patho Exam 1 (final cards)

What is atrophy?

decrease in cell size

What is hypertrophy?

increase in cell size

What is hyperplasia?

increase in cell #

What is dysplasia?

change in cell size, shape, structure

What is metaplasia?

reversible replacement

* of a mature cell by another less mature cell

Why does atrophy occur?

decreased…

* workload
* use
* blood supply
* pressure

What is Cerebral Atrophy?

* decrease in size of cells in the cerebrum
* decrease in the size of neurons

Why does hypertrophy occur?

increase functional demand

Cardiac Hypertrophy Clinical Manifestation

* SOB
* Chest pain
* syncope
* impaired cardiac function

What is the precursor to cancer

Dysplasia

What is Apoptosis?

programmed cell death

* body send signals → cells kill themself

What is Necrosis?

irreversible cell damage

* death of cell

What Causes Cell Injury?

* physical (break)
* mechanical
* thermal (burn)
* chemical (radiation)

Cervical Metaplasia & Dysplasia Pathology

cellular adaptation of the squamous & epithelial columnar cells in the transformation zone of the cervix.

Cervical Metaplasia & Dysplasia Risk Factors

* early sex activity
* multiple sexual partners
* smoking
* HPV

Cervical Metaplasia & Dysplasia Treatment

* Abalation → removal of superficial cells
* Cold Coagulatation
* surgical excision

What is Cellular Proliferation?

new daughter cells generated from division of parent cells

Meiosis

results is ooeytes & sperm

Mitosis

division & proliferation of all nongerm cell

* is continuous

Cellular Differentiation

orderly process of cellular maturation to achieve a specific function

Stem Cells

cells that haven’t decided what they wanted to be yet

Progenitor Cells

cells that have an assignment

* know what they wanna be

Altered Cellular Proliferation & Differention

* gene malfunction goes unrepaired
* cell is allowed to grow uncontrollably
* cell loses ability to carry out its specific function

Carcinogens

* radiation
* tobacco
* hormones
* microbes
* chemicals

Carcinogenesis

origin & development of cancer

Oncogenes

code for proteins involved in cell growth or regulation

Tumor-Suppressor Gene

prohibits growth of cells & regulates apoptosis (cell death)

Benign Tumors

* remained localized
* slow growing
* easier to treat
* closely resembles tissue of organ
* may function as normal cells

Malignant Tumors

* invasive & destructive
* proliferates rapidly
* spreads to other sites
* does NOT resemble tissue of origin

Treatment of Cancer

* surgery
* chemo
* radiation
* bone marrow transplant
* immunotherapy
* palliative care
* hormones

Lung Caner Patho

* leading cause of cancer deaths worldwide
* from smoking & industrial exposure
* tumors originate most frequently in epithelial lining of bronchi, bronchioles & alveoli

Lung Caner Clinical Manifestations

* persistent cough
* SOB
* chest pain
* hemoptysis (coughing up blood)

Diagnosing Lung Caner

* Biopsy
* CBC
* Chest X-ray
* Bronchoscopy

Leukemia Patho

malignant neoplasm of blood & blood-forming organs

Leukemia Clinical Manifestations

* anemia
* bone pain
* weight loss
* lymph node enlargement
* fever
* nausea
* bruising

Leukemia Treatment

* chemo
* radiation
* bone marrow OR stem cell replacement

3 Lines of Defense

1. skin & mucous membranes
2. inflammatory response
3. immune response

First Line of defense

healthy skin & tissue

What happens If the invader penetrates the 1st line of defense?

* sloughs off skin
* vomit from the stomach
* coughs up mucus
* flushes out in urine

What do normal flora do

eradicate pathogens

Second Line of defense

VASCULAR RESPONSE

* increase capillary permeability
* tissue creates barriers to prevent spread
* inflammatory mediators help widen/loosen blood vessels

Histamine

MOST IMPORTANT VASODILATOR

* increase vascular permeability
* produced by mast cells
* seen early in inflammation

Acute Inflammation Response Clinical Manifestations

* arterioles constrict briefly
* hyperemia (due to arteriole dilation)
* rubor (redness)
* tumor (swelling)
* exudate
* dolor (pain)
* calor (heat)
* altered functions

Cardinal Signs of Inflammation

* heat
* redness
* swelling
* pain
* loss of function

Mnumonic “DOCTOR”

Dolor

LOss of function

Calor

Tumor

LOss of function

Rubor

Treatment of inflammation

RICE

* rest
* ice
* compression
* elevation

Chronic Inflammation

Persistent injury

* lasting several weeks or longer
* ex: arthritis

Acute Inflammation

the response to sudden body damage

* Ex: cutting your finger

Rheumatoid Arthritis Patho

* chronic inflammation of synovial membrane & hyperplasia

Rheumatoid Arthritis Clinical Manifestation

* mildly-debilitating
* pain, stiffness
* redness, heat, swelling
* decrease mobility

Rheumatoid Arthritis Treatment

* meds that induce remission
* rest/activity balance
* physical therapy
* splints
* surgery
* swimming

Acute Pancreatitis Patho

caused by:

* duct blockage by gallstones
* excessive alcohol use

Acute Pancreatitis Clinical Manifestations

* dull steady ache
* radiating to back
* nausea, vomiting, anorexia, diarrhea

Acute Pancreatitis Treatment

* IV hydration
* Analgesics
* Surgery to remove gallstones

Chronic Pancreatitis Patho

duct obstruction by enzyme & proteins

* ischemia
* loss of function
* excessive alcohol use

Chronic Pancreatitis Clinical Manifestations

Abdominal Pain

* severe but gets better after eating
* mid or upper r.sided → radiating to back
* diarrhea
* weight loss

Chronic Pancreatitis Treatment

* pain management
* surgery
* behavior mods
* stop smoking & drinking
* exercise
* nutrition

Acute Sinusitis Patho

blockage of ostia & outflow of mucus due to allergy, viruses, & other irritants

* impaired clearance of mucus of cilia
* alt mucus quality
* cystic fibrosis

Acute Sinusitis Clinical Manifestations

* facial pain over sinus region
* fever
* nasal congestion
* x-cessive nasla discharge
* persistent cough
* fatigue

Acute Sinusitis Treatment

* antibiotics
* antihistamines
* decongestants
* nasal spray
* surgical

Chronic Sinusitis Patho

MULTIFACTORAL

* environmental factors
* allergens
* persistent factors
* genetic factors
* metabolic abnormalities
* immune deficiencies

Chronic Sinusitis Clinical Manifestions

* nasal congestion
* nasal discharge
* fatigue
* sore throat
* pain/facial discomfort
* headache
* chronic cough
* foul breath

Chronic Sinusitis Treatment

* glucocorticoids
* antibiotics
* nasal saline irrigation
* surgery

What is Innate Immunity?

1ST RESPONDERS

* present @ birth
* cells of the immune system surround invader → invader is killed inside immune system cells (phagocytes)
* made up of skin, cornea, mucous membranes that live in Resp, GI, GU tracts

Major cell types of the innate immune system

* macrophage
* neutrophil
* basophil
* Eosinophil
* dendritic cell
* natural killer T cell

What is Adaptive Immunity

### A type of immunity that develops when a person's immune system responds to a foreign substance or microorganism, such as after an infection or vaccination.

Active immunity

* development of antibodies to antigens (natural)
* achieved by having specific disease or vaccine (vaccination)

Passive Immunity

* immunity transfer from host to recipient
* achieved via mother → infant transfer injection of antibody

Major cell types of the adaptive immune system

* B-cell


* T-cell
* antibodies
* dendritic cell
* natural killer T cell

Specificty

targeted response to an antigen

Diversity

recognizes a multitude on antigens

Memory

rapid-response to a previously known antigen

Self & Non-Self recognition

can tell a foreign antigen from a normal body

* when this malfunctions = auto immune disease

Cytotoxic T-cells

CD8

* A type of immune cell that can **kill certain cells**, including foreign cells, cancer cells, and cells infected with a virus. 

Helper T-cells

CD4 (master switch)

A type of immune cell that stimulates killer T cells, macrophages, and B cells to **make immune responses.** 

Humoral Immunity

production of B-lymphocytes (fight all over)

* antibodies secreted from plasma cells
* IgA, IgD, IgE, IgG, IgM

\*\***MEMORY CELLS** (take 4-5 days to develop)

Primary Adaptive Immune Response

activation w/ 1st recognition of a specific antigen

Secondary Adaptive Immune Response

reactivation w/later recognition of the same antigen

Altered Immune Function - Host Defense Failure

* antigen variation
* viral latency
* immunodeficiency (primary vs secondary)

Altered Immune Function - Hypersensitivity

* Type I

IgE mediated immediate reaction.

* allergies

Altered Immune Function - Hypersensitivity

* Type II

Antibody-mediated reaction (IgG or IgM antibodies)

Altered Immune Function - Hypersensitivity

* Type III

Immune complex-mediated reaction → autoimmune disease

Altered Immune Function - Hypersensitivity

* Type IV

\
Cytotoxic, cell-mediated, delayed hypersensitivity reaction.

Altered Immune Function - Autoimmunity

* failure to distinguish self from non-self
* causes damage to specific organs or to the entire system

Altered Immune Function - Alloimmunity

* graft rejection
* graft vs host disease

Altered Immune Function - clinical models

* Anaphylactic Reaction

Exaggerated systemic immune response due to a type 1 hypersensitivity reaction

* antigen exposure stimulates an IgE mediated response in a previously sensitized individual
* degranulation of mast cells & basophils → causes local & systemic response

Anaphylactic Reaction Triggers

* insect stings
* food allergies
* drug allergies

Anaphylactic Reaction Clinical Manifestation

* Phase 1

* difficulty breathing
* skin flushing & itch
* angioedema

Anaphylactic Reaction Clinical Manifestation

* Phase 2

* difficulty breathing
* severe hypotension
* severe edema

Anaphylactic Reaction Diagnosis

* allergy testing
* HX & physical exam

Anaphylactic Reaction Treatment

* Symptomatic

* drugs to relax bronchial smooth muscle
* drugs to constrict vascular smooth muscle
* limit inflammation

Anaphylactic Reaction Treatment

* Preventative

desensitization to allergy

IF an Rh- woman is carrying an RH+ fetus →…….

Rh+ cells enter her bloodstream during pregnancy or childbirth

* she produces Rh+ anti-bodies

Foreign antigens stimulates women’s body to make antibodies →……

Anti Rh+ antibodies bind antigen on RBC’s of Fetus

* Fetus RBC are destroyed

Rh Isoimmunization Pathology

Type II cytotoxic antibody-mediated reaction

* antibodies against the Rh antigen (anti-D) attack RBC’s causing hemolysis
* often occurs in Rh-negative mothers exposed to fetal Rh- positive antigen

Rh Clinical Manifestations

* fetal effects

* anemia
* hydrops (edema)
* death

Rh Clinical Manifestations

* Infants

* lethargy
* hearing loss
* cerebral palsy
* kernicterus (bilirubin deposits in brain)

Rh treatment

* risk reduction

prenatal visits

Rh treatment

* Prevention

administration of Rh immunoglobulin to prevent maternal sensitization to fetal D antigen

Rh treatment

exchange transfusions to replace damaged RBC’s w/ healthy ones