Pathophysiology Exam 1

Epidemiology

the study of epidemics; distribution of disease (ex. COVID/Plague)

Mortality

number of deaths

Morbidity

occurrence of the disease

• incidence: number of new cases

• prevalence: density/percentage of all cases

Ecology

cause

• genetic components

• congenital (intrauterine factors)

• acquired

• idiopathic: unsure of cause

• iatrogenic: induced by treatment

Signs

what the observer sees

• disorder- 1 dysfunction

• syndrome- group of interrelated signs

Symptoms

subjective to what the patient feels

Acute

anything less than 6 months

Chronic

anything longer than 6 months

Insidious

minor changes occurring until they become more noticeable

Clinical manifestations

• Latent period: developing; asymptomatic

• Prodromal: onset of symptoms

• Aura: no onset; immediately feel (seizures)

Stressor

throws off homeostasis

Physiology is the study of

negative feedback

• to keep you within homeostatic ranges

Pathophysiology

Normal cell function response to stress

1. Adaptation

2. Cell death

1. Alarm phase (body feels pain)

• acute pain: accurate, fast AP, sharp pain

• chronic pain: slow AP, diffuse pain

• immune response (cytokines- immune hormones)

Triggers RAS system!

2. Resistance phase (-FB) to put back into homeostasis

-FB→ homeostasis applied

+FB→ amplify what stressor causes

exhaustion= final phase→ cell death

Atrophy (hypotrophy)

decrease in cell size and protein in a cell (not water)

• result of disuse, denaturation, decrease in endocrine hormones, ischemia

• damaged structures

• malnutrition

Hypertrophy

increase in cell size, increase in protein (not water)

• skeletal muscle, cardiac muscle, kidney, glands (goiter)

• steroids cause hypertrophy

• Ventricle: decrease in chamber volume and increase of heart rate

Hyperplasia

increase in number of cells (neurons, cardiac, and skeletal muscle are discluded)

• hormonal cause, compensatory, pathological

• Hematopoiesis

Metaplasia

1 normal cell replaces another normal cell

• Barrett’s Esophagus

  • stratified squamous (esophagus)

  • ^replaced by simple columnar (stomach) due to esophageal acid exposure

Dysplasia

deranged and abnormal

• mild, moderate, and severe

• severe: neoplasia

• new growth= cancer

Ischemia

hypoxic injury (Angina)

• oxygen, electron transport, Na/K pump

• D BF→D O2→ETC D ATP production

Necrosis

• Coagulative

• Liquefactive

• Caseous

• Fat

Coagulative necrosis

results from ischemia→ anaerobic (lactic acids)

• Ischemia: I Carbonic acid, I CO2

• denature proteins

Liquefactive necrosis

results of release of hydrolytic enzymes→ breaking protein down (neutrophils leak hydrolytic enzymes)

Caseous necrosis

Coagulative and liquefactive necrosis

• cheese like consistency (TB)

Fat necrosis

lipase

• Triglycerides and phospholipids → fatty acids with cations→ saponification (make soap)

Dry gangrene

• Clearly demark able from the artery

• tissue dries out

• associated with coagulative necrosis

Wet gangrene

• stops at veins and causes flood of back pressure

• associated with liquefactive necrosis

• messy; tissue forms blebs (smells)

Gas gangrene

• Clostridium (anaerobic organism)

• Hydrogen sulfide is generated (rotting eggs)

Heavy metal cell alterations

• lead→ calcium

• vanadium→ phosphate

Bacterial infections

• recruit neutrophils to get rid of bacteria

• exotoxin= live bacteria

• endotoxin= dead bacteria (gram -)

  • gram (-) outer membrane releases endotoxin

Roundworms

eosinophils

Virus

lymphocytes

Cellular accumulations

• H20→ ischemia

• Fatty acids→ fatty liver

• Proteins→ thalassemia (Heinz Body)

• Jaundice→ unconjugated bile (lipid soluble)

• Calcium→ hypercalcemia (effects thresholds)

Hypercalcemia effects thresholds

• Increased calcium causes thresholds to rise

• Makes it harder to generate AP

• Metastatic calcification: normal tissue will calcify

• Dystrophic calcification: dead and dying tissue will calcify

Hyperthermia

• partial thickness

• BV vasodilate

  • edema blister (edema under epidermis)

• full thickness

  • fluid loss and loss of protein

Fluid compartments

• most fluid is intracellular

• interstitial fluid: fluid between cells

• blood is 3rd fluid

Hypothermia

ice crystal formation

• slow form: large crystals that disrupt cell membrane

• fast form: small crystals that do not disrupt cell membranes

Vasoconstriction

• cycles into vasodilation

• leaks fluid into tissue causing edema

Beta radiation

penetrates skin and stop

• Lo!

Gamma radiation

penetrate and passes through the body

• High!

Alpha radiation

tritiated H20

• H3 penetrate one cell

• Very Lo!

UV radiation causes

• thymine dimers

• DNA polymerase I fixes dimer

• Cancer: not being able to keep up with dimers

Gene mutations

• spontaneous mutations

• point mutation

• deletion base

Spontaneous mutations

result in substitution

• creates tautomers

  • Transition: purine→ purine, pyrimidine→ pyrimidine

  • Translation: purine→ pyrimidine (vice versa)

Purine

adenine and guanine

Pyrimidine

Cytosine and thymine

Point mutation

1 or more bases are mismatched

Deletion base

frameshift

• changing the base could have no change in amino acid

  • missense: subs. of amino acid

  • Nonsense: sub and get stop codon

Chromosomal disruption

• Deletion (missing a gene)

• Duplication (Duplicate gene)

• Inversion

• Translocation (structural rearrangement)

Fragile sites

Folate deficiency

• breaks and causes gaps

Fragile X syndrome

• CGG→ prone to creating breaks and gaps

Non-disjunction

• anaphase lag

• 1 chromosome doesn’t move during anaphase

• Polyploidy: more than 2N (3N)

• Aneuploidy: not a multiple of 23 in haploid set

Kinds of chromosomal makeups

• XO= Turner’s

• XYY

• XXY= Kleinfelter’s Syndrome

• SRY= Y chromosome male gene

AA

homozygous dominant

• Hgb: more at risk for malaria and separated clumping

Aa

heterozygote

• Hgb: resistant to malaria and partially clumped compartments

aa

homozygous recessive

• Hgb: irregularly Red shaped blood cell (sickle cell); clumped compartments