definitions Flashcards
the study of the cause of disease
etiology
how a disease develops
pathogenesis
disease with no identifiable cause
idiopathic
disease the occurs as a result of medical treatment
iatrogenic
period during which there is a decrease in severity of disease
remission
severity of disease made worse
exacerbation
decrease in size
atrophy
increase in size
hypertrophy
increase in number of cells
hyperplasia
reversible replacement of one mature cell type by another, sometimes less differentiated, cell type
metaplasia
abnormal changes in size, shape, and organization of mature cells
dysplasia
lack of sufficient oxygen for cells
hypoxia
reduced blood supply to cells in one area
ischemia
type of endogenous free radicals that are kept in check by KOS scavengers
reactive oxygen species
caused by hypoxia and infarcts, is the manifestation of protein deviation (coagulation) which causes the tissue to become firm and opaque
coagulative necrosis
a pattern of cell death caused by several etiological factors
liquefactive necrosis
a unique form of cell death in which the tissue maintains a cheese-like appearance
caseous necrosis
A benign condition in which fat tissue in the breast or other organs is damaged by injury, surgery, or radiation therapy
fat necrosis
a condition that occurs due to coagulative necrosis. Skin becomes dry, wrinkles and dark
dry gangrene
a condition that occurs due to liquefactive necrosis, unusually in internal organs, where area becomes cold, swollen, and blck with a foul odor due to bacterial action
wet gangrene
a specific condition caused by infection with a species of bacteria (clostridium species)
gas gangrene
programmed cell death caused by both normal and pathologic tissue changes (cell suicide)
apoptosis
part of the innate (non-specific) immune response to tissue injury or microbial infection. Relatively severe, but short term
acute inflammation
lasts longer than acute inflammation.Your body continues sending inflammatory cells even when there is no outside danger
chronic inflammation
activate the inflammatory response
mast cell
cascade reactions that activate proteins which either kill pathogens directly or intensify reactions of other components of the inflammatory response = very potent defenders against bacteria infection
complement system
one of the first chemicals to be released during acute inflammation. Increases vascular dilation and permeability
histamine
made from long chain fatty acids that produce various effects (induce inflammation, vasoconstriction/dilation) depending upon the tissue. Leukotrienes important cause of asthma and anaphylaxis
prostaglandins and leukotrienes
proteins produced by many cell types to communicate with each other in producing an effective inflammatory response
cytokines
function mainly as chemoattractants to recruit and direct the migration of immune and inflammatory cells
chemokines
low protein content, similar to fluid under a blister
serous exudate
greater injury, increased inflammation and vessels become more permeable, releasing more proteins out into tissue. Flud is sticky and thick, and may have to be removed for healing
fibrinous exudate
“pus”- severe inflammation accompanied by infection. Large pockets may have to be drained for healing to occur
purulent exudate
contains a large amount of RBC. Occurs with severe inflammation
hemorrhagic exudate
an increase in the number of immature cell types among the blood cells in a sample of blood
shift to the left
chemicals released by cells in the injured area attract leukocytes
chemotaxis
a special type of chronic inflammation characterized by often focal collections of macrophages, epithelioid cells and multinucleated giant cells
granulomatous inflammation
injured tissues are returned to almost original structure and function
regeneration
replacement of destroyed tissue with scar tissue
replacement
continually dividing. Epithelial tissue and bone marrow cells
labile cells
normally stop dividing when growth ceases, but can regenerate if simulated. Liver, kidney, smooth muscle cells, and vascular endothelial cells
stable cells
cannot regenerate- will be replaced with scar tissue. Nerve cells, skeletal muscle cells, cardiac muscle cells
fixed cells
grows in from healthy connective tissue at the edges of the wound. Red in colour, delicate, and easily broken down by microbes or stress. Contains blood vessels, fibroblasts, and collagen
granulation tissue
healing from clean incisions. Not much contraction or sealing required
healing by primary intention
healing from open wounds. Requires a lot of sealing, filling in and contraction.
healing by secondary intention
fibrous bands of tissue that attach to internal organs. Typically occurs with healing after surgery. Ay restrict normal movement
adhesions
excessive scar that extends beyond wound boundaries
keloid scar
excessive contraction of wound causes deformity, restricted movement
contracture
sutured wound in which the wound is pulled apart along the suture line
dehiscence
abnormal passageway between two structures that does not normally exist. Develop through disease or surgery
fistula
narrowing of passageway. Can arise through inflammatory processes, scar tissue
stritures
an altered immunologic response to an antigen that results in disease or damage to the individual
hypersensitivity
an inappropriate immune response to tissues normally present in the body
autoimmune response
an immune response to alternative forms of an antigen not found in recipient’s body
alloimmune response
IgE mediated reactions
type I hypersensitivity
antibody-dependent cytotoxic hypersensitivity
type II hypersensitivity
immune complex mediated hypersensitivity
type III hypersensitivity
cell-mediated hypersensitivity
type IV hypersensitivity
the most severe systemic allergic reaction- generally type I mechanism. Triggered by substances that are injected or ingested
anaphylaxis
a state of immunological control whereby an individual does not make a detrimental immune response against their own cells and tissues
immunotolerance
occurs immediately, usually to pre-existing recipient antibody to the donor antigen
hyperacute rejection
occurs within days to months after the transplant- type IV reaction
acute rejection
occurs after months to years. Slow, progressive organ failure of the transplanted tissue/organ due to blood vessel damage and fibrosis- weak type IV hypersensitivity
chronic rejection
when the transplanted tissue contains components of the donor’s immune system that recognize the recipient’s tissue as foreign, and attack it
graft vs. host disease
the failure of the immune system to function normally, resulting in increased susceptibility to infections
immunodeficiency
an antigen involved in an allergic response
allergen
symptom of itching
pruritus
a localized pruritic skin disruption characterized by wheals and hives
urticaria
new growth = tumor
neoplasm
cells acquiring the characteristics of the tissue that they make up
cell differentiation
have lost ability to control proliferation, but growth is usually slow and may come to a stop, made of fairly well-differentiated cells and well organized stroma, do not invade beyond their capsule, no metastasis
benign tumor
more rapid growth rate. Loss of differentiation and tissue organization. Cells are pleomorphic
malignant tumour
from epithelial tissue
carcinoma
from mesenchymal tissue
sarcoma
loss of differentiation
anaplasia
spread far beyond the tissue of origin
metastasis
growth with malignant characteristics in epithelial tissue that has not (yet) invaded local tissue
carcinoma in situ
active enzyme that can lengthen telomeres = dividing without a limit
telomerase
genes that in their normal non-mutant state code for proteins that cause the cell to divide
proto-oncogene
genes that code for proteins that slow the rate of cell division or stop it when the cell is damaged
tumour suppressor gene
substances produced by both benign and malignant cells that are either present in or on tumor cells, or found in blood, spinal fluid, or urine
tumour markers
the secretions surrounding a tumor can contain cells of the tumor. Examination of the secretion can reveal abnormal cells
pap test
according to cellular characteristics. A portion of the tumor is obtained through a biopsy. The closer the tumor cells resemble normal tissue, the lower the grade
grading (of cancer)
includes size and spread of the disease
staging (of cancer)
symptoms triggered by cancer, but not caused by direct local effects of the tumor mass
paraneoplastic syndrome
loss of body mass due to metabolic disturbances caused by a disease and cannot be reversed nutritionally- occurs even with adequate caloric intake
cachexia
chemotherapy given alone
induction chemotherapy
given after surgery to hopefully kill the cells that fluffed off/spread
adjuvant chemotherapy
given before surgery to reduce tumor size for easier removal
neoadjuvant chemotherapy
a decrease in the oxygen carrying capacity of the blood
anemia
vitamin b12 deficiency
Pernicious anemia
small and pale
Microcytic-hypochromic
a condition in which blood lacks adequate healthy red blood cells
iron deficiency anemia
normal color
Normocytic-normochromic
excessive erythrocyte presence
Polycythemia
an early response to infection
Neutrophilia
with severe prolonged infections, production can’t keep up with demand
Neutropenia
extremely low counts of genulocytes. Can be caused by chemotherapy
Agranulocytosis (granulocytopenia)
usually produced through viral infection
Lymphocytosis
immune deficiencies, neoplasia, drugs, no known cause
Lymphocytopenia
acute infection of B lymphocytes by Epstein-Barr virus
Infectious mononucleosis
a reduction in all cellular components of the blood
pancytopenia
rapid growth of immature blood cells. Abrupt onset of disease: short survival time (untreated)
Acute leukemia
slow growth of more mature (differentiated) cells which do not function normally
Chronic leukemia
small spontaneous bleeding without any trauma
Petechiae
larger spontaneous bleeding without any trauma
purpura
too many platelets
thrombocythemia
disease of tunica intima of arteries, fibrous fatty lesions form in large/medium-sized arteries
Atherosclerosis
high blood pressure
hypertension
hypertension, proteinuria, adverse conditions when woman is pregnant
preeclampsia
local outpouching of vessel or heart chamber wall, usually in the abdominal aorta, most commonly caused by atherosclerosis and hypertension
aneurism
veins in which blood has pooled, producing distended, tortuous and palpable vessels
Varicose veins
inadequate venous return over a long period of time, which impairs blood flow to the area
chronic venous insufficiency (CVI)
the development of a thrombus in deep vein
deep vein thrombosis (DVT)
chronic ischemia of heart muscle, usually due to coronary artery disease
Chronic ischemic heart disease
the surface of a plaque experiences small disruptions, leading to the development of small thromboses, which cause periods of occlusion
Unstable angina
the clot lodges permanently in the vessel and the entire thickness of the myocardium becomes ischemic
STEMI
sometimes thrombus disintegrates before complete tissue necrosis: only sub endocardium affected
Non-STEMI
able to see due to necrosis and MI
Cardiac biomarkers
chest pain caused by transient myocardial ischemia not severe enough to cause necrosis
Stable angina pectoris
diverse group of diseases that primarily affect the myocardium, itself
Cardiomyopathy
narrowing of valve opening, causing turbulent flow and enlargement of emptying chamber
Stenosis
permits backward flow
Incompetent (regurgitant) valve
range from occasional “missed” or rapid beats to serious disturbances that impair the pumping ability of the heart
Disrhythmias/Arrhythmias
the most serious cardiac arrhythmia
Ventricular fibrillation
occurs when conduction is excessively delayed or stopped at the AV node or bundle of His
Heart block
when the heart is unable to generate an adequate cardiac output
Heart failure
volume of blood in the ventricle at the end of diastole
Preload
the more stretched the ventricle wall, the greater the force of contraction (up to a maximum value)
Frank-Starling law of the heart
resistance to ejection of blood from the left ventricle
Afterload
contractility (force of contraction) of muscle is the ability of the actin and myosin of the heart muscle to interact and shorten against a load
Inotropy
myocardial contractility is impaired, leading to a decrease in ejection fraction and thus cardiac output
Systolic heart failure
inability of right ventricle to move deoxygenated blood from systemic circulation into the pulmonary circulation
Right heart failure
when right heart failure occurs independently of left heart failure, in response to pulmonary disease
Cor pulmonale
decreased cardiac output
Cardiogenic shock
not enough blood volume, caused by loss of whole blood, plasma, or interstitial fluid in large amounts
Hypovolemic shock
result of massive vasodilation such that, although the volume of the blood has not changed, the amount of space containing the blood has increased, resulting in a decrease in BP below that required to drive nutrients across capillary membranes to the cells
Distributive shock
result of massive vasodilation resulting from overstimulation of the parasympathetic nervous system and under-stimulation of the sympathetic nervous system
Neurogenic shock
results from widespread hypersensitivity reaction, known as anaphylaxis
Anaphylactic shock
severe infection with a microorganism has two possible effects: the microorganism releases toxins that stimulate an overwhelming inflammatory response, and/or there is an overwhelming inflammatory response to the microorganism, itself
Septic shock
results from mechanical obstruction of the flow of blood through the central circulation
Obstructive shock
discomfort in breathing
Dyspnea
dyspnea upon lying down
Orthopnea
awakening at night with dyspnea
PND- paroxysmal nocturnal dyspnea
expectoration of blood
Hemoptysis
bluish discoloration of skin and mucous membranes, caused by increased amounts of deoxygenated hemoglobin in the blood
Cyanosis
selective bulbous enlargement of the end of a digit
Clubbing
increased carbon dioxide in the arterial blood
Hypercapnia/Hypercarbia
reduced oxygenation of arterial blood
Hypoxemia
reduced oxygenation of cells
Hypoxia
balance between alveolar ventilation and perfusion
V/Q ratio
blood moving through unventilated parts of the lung where blood physically doesn’t go through the lungs, due to defects in the heart
Physiological right to left shunt
multiple consecutive ribs are broken
Flail chest
presence of air in the pleural space caused by a rupture in the visceral or parietal pleura
Pneumothorax
presence of excess fluid in the pleural space
Pleural effusion
infected pleural effusion. A collection of pus in the pleural space
Empyema
collapse of lung tissue, by external compression, obstructed airways, inhalation of concentrated oxygen, decreased production of surfactant, etc.
Atelectasis
occlusion of a portion of the pulmonary vascular bed by an embolus
Pulmonary embolism
elevated mean pulmonary artery pressure
Pulmonary hypertension
characterized by airway obstruction that causes difficult exhalation
COPD
incomplete expirations
Air trapping
hypersecretion of mucous and chronic productive cough for at least 3 months of the year, for at least 2 consecutive years
Chronic bronchitis
a loss of lung elasticity and abnormal enlargement of the airspace distal to the terminal bronchioles, with destruction of the alveolar walls and capillaries
Emphysema
classic tripod breathing position, with lips pursed to increase lung pressure during exhalation, in an attempt to keep breathing passaged open
Pink puffer
hypoxemia and edema caused by eventual right heart failure
Blue bloater
more severe aspect of ALI
ARDS
inadequate gas exchange, leading to lower PaO2, higher PaCO2 and pH < 7.30
Acute respiratory failure
from V/Q mismatch, impaired diffusion
Hypoxemic respiratory failure
the increase in arterial CO2 is due to a failure in ventilation, which also causes hypoxemia
Hypercapnic/hypoxemic respiratory failure
inspiratory stridor, hoarseness and a barking cough
Croup
wheezing tone produced during inspiration, indicating obstruction of upper respiratory pathway
Stridor
indentations of skin around ribs and sternum, showing use of accessory muscles of respiration
Retraction
the return of stomach contents into the esophagus
GERD
upset stomach
Dyspepsia
a break in the protective mucosal lining of the lower esophagus, stomach or duodenum
Peptic ulcer
black foul smelling stools from digestion of blood
Melena
vomiting of blood, either bright red or “coffee ground” appearing
Hematemesis
chronic inflammatory disease that causes ulceration of the colonic mucosa, most commonly in the rectum and sigmoid colon
Ulcerative colitis
an urge to defecate, even if the colon is empty
Tenesmus
an abrupt increase in diameter of colon that could rupture
Toxic megacolon
inflammatory disease of the intestine, thought to be unregulated response against bacteria
Crohn’s disease
malabsorptive disease where the mucosa fails to absorb digested nutrients
Celiac disease
abnormally high blood pressure in the portal venous system
Portal hypertension
accumulation of fluid in the peritoneal cavity
Ascites
varicose veins in esophageal wall than can easily rupture
Esophageal varices
varices caused by collateral shunts between veins in abdominal wall
Caput medusa
liver dysfunctions and collateral vessels that shunt blood past the liver allow toxins to remain in bloodstream and reach the brain
Hepatic encephalopathy
flapping of hands
Asterixis
jaundice
Icterus
an irreversible inflammatory, fibrotic liver disease, casued by direct damage and inflammation from many disorders
Cirrhosis
nose bleeds
Epistaxis
the formation of gallstones
Cholelithiasis
inflammation of gallbladder
Cholecystitis
