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83 Cards in this Set

  • Front
  • Back

Epidemiology

*Study of disease occurrence in human populations


*Analysis of patterns of people affected by a certain condition


*Determination of how disease is spread, how to control it, prevent it, and eliminate it

Incidence


(Epidemiology)

Number of new cases within a population at risk during a specific time


(Example: number of new cases of Hep. C in heroin addicts)

Prevalence


(Epidemiology)

Measure of existing disease in a population at a given point in time

Morbidity


(Epidemiology)

*Describes the effects an illness has on a person's life


*Persistence and long term consequences of a disease

Mortality


(Epidemiology)

Causes of death in a given population (Example: infant mortality rates)

Natural History

Progression and outcome of a disease without medical intervention

Prognosis

probable outcome and prospect of recovery from a disease; chances of survival

Purpose and Components of the Diagnostic Process

Purpose:


*accumulate info


*assess and evaluate the info collected


*integrate the info




Components:


*Interview


*Physical examination


*Other examinations (labs, imaging studies)

Signs

objective; seen, heard, or felt by another

Symptoms

subjective; only felt by the sick person

Does the interview look for signs or symptoms of the disease?




What other information should be collected during the interview?

Symptoms




family history, lifestyle, social history (smoking, sex, occupation), past medical history, medications (esp. elders), demographics (age, gender)

Physical examination

*Measurement of vital signs (BP, temp, pulse)


*Inspection: visualizing structure; swelling, redness, hair, weight, height


*Palpation: fingertips to feel size, location, etc.


*Percussion: using fingertips to tap over different parts of body


*Auscultation: listening to sounds of body (chest & abdomen with stethoscope)

Medical imaging studies (3)

*MRI: look at soft tissue


*CT scan: 360 degree manner


*X-ray: shadow/silhouette of bones

Etiology

study of the cause (of disease)

Hypoxic injury


*lack of oxygen; cannot undergo oxidative phosphorylation for ATP


Causes:


*Ischemia - insufficient blood supply (most common)


*heart disease, lung disease, RBC disorders

Anemic Hypoxia

*poor oxygen delivery


*iron deficiency, reduced RBCs, shitty hemoglobin

Ischemic Hypoxia

*impaired blood circulation


*inclusion of the artery

Histotoxic Hypoxia

*impaired utilization of oxygen


*tissue poisoning, blocks enzyme systems that work with oxygen

Hypoxemia Hypoxia

*reduced arterial oxygen levels


*lung disease

Effects of Hypoxia

*Hydropic swelling


*Glycolytic pathway


*Cell death


*Reperfusion injury



Hydropic swelling


(Effects of Hypoxia)



*Failure of the injured cells to maintain electrolyte balance through the Na+ / K+ - ATPase pump (needs ATP, lack of oxygen = lack of ATP)


*Decreased functioning of Ca2+ / Mg2+ - ATPase pump; activates enymes which damage the cell

Reperfusion injury


(Effects of Hypoxia)

*Blood supply is suddenly restored to tissue


*Oxygen acts as a free-radical = cell injury



Glycolytic pathway


(Effects of Hypoxia)

*Anaerobic metabolism (lactic acid builds up)

Nutritional deficiencies


(Effects of Hypoxia)

*poor intake (low intake of calories)


*excessive output (not absorbing nutrients)


*altered absorption (not enoughintrinsic factor for absorption of vitamin B12)


*impaired distribution (trans fat > plaques > obesity; excess glucose > diabetes mellitus)


*inefficient cellular uptake (lack of insulin)

Gangrene

*Mass of tissue undergoes cell death


*Caused by a loss of blood supply followed by bacterial growth (infection)




*wet - spreads rapidly & can be fatal; caused by blockage of venous blood flow


*dry - limited to the extremities and spreads slowly; caused by interfering with arterial blood supply to the tissue;

Chemical Injury (2)

Drugs: alcohol, Rx drugs (too much acetaminophen > liver problems), street drugs, OTC




Heavy Metals (Pb): in paint, contaminated soil, makeup; stored in bone, eliminated by kidneys; causes inactivation of enzymes, interference of nerve transmission, brain development

Hypothermia


(physical injury)


*vasoconstriction (to prevent heat loss, protecting internal organs); ischemia


*freezing, ice crystals form, rupture cell

Hyperthermia


(physical injury)

*microvascular coagulation


*speed up of cellular metabolic processes


*protein degradation

Electromagnetic radiation


(physical injury)

*direct breakage of chemical bonds


*ionization


*heat production


*disruption of neural, cardiac impulses


*hyperthermia

Mechanical deformation


(physical injury)

*Non-penetrating or penetrating


*blood loos or obstruction of blood flow


*hypoxia


*inflammation

Patho

disease

physiology

bodily function

health

a state of complete physical, mental, and social wellness

disease

pathologic condition; clinical signs, symptoms, and laboratory findings

Normal white cell count

4.0 - 11.0 x 10^9 / L

Reference Intervals

*usual values for all parameters within a healthy population

Pathogenesis

*the evolution, effect, & duration of a disease


*Onset: acute (sudden) vs. insidious (subtle)


*Duration: acute (one time) vs. chronic (reoccurring)

Syndrome

collection of signs and symptoms that usually occur together in response to a given condition

Signs and Symptoms can be localized or system

localized: one place; example: strep throat, swelling




system: multiple organ systems; example: fever, fatigue

Subclinical stage

no signs or symptoms but abnormal physiology and lab values

Prodromal Stage

Appearance of the first signs of symptoms

Acute Stage

Disease reaches its fullest intesity

sequela (pl. sequelae)


(Outcomes of Disease)

a condition that is the consequence of a disease


(example: neck pain from whiplash)

complications


(Outcomes of Disease)

new or separate process that arises secondarily to the original disease

resolution


(Outcomes of Disease)

return to normal function

Classification of Disease (7):


(the etiology)

*Inherited (from parents / genetic)


*Congenital (occur in utero)


*Toxic (Pb or alcohol poisoning)


*Infectious (caused by microorganisms)


*Neoplastic (new growth; cancer)


*Iatrogenic (caused by medical intervention)


*Idiopathic (unknown cause)

Cells have three responses to challenges:

*Reversible


*Adaptation


*Cell death

Hydropic swelling


(definition & cause)

water & sodium accumulation; Na+/K+ - ATPase pump not working properly; lack of ATP




caused by viruses, alcoholism, etc

Characteristics of hydropic swelling

*large, pale cytoplasm


*dilated endoplasmic reticulum


*swollen mitochondria

Cellular Accumulations


(Reversible Cellular Injury)

*Buildup of toxic substances that cells cannot immediately use or eliminate


*Categorized according to type of substance accumulated


*Example- fatty liver; delivery of free fatty acids is increased and disturbs metabolism


*Causes: diet high in fats, alcoholism, low glucose

Hemosiderosis


(in the liver)

*iron overload disorder


*brown deposits


*caused by intravascular hemolysis (mechanical injury, sickle cell anemia, thalassemia, frequent blood transfusions

Bilirubin Deposition

*Increased bilirubin production


*obstruction of bile duct into intestine


*diseases that affect liver's ability to remove bilirubin from the blood (jaundice)

Asbestosis

*Inhalation of asbestos fibers


*deposits in lung tissue


*scar tissues formation


*causes mesothelioma and lung cancer

Cellular Adaptation

*Atropy


*Hypertrophy


*Hyperplasia


*Metaplasia


*Dysplasia


*Anaplasia

Atrophy

*cellular shrinkage; decreased functional capacity


Causes:


*disuse


*chronic nutrient starvation


*neurological disorder / central nervous system


*denervation (injury to nerve)


*alchemia (cutting off blood supply)

Hypertrophy

*larger in size; increase in functional capactiy


*seen in skeletal and cardiac muscle


Causes:


*increased function (body builders)


*high blood pressure (hypertension)

Hyperplasia

*increase of cell number


*increase in functional capacity


Caused by:


Physiological


*hormonal stimulation (pregnancy)


*chronic irritation


*regeneration (wounds; tumors)


Non-physiological


*hormonal (endometriosis; enlarged lining)


*growth factors (produced by viruses; HPV)

Metaplasia

*persistent injury; chronic irritation & inflammation


*reversible conversion of 1 type to another


*replacement of glandular epithelium with squamous epithelium

Dysplasia

*disorganized appearance of cells


*loss of adaptive effect


*potentially reversible after the stimulus is removed


Causes:


*chronic irritation or infection


*implicated as a precursor to cancer

Papanicolaou (Pap) smear

checks for HPV which leads to cervical cancer; 1:4 to 1:1

Anisocytosis

unequal or different size

Poikilocytosis

abnormal shape

Hyperchromatism

excessive pigmentation

Mitotic figures

abnormal cell division

Anaplasia

*differentiated body cells return to an undifferentiated (irreversible) state


*associated with malignancy


Features:


*loss of polarity


*loss of specialized functions


*vary in shape (pleomorphism)


*altered nucleus


*hyperchromatism

Neoplasia

New growth (cancer)

Neoplasm

Abnormal mass of proliferating cells


Benign - grow slowly; stays confined in the tissue it originated in


Malignant - fast growth rate; poorly differentiated; spreads

Cell death (two types)



*Occurs when an injury is too severe or prolonged to allow cellular adaptation or repair




*Apoptosis - normal cell death (beneficial)


*Necrosis - abnormal cell death

Apoptosis

*Elimination of injured or aged cells


*"Programmed cell death"


*Responsible for localized deletion of cell during normal cell development

Characteristics of Apoptosis

*Shrinkage and condensation of nucleus and cytoplasm


*Chromatin aggregation at the nuclear envelope


*Nuclear fragmentation


*Apoptotic bodies

Nuclear changes during apoptosis

*Pyknosis - irreversible condensation of chromatin in the nucleus


*Karyorrhexis - fragmentation of the pyknotic nucleus


*Karyolysis - complete dissolution of chromatin

Normal physiologic processes of Apoptosis

*Embryonic development (fingers and toes)


*Maintenance of homeostasis


*Immune system (rids of B & T cells that produce autoimmune response)

Two basic pathways of Apoptosis

Extrinsic (death receptor)


*Extracellular signaling proteins bind to the cell surface molecules and trigger apoptosis




Intrinsic (mitochondrial)


*Cytochrome c (from mitocondria moves to cytoplasm)


*Activated by conditions such as DNA damage, hypoxia, decreased ATP levels



Necrosis

*Pathologic cell death


*Unregulated enzymatic digestion of cellular components


*Loss of plasma membrane integrity (intracellular > extracellular; provokes immune response)


*Interferes with cell replacement and tissue regeneration

Nuclear changes during necrosis

*Pyknosis - irreversible condensation of chromatin in the nucleus


*Karyorrhexis - fragmentation of the pyknotic nucleus


*Karyolysis - complete dissolution of chromatin

Other cell changes during necrosis


(that don't occur during apoptosis)

*swollen cell volume


*dispersed ribosomes


*disrupted plasma membrane


*disrupted organelle membranes

Types of Necrosis

*Coagulative


*Liquefactive


*Fat


*Caseous

Coagulative Necrosis

*Most common


*Retention of architectural pattern (you can tell what it looked like)


*Dense in comparison to surrounding tissue


*acidic pH, breaks down enzymes


*Mechanism = hypoxic injury



*Appearance of Coagulative Necrosis

*Composed of denatured proteins that are dissolved by proteolytic enzymes and replaced by scar tissue




*Example: Gangrene

Liquefactive Necrosis

*Cells die, enzymes are not destroyed


*transformation of tissue into viscous liquid mass


*formation of cyst (fluid, puss, air)


*associated with injury in brain and following infections


*seen when dissolution of dead cells occurs quickly


*liquefied area of dissolved tissue




*Example: lung

Fat Necrosis (from Acute pancreatitis)

*leakage of enzymes (lipase)


*break down adipose cells and split triglycerides within the cells


*release of fatty acids


*Fatty acids combine with Ca2+ to form chalky white areas called soaps

Fat Necrosis (from Trauma / Mechanical injury)

*Physical injury of adipocytes releases triglycerides


*Triglycerides are hydrolyzed by serum lipases to free fatty acids


*Free fatty acids combine with Ca2+

Caseous Necrosis

*Characteristic of injury to lung tissue by mycobacteria


*No histologic architecture is preserved


*dead cells remain indefinitely as a soft, clumpy debris (clumpy cheese)




*Example: mycobacterium tuberculosis