Cellular Concepts PPT

Cell functions

-growth

-energy production

-metabolism

-DNA replication

-protein synthesis

Sodium-Potassium Pump

-uses ATP (active transport!)

-Na+ = extracellular

-K+ = intracellular

Na-K+ pump rate

pump 3 Na+ out

bring 2 K+ in

Na-K+ pump roles

1) establish resting membrane potential

2) maintains fluid volume

Mitochondrion “cell powerhouse”

-converts nutrients → ATP

-contain own DNA, can replicate when more ATP is needed

-different cell types have various # of mitochondria based on metabolic needs

DNA mutations in mitochondria can occur from…

free radicals

Aerobic metabolism

oxygen → mitochondria → 34 ATP

3 types of cells that have different # of mitochondria based on metabolic needs

1) cardiac

2) skeletal muscle

3) bones

2 types of cellular metabolic processes

1) Anaerobic metabolism (glycolysis)

2) Anaerobic metabolism (krebs cycle)

Anaerobic Metabolism (i.e. Glycolysis)

= no oxygen

produces 2 ATP + lactic acid

Aerobic Metabolism (i.e. Kreb’s cycle)

= requires oxygen
produces 34-36 ATP per glucose

Disease Etiology

The study of the causes or origins of diseases, including genetic, environmental, and infectious factors that contribute to health conditions.

Etiology

-original cause of cell alteration or disease

ex) infection, trauma

Characteristic changes with specific etiologic agents

ex) atrophy of skeletal muscle cells with paralysis, HPV may lead to cervical dysplasia

In response to an etiologic agent, the cell may…

-develop adaptive, compensatory changes

-develop maladaptive changes

Types of Cellular Adaptations

-atrophy

-hypertrophy

-hyperplasia

-metaplasia

-dysplasia

Left Ventricular Hypertrophy

thickened muscle wall of LV, due to heart disease or hypertension or overworking

Gingival hyperplasia

enlargement of gum tissue, often due to medications or chronic inflammation.

Benign Prostatic Hyperplasia

A non-cancerous enlargement of the prostate gland, commonly occurring in older men, which can lead to urinary symptoms

-urine may go back up inside of exiting out the urethra

Metaplasia: Barrett’s Esophagus

condition where normal squamous cells of the esophagus are replaced by columnar tissue, from chronic acid exposure from GERD

-duodenal bile reflux + gastric acid reflux

Metaplasia v.s. Dysplasia - conditions of the normal ciliated epithelium

metaplasia: chronic injury/irritation

dysplasia: persistent severe injury or irritiation

Neoplasia

-new growth

-disorganized, uncoordinated

-tumor

Neoplasia tumors

can be benign or malignant

*assess for differentiation

well differentiated cells = good (benign)

poorly-differentiated cells = bad (malignant)

Benign Neoplasms

-cells resemble normal cells

-well differentiated

-do not metastasize

-well defined borders

Malignant Neoplasm

-cells appear different from healthy cells

-poorly differentiated

-increased likelihood of metastasis

-poorly defined borders

Cellular injury pathways

*VIEW IMG - Refers to the various mechanisms through which cells can sustain damage due to stressors, leading to functional impairment or cell death. These pathways include necrosis, apoptosis, and autophagy.

Changes that occur in cell injury

-dysfunction of Na+/K+ pump

-loss of plasma membrane integrity

-mitochondria dysfunction

-defects in protein synthesis ability

-intracellular accumulations

-cell swelling

-gene damage

Dysfunction of Na+/K+ pump

cause: lack of ATP

-too much Na+ in cells → cell swelling

-loss of electrochemical gradient

Cellular Injury Mechanisms

-hypoxic injury

-free radical injury (oxidative stress)

-physical agents of injury

-chem injury

-infectious injury

-immunologic injury

-gene defects

-nutritional imbalance

Cellular Hypoxia

cell hypoxia → anaerobic metabolism → 2 ATP + pyruvate → LACTIC acid

More on Cellular Injury

-single, unpaired electron that create instability and reactivity w/ adjacent molecules

-react w/ plasma mem. and organelles (including nucleus/DNA) → oxidative degradation

-free radicals can be removed by the cell, but it may be overwhelming and cause oxidative stress

Cellular Injury: Physical injuries

-trauma (laceration, fall, gun shot wound)

-burns (sunburn, electrical)

-frostbite

Cellular Injury: Chemical injuries

-hypernatremia (cell dehydration)

-hyperglycemia → damage endothelial cells that line arteries

-medications (nephron/neurotoxic), pollutants, poisons

Cellular Injury: Infectious agents

-bacteria, virus, fungi, parasites

i.e.) HPV can cause cervical dysplasia

i.e.) H. Pylori causes gastric and duodenal ulcers

Cellular Injury: Immunological agents

-autoimmune, ex) RA

-chronic inflammation

Cellular Injury: Genetic Defects

damage and mutation to DNA → RNA → ribosomes → proteins

Cellular Injury: Nutritional imbalances

-starvation: not enough protein, carb, lipid, vitamins, minerals

-inadequate protein: = low albumin = fluid shift from vascular space into interstitial space (i.e. peritoneal cavity)

-obesity: fat accumulation, stress on heart, increased metabolic needs

What can happen with inadequate protein intake?

this leads to low albumin, so fluid will shift from the vascular space → interstitial spaces such as the peritoneal cavity

Endothelial Cells

-line arterial BV
-”largest organ” → responsive and secretory tissue

-key in angiogenesis

-have Nitric Oxide (NO) → vasodilator

-have Endothelin → vasoconstrict

Endothelial Cells in Angiogenesis

-vascular endothelial growth factor (VEGF)

-stimulates collateral BV branches

Nitric Oxide (NO) is a ….

vasodilator

Endothelin is a …

vasoconstrictor

Endothelial Cell Injury

initiates arteriosclerosis and cell changes of CV disease

Significant Injurious agents that cause Endothelial Cell Injury

-HTN

-DM/hyperglycemia

-Free radicals

-Persistent secretion of Angiotensin II

-LDL cholesterol

Inflammatory Response to cell injury

-caused by a variety of things

-local manifestations (signs / symptoms) → redness, heat, swelling, pain, loss of function

Things that cause an inflammatory response to cell injury

infection, mechanical damage, ischemia, nutrient deprivation, temp. extremes, radiation, etc.

Inflammatory Response - Vascular

1) blood vessel dilation

2) increased vascular permeability + leakage

3) WBC adherence

3 Stages of Acute Inflammatory Rxn

1) Vasodilation — histamine, bradykinin, prostaglandin

2) Vascular Permeability

3) Cellular Migration — WBC, platelets

5 Markers of Inflammation

1) CRP - c reactive protein

2) ESR - erythrocyte sedimentation rate

3) Leukocytosis

4) Calcitonin

5) Lactic Acid (marker of sepsis!)

Sepsis is defined as…

Systemic Inflammatory Response Syndrome (SIRS) that is due to infection

Leukocytosis = high WBC

how many cells is this??

approx. 5,000-10,000 cells/cm

Necrosis

cell death due to overwhelming stressors or injury

-irreversible → lysosomes break open, initiating autolysis

-inflammatory rxn results

Apoptosis

programmed cell death in an organized process

-no inflammation

ex) WBCs undergo apoptosis after their participation in an inflammatory rxn

Ischemia

lack of blood

Necrosis (short answer)

cell death

Infarction

tissue death caused by prolonged ischemia (lack of blood)

Prolonged ischemia leads to…

Ischemic necrosis

CKmb

a cardiac enzyme released during myocardial infarction (MI)

troponin

a protein complex found in cardiac muscle that is released into the bloodstream during myocardial injury or MI

Any tissues that sustains prolonged ischemia is susceptible to… ???

infarction

Individual cells have different tolerances to ischemia

Brain: 6 min

Heart: 20 min

Skeletal muscle: several hours

2 things that may come up during MI and/or heart infection

1) CKmb = cardiac enzyme

2) troponin = cardiac protein