gangrenous necrosis
Organelle Changes
•Organelles, like cells, can undergo hypertrophy or atrophy
•Example: Liver - increased smooth ER with barbiturate use. Increased cytochrome p450 2C can metabolize other drugs or toxins more quickly
•Injured organelles: Mallory body in liver from alcohol or other injury - clump of intermediate filaments
•Injured organelles: Neurofibrillary tangles in brain in Alzheimer's patient
Abnormal Storage Products
•Fatty change of liver –Common & nonspecific –See with: alcoholism, obesity, starvation, toxins
•Glycogen accumulation –In liver in diabetes –In glycogen storage disease –In certain tumors
•Lipid storage –Lipid storage disease - Fabry's - Gaucher's –In vessels in atherosclerosis
Brown Storage Products
•Lipofuscin - degraded lipid in lysosomes –increases with age, free radical damage
•Bilirubin - hemoglobin breakdown product –normally present in bile –increased with biliary obstruction & hepatocyte disorders –too much causes jaundice / icterus
•Hemosiderin - iron containing pigment –Increased with excessive iron absorption, bleeding into tissues
Protein Storage
•Intracellular: –α-1-antitrypsin deficiency –Russell bodies in plasma cells
•Extracellular –Amyloid
•Beta pleated sheet protein accumulations
•Can be more than a dozen different protein types
•Occurs in a variety of diseases
•Seen in vessels, brain, heart, glomeruli, tumors, and other sites
Misc. Storage Products
•Anthracosis - carbon pigment –Harmless, but other harmful materials can be deposited with it (silica, asbestos) –Mostly in lungs
•Calcification –Dystrophic Calcification - into damaged tissue –Metastatic Calcification - into normal tissue
•Disorder of calcium metabolism (renal failure, hyperparathyroidism, malignancy)
Hypertrophy
enlargement in response to stimulus.
Hormonal, chemical signaling, stress
Cachexia
Generalized wasting. caused by starvation, disseminated, tumors, and chronic inflamatory diseases such as advance tb and AIDS.
proteins degrated by ubiquitin-proteosome
lipids and lipid bound structures degraded in lysosome.
Reversible cell injury
cell must mantain its integrity. the cell membrane, mitochondria, basic bioxynthetic pathways, and DNA.
Irreversibe cell injury
holes in the cell membrane
large prolonged influx of Ca into cytoplasm
mitochondrial damage with or w/out mito death signaling
lysosomal liakage w/diagestion of cytoplasmic contents
nuclear pyknosis
2 kinds of cell death: necrosis and apoptosis
Kinds of Inflammation
•Acute –Begins almost immediately, lasts minutes to days –Neutrophils, vessels, mast cells
•Chronic –Begins ~1 or more days later –Lymphocytes, macrophages, ± plasma cells
•Granulomatous –Variant of chronic inflammation –Aggregates of epithelioid histiocytes, giant cells, lymphocytes
5 Clinical Signs of Inflammation
5 Clinical Signs of Inflammation
•Rubor - redness
•Tumor - swelling
•Calor - warmth
•Dolor - pain
•Loss of function
Fever
Temperature > 37.2oC (99oF).
•Can have vasodilation or vasoconstriction.
•Can have shivering (chills), sweating.
•Due to infection, hormones, drugs, mediated by certain cytokines (esp. IL-1, TNF-α).
•Changes temperature regulation set point in hypothalamus.
•Malignant hyperthermia.
•"Sell at 106" i.e. serious tissue damage at 104-106oF / 40-1oC. Often fatal at 108oF / 42.2oC.
Vessels are Crucial in Inflammation
•Small vessels, esp. venules, develop endothelial cell retraction
•Plasma seeps through the gaps
•Forms exudate - fluid rich in proteins
•DDx - transudate (low specific gravity, protein, & LDH) from hemodynamic problems
•Vessels also recruit inflammatory cells to site
Laboratory Signs of Inflammation
•Leukocytosis with neutrophilia - acute inflammation - think bacterial infection
•Leukocytosis with lymphocytosis - chronic inflammation - think viral infection
•Eosinophilia - parasitic infection, autoimmune, asthma/allergic, tumors
•Thrombocytosis or thrombocytopenia can occur
Laboratory Signs of Inflammation
Increased sedimentation rate
CRP (C - reactive protein)
Other markers for cellular injury
•Troponin - myocardial damage (as in infarct)
•Transaminases - AST, ALT - liver injury / hepatitis
•LDH (also present in many tissues)
•Alkaline phosphatase - liver biliary obstructive injury.
•CPK (creatine phosphokinase) - muscle injury
•Amylase & lipase - pancreatitis
Cells in acute inflammation
•Mast cells
•Neutrophils
•Endothelium
Mast Cells
•Activated by trauma, burns, etc., IgE cross-linking, toxins, endogenous mediators
•Degranulate, secreting: –Histamine –TNF-α, IL-4 –Chemokines –Proteases (tryptase) –Heparin
•Also secrete leukotrienes / prostaglandins
Neutrophil activity
Phagocytose bacteria-degranulation can cause tissue damage.
In accute inflamation-permanent damage can occur, scaring can occur. If inciting agent can't be removed infiltration continues causing abscess.
Granulomatos form if inciting agent is phagocytosed but not killed.
Cells in Chronic Inflammation
•Lymphocytes (sometimes plasma cells too)
•Macrophages
•Sometimes eosinophils
•Fibroblasts and new vessels in tissue repair
Chemical Mediators of Inflammation
•Cytokines –Small proteins –Chemokines
•Cause chemotaxis or activation
•Specific structure with nearby cystine –Can have effects on, Same cell that secreted it (autocrine); Nearby cells (paracrine) ; Cells throughout the body (endocrine)
Complement
•Cascade of proteases
•Amplify, mediate effects of immunoglobulins
•Also activated by innate immune mechanisms and neutrophil proteases
Arachidonic Acid Metabolites
•Crucial inflammatory mediators
•Cyclooxygenase pathway * –Prostaglandins –Prostacyclins
–Thromboxanes
•5-Lipooxygenase pathway –Leukotrienes* Major target of antiinflammatory drugs - NSAIDS (nonsteroidal antiinflammatory agents).
Kinin cascade
Activates and is activated by clotting factor 12 and results in the accute inflamatory mediator bradykinin, which causes vascular changes and pain in accute inflamation.
Toxic Shock Syndrome
abrupt onset of fever with chills, vomiting, diarrhea, muscle aches, and rash
Cause by Staph aureus sepsis with staph toxin (TSST1)
EDEMA
•Dependent edema - legs or lower part of body.
•Pulmonary edema - often from heart failure.
•Anasarca - edema of the whole body.
•Periorbital edema - puffiness around eyes.
•Localized edema - area of infection, trauma, circulatory problem.
•Renal failure & thyroid deficiency often cause periorbital edema or anasarca.
RegeneratioN and cell type dependent
–Stem cells - Primitive cell type that can proliferate and can differentiate to mature cell type(s)
–Labile cells - Normally proliferate, but not necessarily a primitive cell type such as a stem cell.
–Stable cells - Can proliferate in response to injury etc., but does not do so normally. (Hepatocytes)
–Permanent cells - Cannot proliferate. Mostly cannot be replaced if lost. (Neurons, cardiac myocytes)
kLEOIDS
ENLARGED HYPERTROPHIC SCAR, CAUSED BY ESCESSIVE COLLAGEN LAID DOWN. gENERALLY FORMS IN DARK SKINNED INDIVIDUALS
WOUND dIHISCENCE
THE REOPENING F A WOUND WHEN WOUNDS DO NOT HEAL APPROPRIATELY
LIVER REPAIR
GREAT GENERATIVE CAPACITY
CIRRHOSIS-RESULT OF INFLAMATION CAUSING SCARING AND INHIBITED REGROWTH OF PORTAL TRACKS AND CENTRAL VEINS.
PORTAL HYPERTENSION
HEART REPAIR
INFARCT CAUSES GRANULATION TISSUE AND SCARRING WITHOUT REGENERATION
VENTRICULAR ANEURYSM
KIDNEY
GLOMERULI CANNOT REGENERATE. RENAL MEDULA REGENERATES POORLY
BRAIN
INFARCTS UNDERGO LIQUEFACTIVE NECROSIS
LUNG
CYSTIC CAVITY IF MANY ADJECENT ALVEOLI ARE LOST-EMPHYSIMA
IF IT HAPPENS IN THE BRONCHIOLES BOOP (BRONCHIOLITIS OBLITERANS OBSTRUCTIVE PNEUMONIA)
SEROSAL SITES:
PLEURA, PERITONEUM AND PERICARDIUM
FIBRIN DEPOSITION -CAN CAUSE OBSTRUCTION AND BLOOD SUPPLY INTERFERANCE, CAUSING BOWEL NECROSIS AND INFARCTION
WHAT IS A NEOPLASM
UNCONTROLLED GROWTH OF CELLS, GENERALLY A CLONE-THE POGENY OF A SINGLE INITIAL TUMOR CELL
BENIGN IF IT DOESN'T METASTASIZE OR MALIGNANT IF IT DOES
Neoplasm
An uncontrolled growth of cells
•Usually a single clone (progeny of a single cell)
•Names usually end in -oma
•A benign epithelial tumor is an adenoma (if glandular),
a papilloma (if papillary)
•A malignant:
–Epithelial tumor is a carcinoma
–Mesenchymal tumor is a sarcoma
–Lymphoid tumor is a lymphoma
–Tumor of hematopoietic cells is a leukemia
Carcinoma
•Most common kind of malignancy –Usually has cytologic features of malignancy
•Nuclear enlargement and anisocytosis (different cells look different)
•Abundant and abnormal (sometimes) mitotic figures
•High nuclear : cytoplasmic ratio –These are general features. The specific rules vary with site and situation. –Most often metastasizes to regional lymph nodes; can metastasize hematogenously
• –MOST IMPORTANT FEATURE IS INVASION!
How Many Cells in a Tumor?
A 1 cm diameter tumor has ~109 cells 30 doublings
•A 10 cm diameter tumor has ~1012 cells~40 doublings)
•Roughly 3/4 of the doublings a tumor undergoes are before it is discovered
•tumor grows for 5-10 or more before it becomes visible.