Homeostasis And Cellular Adaptation

Front 1

Homeostasis

Back 1

-Intracellular and extracellular fluids
-pH
-Nutrients and waste
-Electrolytes
-Fluid volumes and pressures

Front 2

Negative Feedback

Back 2

-Controlled by receptors, hormones, nervous system, enzymes
-The body is telling system to stop once it reaches a normal level

Front 3

Positive Feedback

Back 3

-Tells system to keeping doing what it is doing

Front 4

Cell Injury

Back 4

Can be d/t:
-Infection
-Hypoxia
-Chemicals
-Trauma
-Genetics
-AI: auto immune
-Nutrition

Front 5

Atrophy

Back 5

-There is a ⇓ in cellular size.
-Most commonly affects skeletal muscle, the heart, secondary sex organs, and the brain.
ex.
-Physiological: Normal process Aging (alzheimer's)
-Pathological: abnl.
Osteoporosis, muscle atrophy d/t immobilization

Front 6

Osteoporosis

Back 6

-Osteopenia: weakening of the bone
-There is a ⇓ in bone mass
Causes:
-Estrogen deficiency
-Post menopausal
-Calcium deficiency
-⇑ cortisol
-Renal, Multiple Myeloma, or Vitamin D deficiency
S/S:
-Kyphosis, compression fx, radiolucency
Testing:
-Bone density scan (DEXA) T-score < -2.5 (-1 to -2.5 osteopenia)

Front 7

Alzheimer's

Back 7

-Progressive destruction of the brain
Causes:
-Genetics- can be detected early
-FHX, Age, Down’s syndrome
S/S:
-Amyloid plaques (infl.)- like scabs on the nerves; neuritic plaques + cell death, Cortical Atrophy
-Accumulation of tau protein neurofibrillary tangles + dystrophy
-Decr. acetylcholine
-Problems w/ memory, judgment, behavior, reasoning
Testing:
-R/O other possible causes

Front 8

Intracellular Accumulation

Back 8

Pathological
-Lipids – Liver disease
-Iron – Hemochromatosis
-Copper – Wilson’s disease ciser flisure)
-Uric Acid – Gout
-Beta-Amyloids- Alzheimer's
-Bilirubin- Liver, GB, Pancreas
-Melanin - Addison’s
-Dystrophic Calcification – Atherosclerosis
-Malignant Calcification – Hyperparathyroism, Malignancy

Front 9

Hemochromatosis

Back 9

-Increased iron absorption (30% - Normal 10%) and storage
Causes:
-Primary – Genetic
-Autosomal recessive – Disease
-Secondary – other disorders, alcoholism
S/S:
Fatigue, Arthritis
Deposits in liver (cirrhosis), pancreas (DM), heart (HF), anterior pituitary and other organs
-Gray or bronze skin tone
Testing:
-Serum Fe
-ferritin- storage form of Fe
-transferrin saturation (>45%), TIBC- Total iron binding capacity
-Glucose
-FSH/LH
-reproductive hormone,
-EKG
-Imaging
-DNA testing
Management:
-Therapeutic Phlebotomy
-Vitamin C: need to limit Vit C intake because it binds with Fe

Front 10

Hypertrophy

Back 10

-There is an increase in size of cells and the affected organ.
ex.
-Physiological: hypertrophy during pregnancy
-Pathologically:
BPH, CHF, left ventricular hypertrophy, HTN

Front 11

Hyperplasia

Back 11

-Increase in the number of cells d/t ⇑ rate of cell division
-Physiological:
-Compensatory hyperplasia (1)
*kidney or liver (ectomy) or failure
*callous
-Hormonal hyperplasia (2)
*pregnancy
-Pathological:
-can occur as a response to excessive hormonal stimulation ex. endometrial hyperplasia, BPH, fatty liver (NASH)

Front 12

Dysplasia

Back 12

-There are abnl. changes w/in mature cells to include size, shape, and organization.
-Referred to as atypical hyperplasia
-There is only pathological dysplasia
-usually occurs in epithelial tissue and associated with neoplastic growths r/t Cancer
-can be reversible if caught and corrected early
-commonly seen in cervix and resp. tract

Front 13

Metaplasia

Back 13

-Reversible replacement of one mature cell by another less differentiated cell.
-Always pathological
-Ex. smoker lungs. the cells that are replaced do not secrete mucous or have cilia. Replaced d/t damage from smoke inhalation
-If smoking stopped cells can be corrected if not risk for dsyplasia (cancer cells)
- Squamous to glandular epithelium
- Barrett’s esophagus can turn into a cancer

Front 14

Cell Adaptation

Back 14

Front 15

Coagulative Necrosis

Back 15

-occurs in kidney, heart, and adrenal glands as a result of hypoxia
-The necrotic tissue appears firm and slightly swollen

Front 16

Liquefactive Necrosis

Back 16

-results from ischemic injury (Cerebral ischemia) or Bacterial infection
The tissue becomes soft, liquefies, forms cyst

Front 17

Caseous Necrosis

Back 17

- Commonly results from TB lung infection and Histoplasmosis
-It's a combination of coagulative and liquefactive necrosis
-Tissues resemble cottage cheese.
-(lipids+macrophages)
-Develop granulomas

Front 18

Fat Necrosis

Back 18

-High Fat content
-Can occur in breast, pancreas, and other abd structures.
Necrotic tissue appears opaque and chalky white

Front 19

Gangrenous Necrosis

Back 19

-Death of tissue r/t severe hypoxic injury
-Dry (Ischemic) usually d/t coagulative necrosis (skin dry and shrinks)
-Wet (Bacterial) looks cold, swollen, and black. There is a foul odor and pus

Front 20

Cells Involved with Inflammation

Back 20

-Neutrophils- First responders and initiate the inflammatory process
-Eosinophils- Involved with allergic rxns and parasites
Basophils- Releases histamine
Macrophages- Do the cleaning up and usually appear towards the end of the inflammation process.
-Lymphocytes-
B cell antibodies
--Immunoglobulins
-IGM-(The initial or primary response) starts early in neonatal life
-IGD- Not alot of info on it, unknown fx.
-IGG- Long term immunity
-IGA- found in mucosal membranes
-IGE- works against allergic rxns and parasite infections
T cells
-Tell immune system to turn on and off.
-Platelets- Coagulation

Front 21

Genetics

Back 21

- DNA- Housed in the nucleus and is the "body cook book"
- Chromosomes- Packages of DNA (23 pairs)
-Males XY
-Females XX
Traits
-Physical – ex. Hair, eye and skin color
-Behavioral – ex. Herding dog
-Familiar predispositions – Sickle cell, CVD, CA, Mental illness

Front 22

Genetics

Back 22

-Dominant: the disease was given to child by one parent. The person who passed it on usually has that disease also
-Recessive: both the parents passed on the disease but do not have the disease. Just carriers
-Sex-linked: effects the X and Y
-Autosomal: out side of sexlinked
-Multifactorial: ex. pre disposition of DM. Environmental and Lifestyle related

Front 23

Chromosomal

Back 23

Disease related to Abnl. Chromosomes

Front 24

Down's Syndrome

Back 24

-Trisomy 21 with physical and mental disorders
Causes:
-Chromosomal disorder
-Maternal age
--35 – 1/385
--40 – 1/106
--45 – 1/30
S/S:
-Small head with flat facial features
-Slanted eyes, Single crease in palm of hand
-Heart defects, leukemia, dementia, decr. IS
-May have decreased IQ and speech difficulties
-Risk for Early Alzheimer’s
Testing:
-Prenatal care – US or amniocentesis

Front 25

Down's Syndrome

Back 25

Front 26

Klinefelter's Syndome

Back 26

Causes:
Chromosomal disorder XXY
1/500 -1000
S/S:
-Generally male with both male and female sexual characteristics
- ⇓ testosterone less body and facial hair, gynecomastia (risk breast CA), weak muscles and bones (osteoporosis), shy
-Infertility
Testing:
-Clinical Exam
-Chromosomal testing
-Hormones

Front 27

Klinefelter's Syndrome

Back 27

Front 28

Turner's Syndrome

Back 28

Causes:
- Chromosomal disorder w/ women
- contain X only also called XO
S/S:
- Short stature
- No or irregular menstrual periods; ovarian failure, risk for ovarian Ca.
- No breast development
- Infertility
- Aortic stenosis or coarctation; pulses stronger on upper extremities compared to lower
- Web neck
- Nipples are wider apart
Testing:
- Clinical
- Chromosomal testing
- Echo
- Reproductive Hormones

Front 29

Turner Syndrome

Back 29

Front 30

Dominant

Back 30

Disease given by ONE parent and usually has the disease also

Front 31

Hunington's Chorea

Back 31

-Progressive degeneration of nerve cells
Causes:
-Genetic- Autosomal dominant
-FHX
-Middle age onset
S/S:
-Chorea ⇒ jerky movements
-Problems ⇒ Speech, Balance, Swallowing
Cognitive Impairment, Behavioral/Personality Changes
Testing:
-CT/MRI
-Genetic testing

Front 32

Dwarfism

Back 32

Adult height of less than 4 feet 10 inches or less”
Causes:
- ⇓ GH
- Achondroplasia (autosomal dominant) ⇒ Most Common ⇒ no cartilageproduction ⇒ no bone production
- problem is below the hips; shorter than nl. and leads to hip problems
Primordial dwarfism ⇒ autosomal recessive
S/S:
- Hip deformities
- Clubfoot
- Scoliosis and lordosis
Testing:
- Clinical exam ⇒ height percentiles
- Hormones
- X-Ray/CT
- Genetic testing

Front 33

Recessive

Back 33

Both parents passed the disease but do not have the disease (Carriers)

Front 34

Cystic Fibrosis

Back 34

Causes:
Autosomal recessive ⇒ ⇓ Cl metabolism ⇒ ⇑ Na and H2O reabsorption ⇒ sticky mucus
S/S:
- Respiratory- cough, wheezing, freq. infection (Pseudomonas), clubbing, bronchiectasis
- GI –meconium ileus, abnormal fat metabolism⇒ steatorrhea, fecal impaction, fat absorption is not absorbed well which causes decrease in vitamin absorption, brain tissue, cholestrol (Makes our steroid hormones)
- Pancreas – decr. exocrine function ⇒ digestive enzymes
-Liver – thick bile
-Growth- failure to thrive
-Reproductive – infertile males and some females
Testing:
- Sweat test ⇒ NaCl
- Genetic Testing

Front 35

Muscular Dystrophy

Back 35

- Skeletal Muscle degeneration
Dystrophin deficiency (protein responsible for intracellular structure and support)
- Wheelchair by age 12
- Excessive fat tissue and effects lower legs (calves)
Cause:
-Duchenne MD
-- MC, severe, early onset (1)
-- X-linked recessive – male children
-- Weakness in proximal muscles – necrosis of muscle fibers – replacement with fatty tissue – pseudohypertrophy
-- Pneumonia
-- Decr. IQ, cardiomyopathy, incr. intestinal transit time
- Becker MD
-- Less severe than Duchenne’s
Testing:
-Incr. CK
-EMG (electromyogram)
-Genetic
-Biopsy

Front 36

Sickle Cell Anemia

Back 36

Causes:
- Sickle cell disease ⇒ Autosomal recessive
- Sickle cell trait⇒ one defective gene ⇒ have both Hb A and S
- African American
- Hb S instead of Hb A ⇒ live only ~ 16 days
- Hb F
S/S:
- Sickling of cells ⇒ Hypoxia, dehydration, acidosis, cold temps, infection
abdominal and bone pain, ulcerations, thrombi, infarcts
- Acute Chest Syndrome ⇒ damage to lung tissue, cardiomyopathy
- Hemolytic crisis ⇒ Jaundice and hematuria
- NO def. due to incr. lysed cells
- Splenic sequestration crisis ⇒ HSM
- Aplastic crisis
- Higher risk osteomyelitis and aseptic necrosis
- Retinal hemorrhage/ detachment, Priapism

Front 37

Sickle Cell Anemia

Back 37

Testing (high, low, normal)
- Bilirubin (high)
- Potassium (high)
- WBC’s (high)
- Hemoglobin (low)
- Reticulocytes: immature blood cells (high)

- Newborn screening
CBC – diff., reticulocytes, Hb Electrophoresis