Pathophysiology Katia Ferdowsi UCF Exam 1, PATHo!

Patho

suffering

Physio

Nature

ology

the study of

Pathophysiology

study of abnormalities in physiologic function of living things

What is the purpose of studying Pathophysiology?

Reveals physiologic responses of the body to

disruptions

four interrelated topics of Pathophysiology

Etiology

Pathogenesis

Clinical manifestations

Treatment implications

Etiology

study of causes & reason. identify causal factors that cause the disease

Risk factor

When factor is present it increases likelihood of disease. Knowing this prevents disease

Idiopathic etiology

unknown cause

Iatrogenic

causes from unintended/unwanted medical treatment

some etiologic classifications of disease

Congenital (inborn) diseases or birth defects

Degenerative diseases

Immunologic diseases

Infectious diseases

Pathogenesis

Developtment of disease. Starting from 1st stimulus to expression.

Pathogenesis describes

Describes how etiologic factors can alter physiologic function and lead to develop disease.

Symptoms

subjective abnormal feeling. ex: headache, nausea, pain

Signs

objective, observed manifestation of disease

Syndrome

set of symptoms & signs typically associated with a particular disease or condition

Latent Period

Time between exposure of infectious agent to first appearance of sign and symptoms

Prodromal period

first appearance of signs and symptoms indicating disease

Acute phase

disease in full intensity

Acute clinical course

less than a month, short lived sever manifestation. Short incubation period

Chronic clinical course

More than 1-3 months. can last month to years

Exacerbation

increased severity of signs and symptoms

Remission

decrease in severity; sign of cure >5yrs

Convalescence

stage of recovery after disease or surgery.

Sequela

Subsequent (coming after) condition result from acute illness. Ex: Paralysis is sequela of stroke

Complication

Secondary pathologic condition produced by the original problem

Treatment

Understanding the etiology, pathogenesis, and clinical

consequences of a particular disorder/disease/illness to help

general ______

three main Individual Factors affecting health and disease?

Culture,Age,Gender

Withstand the assault (Reversible cell injury)

if change is short lived the cell can withstand and then go back to normal

Cellular adaptation (reversible)

cell adapts by changing structure or function that can stand injury

Cellular death (irreversible)

cell death occurs if problem is prolonged

Ischemia

Most common cause of cell injury. This is inadequate blood supply to an organ. It injures cell faster than hypoxia. Ischemia deals with hypoxia

Hypoxia

lack of oxygen

Nutritional injury

inadequate of sufficient amount of fats,carbs,protein,vitamin, & minerals. this can injure the cell. Some cells are more susceptible than others.

infectious & immuno injury

Bacteria & viruses

chemical injury

Toxic chemicals or poisons can cause cellular injury

Physical mechanical injury

Temp, pain, electrical etc. Ex: Hypothermia from cold temperature

Reversible cell injury

Cellular swelling (hydropic) & Accumulation of excess substance in cell

Cause of swelling

- 1st manifestation could be malfunction in sodium- potassium pump. Accumulate sodium ions in cell. -

- Also injury with loss of ATP cause swelling.

Hydropic swelling Characterized by

large, pale cytoplasm; dilated endoplasmic reticulum; and swollen mitochondria

megaly

increase in size and weight

Intracellular accumulation

Space is taken up within cell so it can't grow. Accumulation of substance in cell = injury. Toxicity immune response, taking up space

Common site of intracellular accumulation

liver

Complex substrate + enzyme= soluble product

Without this enzyme the cell is filled with substrates that aren't soluble.

Chaperone protein

if there is protein damage then the number of ________________ increase to refold the protein. This accumulates within the cell.

Ubiquitin proteasome enzyme

degrades unfolded protein. This activates caspases which then leads to apoptosis

Atrophy

Respond to injury by reducing cell size.

Caused by:

-Disuse

-Ischmeia

-aging

- Nutrient starvation

Hypertrophy

Cell size increases with function. Ex: increase sex hormone= increase breast size or increase muscle= harder for ventricles to pump blood

Hyperplasia

increase cell #. This can be physio or abnormal due to mitotic division. Ex: callus on foot, rubbing/ irritation = accumulated cell death .

Metaplasia

replacement of differentiated cell type due to adaptation of persistent injury. Reversible

Ex: Barret syndrome: change of esophageal cells due to acid reflux burns. Goes back to normal once done.

Dysplasia

disorganized look on cells due to abnormal cell variation. adaptive effort gone bad. This can cause cancer. Preneoplastic lesion

Indication of cell death

pain, elevated enzyme levels, inflammation, loss of function.

Ex: Troponin enzyme level increases during a heart attack. This means cell death

Necrosis

Stage of dying, turns dark.

Consequences of ischemia/ injury.

Cell ruptures and spill components.

has inflammation

Apoptosis

Programmed cell death.

This can come with necrosis.

This is good in cancer so it can kill malignant cells

No inflammation

Coagulative Necrosis

Most common. Process begins with ischemia and then ends plasma membrane degradation. It is a solid substance. Gangrene is a form.

Liquefactive

occurs with dissolution of dead cells, liquification of lysosomal enzymes, and formation of abscess or cyst from dissolved dead tissue. Cell ruptures and the material flows out

Fat necrosis

Degeneration of fat cells. This comes from cell trauma or pancreatitis. Appears white and chalky.

Caseous necrosis

degeneration and death of tissue with a cheese-like appearance. Happens in lungs from tuberculosis

Gangren

cell death in large area due to interrupted blood flow.

Dry gangrene

form of coagulation necrosis. Blackened dry tissue. Separated from a line of demarcation of healthy tissue. caused by microorganism.

Wet gangrene

fatal. A form of liquefactive necrosis in internal organs

gas gangrene

fatal. Formation of gas due to microorganism. formation of damage muscle tissue in gas bubble form.

- result in infection of necrotic tissue by anaerobic bacteria (Clostridum).

Apoptosis

respond to injury that does not directly kil the cell.

- triggers intracellular cascades

- activate cell suicide response

- Not always pathologic

-No inflammation

Apoptosis is triggered by

Extrinsic (death receptor) & Intrinsic (mitochondrial response)

Extrinsic "death receptor"

Withdraws survival signal that stops apoptotic pathway.

- extracellular signal FAS ligand binds to cell and then triggers death cascade through "death receptors"

intrinsic mitochondrial pathway

response to cell damage.Protein P53 is normally in a low count but is increase one cell DNA has been damaged. This causes its own cell death.

Main component: Caspases.

Cellular aging

cell ages and functions/ size decreases

cumulative result factors of aging

1. progressive decline in repair of cells

2. exposure environmental factors.

Somatic death

Death of entire organism. No inflammation before death occurs.

To declare Death

- no cessation of respiration & heartbeat.

- Presence of stiff muscles (rigor mortis) due to release of lytic enzyme in body tissue (post mortem autolysis)

- brain dead= proof of somatic death

Congenital disorder

At birth, genetic or environment or both

Congenital malformation

structural defects caused by error in fetal development. Mainly due to genetics. If caused by environmental it is mostly unknown.

Inherited genetic disorder

found later in life. Not congenital

Gregor Mendel

discovered traits are passed down from parents to offspring

Chromosome characteristics

The total size

length arm of X

banding pattern once exposed to stain

Chromatids

2 identical linear chromosomes, separated in meiosis

Centromere

where the chromatids join

Diploid

- one member of pair from each parent

- pairs are homologous with different DNA sequence

- 23 pair total, 22 auto some (homologous), 1 sex chromosome.

- Female 2x Male 1X 1Y

Phenotype

physical appearance & biochemical attributes

Meiosis

2 germ cells (1 egg sperm) combine to make 46 chromosomes.

- Produce 4 haploid.

- Each germ cell has 23 chromosomes

- 2 divisions

Genetic Traits

Genes code for specific trait.

- Has particular position on chromosomes

- has several alleles

- 2 alleles for each gene (1 from each parent)

Codominant

allele not clearly dominant or recessive

Monogenic

results from interaction of 1 gene loci

Polygenic

interaction from several gene loci

- inheritable

-difficult to predict

-affected by environment factor (multifactoral)

Permanent change in DNA

is rare. Can be environmental due to potential mutagens : Radiation, chemicals, viruses

Point mutation

single base pair substitution

May cause affected codon (3 base pair) to signify abnormal amino acid

- Affects one amino acid

frameshift mutation

- Causes dramatic change in genetic code

- Addition/ subtraction of 1 or more base reading frame

- remaining codon triplets have altered the rest of the amino acid sequence.

Single strand vs double strand

single strand is easier to break.

Double strands are harder to break and can cause a permanent loss of genetic info at break point

Medelian gene disorders

loci & allele on chromosome is changed. A trait that can be predicted

Multifactorial

Caused by contributing factors other than genes. Ex: diabetes is caused by genes and other factors

Abnormal (aberrant) chromosome structure

caused by separation during meiosis

Anueploidy

Abnormal number of chromosomes, more or less than 23

Nondisjunction

failure of pairs to separate.

1st meiotic division failure to separate = 22 chromosomes

2nd meiotic division = 24 chromosomes

Combine abnormal with normal

produces fertilized cell with 45 or 47 chromosomes

Monosomy

Daughter cell with a deficiency of 1 chromosome
Usually not compatible with life

ex: Turner Syndrome

Similar to Anaphase lag (One chromosome left out of newly formed cell nucleus)

Polysomy

Daughter cell with to many chromosomes

- viable life with disability

- extra or missing chromosome

Abnormal chromsome structure

breakage/ loss/ rearranged pieces of chromosome during meiosis & mitosis

Meiosis errors

during crossing over

- chromosome portion is lost

- attach upside down

- attach wrong chromosomes

Mitosis errors

opportunity for it to break or rearrange

Translocation

exchange DNA pieces between non homologous chromosome