Patho Exam 1 Flashcards
CONTROL CENTER of the cell, contains GENETIC INFORMATION
Nucleus
phospholipid BILAYER made of fatty acids tails on inside & water-soluble heads on the outer
plasma membrane
assembles RIBOSOMES
nucleolus
PROTEIN factory, builds proteins out of amino acids which are the building blocks
ribosome
“HOUSEKEEPER”, gets rid of wastes & breaks down cells & substances
lysosomes
-“POWERHOUSE” of the cell
-converts organic nutrients into cell energy (makes ATP)
-aerobic
-get it from your mother
mitochondria
PROTEIN SYNTHESIS, houses ribosomes, like a maze
endoplasmic membrane
PROTEIN synthesis from attached RIBOSOMES
rough ER
produce LIPIDS, FAT transportation & SEX HORMONES
smooth ER
they release long/stiff fibers called microtubules that split the cell apart during cell division
centriole
“DETOXIFIES” products in cell by oxidation/ produces TOXINS to NEUTRALIZE free radicals
peroxisomes
“POST OFFICE” can synthesize large carbs/ PACKS PROTEINS & LIPIDS, like insulin, for later secretion through vesicles
Gold Apparatus
what type of substances can pass more easily across a cell membrane?
LIPID soluble substances (not water soluble substances!)
how does cell communication occur?
receptors act like LOCKS & KEYS
-things that act w/ these receptors are hormones, meds, neurotransmitters
-protein channels let things in/out
What happens in oxidation which is a type of aerobic metabolism?
oxidation- process of losing electrons & gaining oxygen
aerobic metabolism- max amount of ATP, most cells function this way
what is the difference in transcription & translation?
Translation- DNA to RNA (takes place in nucleus)
Transcription- mRNA to amino acids (takes place in the RIBOSOMES)
what is the difference between passive and active transport?
passive- does NOT require ATP, moves down a concentration gradient
active- requires ATP
what type of transport is Sodium Potassium Pump?
Active Transport!
sodium potassium pump= Na on outside, K on inside… 3 Na pump out for every 2 K in
maintains levels in the pump which is crucial to balance the function of homeostasis
which cells regenerate themselves & which do not?
Regenerate cells: WBC, RBC, Platelets, liver
non-regenerate: hepatocytes (liver), neurons in brain, cardiac muscle
what are the types of cell adaptation and give examples
- Atrophy- declining (ex: muscle atrophy/paralysis (low nerve simulation)/low nutrition/ischemia/ aging
- Hypertrophy- increasing (ex: hypertension= overused big heart/ weightlifting/ fever)
- dysplasia- disordered cell, functions differently, not the true adaptation of cell, abnormal change (ex: cervical cancer- change of cells in cervix)
- hyperplasia- increase in number of cells (breast tissue w/ pregnancy, keloid scar, BPH aka benign prosthetic hyperplasia)
- metaplasia - cells look different, one cell changes to another (Ex: Barrett’s esophagus/ GERD)
- neoplasia- lack adhesion to other cells, lack normal function (Ex: cancer - any time cells undergo mitosis = risk for cancer)
well differentiated, NOT metastasized aka spreading
BENIGN
poorly differentiated, cells are completely different, possible metastasize aka spreading
MALIGNANT
what are the 8 categories of cell injury?
hypoxic injury
free radical injury
chemical injury
physical injury
infectious agents injury
nutrition imbalances
genetic defects
injurious immunological reactions
type of cell injury that lacks O2
hypoxic injury
type of cell injury that is reactive oxidative stress, antioxidants fight them off
(ex: uncontrolled diabetes- high glucose conc. , uncontrolled hypertension- high bp)
**all cause high O2 consumption
fever, cancer, radiation also can cause these!
examples of disorders that are associated with this type of cell injury included Alzheimers, atherosclerotic heart disease, cataracts, cancer, emphysema, aging
free radical injury
type of cell injury where poisons such as led poison, carbon monoxide, & alcohol attack membrane first
chemical injury
type of cell injury that includes a cut, falling, MVA
physical injury
type of cell injury where there is too much fat & cholesterol
nutritional imbalances
type of cell injury that includes down syndrome, turner’s disease
genetic defects
type of cell injury includes autoimmune disorders like diabetes, lupus, COPD, anaphylactic reactions like allergic reaction asthma
immunological reactions injury
type of cell injury that includes viruses, bacteria, fungi, parasites. Each microorganism carries out injurious cell processes in a distinctive manner. Ex: HIV, helicobacter pylori which causes peptic ulcer disease
infectious agents of injury
things that can accumulate in the cell & cause problems
Intracellular accumulations
examples, signs/symptoms of intracellular accumulation
-too much glucose in the cell
-too much cholesterol which causes irritation to our arteries
-enzymes not being eliminated by digestion so they build up
types of cell death
- apoptosis- genetically programmed cell death, eliminates unwanted cells….. cells that resist apoptosis can give rise to cancer (ex: hashimoto’s causes gradual failure of thyroid gland bc of increased apoptotic cell death)
- ischemia- blood flow is restricted to a body part (lack of O2) … only certain types of cells have so long once in ischemia (brain; 6 mins, heart; 20 mins, skeletal muscles; several hours)
- prolonged ischemia- infarction cell death (ex: mitochondrial infarction)
- infarction- ischemic necrosis
- necrosis- “messy” process of cell death, due to stressors or insults that overwhelm their ability to survive, irreversible.. brain liquifies (bacterial meningitis cross through blood brain barrier), lung tissue destroyed by TB becomes dense & cheese like, gangrene (fatal unless surgical debridement, amputation, antibiotics…EX of gangrene= clostridium perfringens which emits gas odor, anaerobic bacteria)
what is regenerative therapy & cloning
-cells taken away from embryo in blastocyst stage, cells have potential to become any new organ
-proposed future treatment for sickle cell, Parkinson’s, tissue repair, replacement organs aka cloning (ex: skin grafts for burns)
explain how genetic damage affects DNA? What are the genes that trigger cancer cell mutations? what is a common cause of this cancer gene mutation?
-codons of mutations on a gene from a specific allele
-this happens during transcription & translation maybe from radiation or another outside environmental like smoking
x-rays, radiation treatment, chemo are examples of what?
ionizing radiation
What happens in the cell when there is hypoxic injury?
decrease of O2 so there is a decrease in ATP production
what is a free radical & what can protect against them?
it is a harmful agent.
antioxidants (vitamins) protect against them!
examples of antioxidants
vitamins such as A, C, E and minerals such as copper, zinc, selenium
how are antioxidants helpful?
they neutralize free radicals aka a harmful agent
the study of the interactions of all the nucleotide sequences (not just genes) within an organism …. study of genes & their interactions
genomics
foundation to study gene function in health, disease, & responses to medications (how genes influence an individual’s response to meds)
pharmacogenomics
when cells aren’t in the process of dividing, in loose form in nucleus
chromatin (noodle shape)
when cells are ready to divide, chromatin condense and coils into this
chromatid (picture top half of chromosome)
2 chromatids attached in the middle by centromere in each of the chromatid pairs, one comes from mom and 1 from dad
chromosome (x shaped)
what is DNA made of
pentose sugar (deoxyribose)
phosphate molecule
nitrogenous base
single stranded, ribose, uracil instead of thymine
RNA
segments of 3 nitrogenous base pairs which represent an animo acid … these make up proteins!
codon
occurs when a gene is damaged or changed in such a way that it alters the genetic code carried by that gene… can be inherited or sporadic (by chance in the absence of mutagens aka mutation causing agent)
mutation
change in DNA or RNA, some of these changes may cause a disease..
caused by radiation, industrial chemicals, smoke…
common changes in DNA sequence are called polymorphisms
mutation
gene vs genotype
gene- basic unit of inheritance made of sequence of DNA
genotype- the composition of genes at a given locus
this predicts the genotypes of a particular cross or breeding experiment
Punnett square
appearance of an individual, the result of both genotype & environment
phenotype
an ordered display of an individual’s 23 pairs of chromosomes, identifies an individual like how fingerprints are used
karyotype
body traits, 22 pairs of the 23 pairs of chromosome (the 23rd is the sex chromosome)
autosomes
2 specific genes (an allele) for the SAME trait
homozygous (HH or hh)
alleles that are different
Heterozygous (Hh)
traits that are not sex linked
autosomal traits
trait expressed only when inheriting defective gene from BOTH parents, individual is homozygous for the abnormal gene, 25% chance that the offspring will be affected by the disease, 50% they will be a carrier… both parents have to be carriers (Ex: cystic fibrosis, sickle cell)
autosomal recessive
trait expressed whenever the gene is present from EITHER parent, any child who inherits the trait will develop this disease, 50% chance offspring will be affected (Huntington Disease or Marfan Syndrome aka tall)
autosomal dominant
trait that is expressed in any male that carries the affected gene. males are affects, females are carries! (Ex: klinefelters aka men have extra X, turner’s syndrome aka women missing an X)
X- linked
what causes cystic fibrosis?
auto recessive; thick mucus produced by the exocrine glands, affects most body systems, shortened life expectancy, salty sweat, whites of Northern European , neither parent has it but BOTH are carriers
what causes sickle cell anemia?
auto recessive; both parents are carriers, sickle cells get stuck in smaller arteries/veins, causes RBCs to become sickle shaped, increased in African Americans, vast-occlusion: pain/damage to tissues throughout body
what causes Tay-Sachs disease?
auto recessive, lysosomal storage disease, inability of lysosomes to break down cell membranes, distention & cell death, appear normal til 6 months and death by age 3, cherry red spots on retina, causes poor motor coordination lethargy, muscle flaccidity, increase cognitive impairment
monosomy of the sex chromosome, girl who has only 1 X chromosome, webbed beck, shield like chest with underdeveloped breasts, widely spaced nipples, imperfectly developed ovaries, hypothyroidism, short stature, female genitalia
Turner’s syndrome
boy born with extra X chromosome, XXY, testosterone deficiency, small testes, absent body hair, long limbs, sterile, decreased muscle mass, gynecomastia (bigger breasts)
Klinefelter’s Syndrome
Trisomy 21; have an extra chromosome, 3 of the 21st chromosome, heart defects, mental retardations, shorter life, hypothyroidism, leukemia, greater risk in moms over 30 yrs
Down syndrome
disorder caused by multiple gene abnormalities & environmental factors, Cleft lip and palate, congenital hip dislocation, diabetes, heart disease, possible schizophrenia, tend to involve malformations of a single organ, runs in families, Cancers of the breast, ovaries, bowel, prostate, and skin. High blood pressure and high cholesterol.
multifactorial defects
3 lines of defense against invaders/injury
-1st line of defense: mechanical/chemical barriers
-2nd line of defense: inflammation response, phagocytosis
-3rd line of defense- specific immune responses, natural killer cells
fast, non-specific, no memory
inflammatory response
slower, specific, has memory
immune response
what triggers acute inflammation?
cellular & tissue injury
5 local cardinal signs of inflammation
- rubor (redness)- histamine
- tumor (swelling)- increase in vascular permeability, WBS leak out
- calor (heat)- histamine
- dolor (pain)
- loss of function
-inflammatory mediates (histamine & bradykinin)- blood vessels dilate & become permeable
-permeability: fluids, WBCs, platelets travel out the site of injury or infection
-vasodilation: enhanced capillary permeability
-allowing fluid to flow out of blood vessels to the injured tissues
-swelling
What stage of acute inflammation is this?
Stage 1: Vascular Permeability
3 stages of acute inflammation
Stage 1. vascular permeability
Stage 2. cellular chemotaxis
Stage 3. systemic responses
-attract microbial agents, endothelial cells, WBCs to the site of injury/infection
-line up along area of inflammation (margination)
-releases inflammatory mediators that amplify the inflammatory process
What stage of acute inflammation is this?
Stage 2: Cellular Chemotaxis
-fever, pain, general malaise, lymphadenopathy, anorexia, sleepiness, lethargy, anemia, weight loos
What stage of acute inflammation is this?
Stage 3: Systemic Responses
chemical signal from microbial agents, endothelial cells, WBCs attracts platelets & other WBCs to the site of injury
chemotaxis
s/s of inflammation
acute- fever, pain, general malaise, lymphadenopathy, anorexia, sleepiness, lethargy, anemia, weight loss
what is a pyrogen & what chemical mediator is released to cause fever?
pyrogen- substances that cause fever
chemical mediator- cells (cytokines) or the bacteria (prostaglandins)
**pyrogens activate prostaglandins to reset the hypothalamic temperature regulating center in the brain to a higher level.
**An antipyretic agent = drug that brings down fever
meds that are antipyretic
Tylenol, ibuprofen, acetaminophen, aspirin
**NEVER give kids aspirin or any salicylate-containing products for fever
normal range of WBC
5,000-10,000
bacterial, acute inflammatory process is occurring. Neutrophils & bands will be above normal range
shift to the left WBC
viral
shift to the right WBC
immature neutrophils
bands
measures the total number of WBCs and calculates the percentages of specific types of WBCs within the total
differential count
cells involved in inflammation (WBCs)
-neutrophils
-lymphocytes
-eosinophils
-basophils
-monocytes
What leukocytes arrive first?
neutrophils are 1st responders and begin the process of phagocytosis
bacteria that’s resistant to being killed by macrophages
TB, Mycobacterium
what does release of histamine cause?
-increase in arteriolar vasodilation
-large artery vasoconstriction
-increased permeability of venuoles
These amplify or deactivate inflammation (messengers, signaling proteins)
cytokines
3 major types of cytokines
- tumor necrosis factor alpha (TNFa): cell signaling protein involved in systemic inflammation and is one of the cytokines that make up the acute phase reaction
- Interleukins (IL-1): causes fever/systemic response
- Interferons (effective against viruses): a group of signaling proteins made and released by host cells in response to the presence of several viruses
involves recognition and attachment of the leukocyte to the foreign matter, engulfment, and degradation or killing of ingested matter
phagocytosis
these are also referred to as polymorphonuclear leukocytes (PMNs), also called bands or stabs in immature form
neutrophils
mass of cells/fluid that seep out of blood vessels or an organ, especially in inflammation
exudate
fluids that pass through a membrane or squeeze through tissue or into the EXTRACELLULAR SPACE of TISSUES.
transudate
serous
clear
sanguineous
bright red
serosanguinous
pink
purulent
yellow, stinky, thick
acute vs. chronic inflammation
acute: occurs rapidly in reaction to cell injury, rids the body of the offending agent, enhances healing, terminates after a short period of hours or days.
chronic: occupes when inflammatory reaction persists, inhibits healing, causes continual cellular damage and organ dysfunction, long term… this often causes a granuloma
example of disorders associated with chronic inflammation
TB, RA, atherosclerosis
injured cells are replaced with same cell type & structure & function is returned
regeneration
replacement with connective fibrotic tissues (formation of scar tissue) that doesn’t function the same way as original cells
repair
5 stages of cell cycle
Interphase: growth phase, cell spends most of its time in this phase
G0 (resting): cells are resting, not undergoing mitotic division
G1 (growth): cells enter cycle during this stage, prep for mitosis
S (synthesis): cells duplicate in prep for mitotic division
G2 (gap): cells undergo actives before mitosis, RNA and protein synthesis occurs during this phase
M (mitosis): cell complete mitosis, divides to regenerate itself. Includes nuclear and cytooplasmic division
3 classifications of cells according to their regenerative potential
Labile
Stable
Permanent
What is a classification of cells according to their regenerative potential that …
continually divides/replicates throughout life, replaces cells that are constantly eliminated (Ex: skin, hair, nail, cancer cells)
Labile
What is a classification of cells according to their regenerative potential that …
cells are resting stage until stimulate, when they enter the cell cycle (Ex: none cells, hepatocytes)
Stable
What is a classification of cells according to their regenerative potential that …
cannot regenerate, don’t enter the cell cycle (Ex: neurons, cardiac myocytes)
*adult stem calls can be stimulate to regenerate permanent cells
Permanent
3 phases of wound healing process
primary intention: aka primary union, lease complicated type, simple rapid healing (ex: surgical wound), no missing tissue
secondary intention: when there is extensive loss of tissue within wound, repair is more complex. regeneration isn’t possible. substantial scar formation and thinning of epidermis occurs. wounds are highly susceptible to infection, complications, deformity (ex: decubitus ulcer)
tertiary: aka tertiary union, would is missing large amount of deep tissues and is contaminated. it’s cleaned & left open x4-5days before closure. may require packing of sterile gauze, drainage tube, commonly requires skin graft
new capillaries begin to form to provide blood / oxygen, needed to nourish growth of fabulation tissue & epithelial cells, fibroblasts release growth factors attracting epithelial cells
Angiogenesis
fibroblasts form fragile, moist, red tissue collagen bed (24-48hrs), fills wound, fibroblasts product collage for days, weeks, months
granulation tissue
epithelial cells begin to grow into wood from healthy surrounding tissue, gradually matures covering wound in epidermal layers, requires a moist wound bed of granulation tissue with no necrotic tissue, slowed if basement membrane not intact
Epithelialization
granulation is replaced and fibroblasts die off, collagen and other substances fill the wound/scar tissue
collagen deposition
connective tissue that synthesizes collagen, provides the extracellular matrix
fibroblasts
4 types of tissue
epithelial
connective
muscle
nervous
3 types of muscle tissue
- cardiac- involuntary/no striation
- smooth- involuntary/ no striation
- skeletal- voluntary/ striation
why might a would develop scar tissue?
when myofibroblasts overproduce collagen during the healing process
factors that affect wound healing
- nutrition - lack of nutrients
- oxygenation
- circulation - lack of circulation
- immune strength - diabetes, cancer, aging, corticosteroids use
- contamination- surgically inserted foreign bodies like pacemaker, heart valves, implants
- age - regeneration is better in young people
- mechanical factors- excessive fat tissue, torsion
complications (dysfunctional) of would healing
- keloid- scar tissue
- contractures: shrinkage of wound tissue that pulls edges toward center of wound
- dehiscence: opening of wound’s suture line
- evisceration- opening of would with extrusion of tissue/organs
- stricture- narrowing of body
- fistula- abnormal connection between tow organs or vessels that normally don’t connect
- adhesions- internal scar tissue between tissues or organs
wound rupture
also known as dehiscence.
in rare instances, internal tissues and organs can extrude from open wound which is called wound evisceration.
type of tumor that grows slowly, well-differentiated, does NOT metastasize
benign
type of tumor that grows rapidly, poorly differentiated, metastasizes
malignant
substances that are produced by cancer cells
tumor markers (EX: PSA for prostate cancer)
helpful: bc it screens high risk patients, can diagnosis a specific type of tumor, follows course of cancer/response to treatment
drawback: non-malignant cells can also show markers, so not used alone for diagnosis of cancer
why does the risk of cancer increase with aging?
-more time for damage in the cells to build up!
develop 2nd hit, lose telomerase (protective cap) over time
BRCA1 or BRCA2
increases risk for breast and ovarian cancer
development of blood vessels
angiogenesis
changes necessary for local spread and metastasis of cancer cells
-cellular proliferation
-angiogenesis
-digestion of capsules and barriers by lytic enzymes
-decreased cell to cell adhesion , increase motility of tumor cells
what are known causes of cancer
-chemical carcinogens: tobacco, pesticide)
-viruses: Hep B, HPV, Hep C
-immune system (AIDS, immunosuppressant drugs)
- heredity
-obesity
-hormones
-bacteria
-chronic inflammation
-radiation exposure
how does the immune system help fight against cancer? What happens with age?
-immune system has potential for recognizing and destroying cancer cells
-immune system gets weaker as you age
*IDEA: stop or interrupt the synthesis and mitosis stage
progressive loss of body fat and lean body mass
cachexia
what does cachexia cause?
weight loss
decrease muscle mass
malnutrition / muscle wasting
weakness, anemia, emaciation, decrease quality of life
interrupts cell cycle during synthesis phase and some mitosis phase, this destroys fast growing cells
chemotherapy
different types of bone cancer
-osteosarcoma: cancer that produces immature bone
-chondrosarcoma: malignant tumor composed of cartilage producing cells
-ewing’s sarcoma: rare type that occurs in bones or soft tissues around bones
