Chapter 1-3 Patho SG

Cellular Adaptation

Physiological vs. Pathogenic; can be good or bad

atrophy definition

Decrease in cellular size; reversible. The cell decreased because the demand for use decreased.

atrophy

·      Disuse

·      Ischemia-inadequate blood supply

·      Endocrine Dysfunction

·      Persistent cell injury

·      Aging

hypertrophy definition

increase in cellular size; physiologic or pathologic

hypertrophy

·      Physiologic

o   __Normal; weightlifting__

·      Pathologic

o   __Abnormal; enlarged organs__

hyperplasia definiton

·      __Physiologic- breast and uterine enlargement__

·      __Pathologic- enlargement of the prostate gland__

metaplasia definition

replacement of one cell type to another

metaplasia

1. Cell retains the same primary tissue type
2. Usually occurs in response to chronic irritation and inflammation


1. Reversible

dysplasia definition

deranged cellular growth

dysplasia

• Cells mutate with abnormal variations in size, shape, and arrangement


1. Abnormal
2. May be reversible


1. Strongly implicated as a precursor to cancer

Hypoxia injury definition

lack of oxygen; the single most common cause of cellular injury

hypoxia

·      Reduced oxygen in the air

·      Loss of hemoglobin or decreased hemoglobin

·      Decreased production of red blood cells

·      Respiratory and cardiovascular diseases occur

·      Carbon monoxide poisoning 

Ischemic injury definition

lack of blood supply; most common cause of Hypoxia; reperfusion injury

ischemic injury

·      It can be progressive or acute

·      Caused by:

o   __Arteriosclerosis- gradual narrowing of arteries__

o   __Thrombosis- complete blockage by blood clots__

 

Necrosis-

early or premature cell death due in tissues by autolysis; caused by external factors to the cell or tissue

Apoptosis

the process of eliminating unwanted cells (known as programmed cell death); may result from environmental and developmental triggers

General adaptation syndrome (GAS)

protective stress response; Dr. Hans Seyle

GAS stages

·      Includes three stages__: alarm, resistance, and exhaustion__

·      __Alarm Stage__

o   Emergency reaction “fight or flight.”

·      __Resistance__

o   Attempts homeostasis; actions of adrenal hormones that help coping mechanisms.

·      __Exhaustion Stage/allostatic overload__

o   No longer can produce hormones; the body’s systems cannot cope with the stress, leaving you vulnerable to disease.

HPA axis

Hypothalamus \*\*control center\*\* secretes → corticotropin-releasing hormone (CRH)

Pituitary releases→ adrenocorticotropin hormone (ACTH)

Adrenals secrets →cortisol and catecholamines

Cortisol

secreted during stress which reaches all the tissues and stimulates gluconeogenesis.

abnormal cortisol levels

·      Obesity

·      Sleep deprivation

·      HTN (hypertension)

·      Diabetes

·      Atherosclerosis

·      Loss of bone density

·      Elevated lipid levels

·      Glycolysis-carbohydrates splitting pyruvates

Cortisol can

·      Elevate blood glucose

·      increase Protein metabolism

·      Promotes repair and resolution

·      Induce T-cell apoptosis

·      Influences all immune cells

·      Cognitive impairments

·      Used for anti-inflammatory/immunosuppressive agents

Catecholamines

Released from the adrenal medulla

·      80% epinephrine and 20% norepinephrine is released

·      α-adrenergic receptors

o   α1 and α2

·      β-adrenergic receptors

o   β1 and β2

·      Mimic direct sympathetic stimulation

·      Increases proinflammatory cytokine production

Catecholamines regulates

·      Cardiovascular-peripheral vasoconstriction, increased rate, and force contraction of the heart

·      Pulmonary- bronchodilation

·      Hepatic

·      Skeletal muscle

·      Immune system

·      Increased blood flow and increased glucose metabolism in the brain\`

fluid movement

Passive transport or osmosis

Osmolality

solutes/particles per kg of water

Osmotic pressure

–pulling pressure

Oncotic pressure

osmotic pressure of plasma proteins

Hydrostatic pressure

– pushing pressure against the cell membrane or vessel wall

Lymphatics can

pick up waste and fluids (sore throat-swollen lymph nodes)

Net filtration

fluid movement between plasma and interstitial space

Edema

too much fluid filling in the interstitial spaces/localized and generalized, an increase of hydrostatic pressure

Lymphedema

swelling in the lymph nodes

Pitting Edema

imprints left in the skin

Third spacing

The body is not using the fluid. Fluid moves from the intravascular spaces (blood vessels) to the interstitial spaces (tissue spaces). This can lead to edema and reduced blood volume. It occurs in conditions like burns, trauma, and infections.

Feet edema

pedal edema

eye edema

periorbital edema

extremities edema

peripheral edema

brain edema

cerebral edema

causes/pathology of edema

·      Increase in capillary hydrostatic pressure

·      Decrease in plasma oncotic pressure

·      Increase in capillary permeability

·      Lymph obstruction

·      Increase in tissue oncotic pressure

ADH

tap water hormone(vasopressin)  

·      Helps kidneys to reabsorb water; makes a smaller amount of urine more concentrated.

Aldosterone

a saltwater hormone

·      Helps kidneys reabsorb salt and water, a smaller volume of urine.’

ANH and BNP

stops the ADH system

ADH

the antidiuretic hormone

High plasma osmolality

more solutes than water

RAAS

The Renin-Angiotensin-Aldosterone System

Decreased circulation or blood pressure is sensed by the kidneys →kidneys secrete RENNIN which stimulates the liver

Angiotensin

·      Lungs convert to Angiotensin I; then ACE transforms I into Angiotensin II →stimulates peripheral vasoconstriction, which raises the BP.

·      ACE inhibitor helps lower blood pressure.

Volume Excess

Excessive sodium or water intake or Inadequate sodium or water elimination

Volume Deficit

Inadequate fluid intake or Excessive fluid or sodium loss

Sodium value/info

136-145 mEq/L; ECF electrolyte

Potassium values/info

3\.5-5 mEq/L; major intracellular electrolyte… concentration maintained by Na+/K+ pump

Calcium value/info

9-10.5 mg/dl; 99% is stored in teeth and bones

Magnesium value/ info

1\.3-2.1 mEq/L; largely stored in bones, intracellular cations

Phosphate

3-4.5 mg/dL; controlled with calcium… if one is elevated other is decreased

Roles of sodium

* Generation and transmission of nerve impulses and muscle contractility 
* Acid-base balance 
* Cellular chemical reactions 
* Membran transport 
* Water balance and plasma osmoality

Hyponatremia

* Too little sodium in the blood
* Serum Na+

Etiology of Hyponatremia

* Loss of sodium 
* Inadequate intake of sodium 
* Sodium dilution from too much water 

CMs of Hyponatremia

* Lethargy 
* Confusion 
* Decreased reflexes
* Muscle cramps and fatigue
* Most serious CMs
* Cerebral Edema 
* Increased intracranial pressure 
* Sezisures 
* Coma

Hyper__na__tremia

* Too much sodium in the blood 
* Serum Na+> 145 mEq/L
* Related to sodium gain, water loss 
* Sodium overload causes plasma hyperosmoality and cellular shrinking 
* Increased serum osmoality 
* Faster action potential

Etiology of Hypernatremia

* Inadeqaute water intake 


* Loss of water 
* Increased concentration of sodium (ECF) 

CMs of Hypernatremia

* Thirst 
* Weigh Loss 
* Increased blood pressure 
* Muscle twitching 
* Increased reflexes 
* Serious CMs: 
* Coma 
* Convulsions 
* Cerebral hemorrahge 
* Seizures

Potassium Levels (Drip never push) 

* Changes in ph affects K+ balance
* Hydrogen ions accumulate on ICF during acidosis.  K+ shifts out to maintain a balance of cations across the membranes. 
* Aldosterone, insulin, and catecholamines influence serum potassium levels 
* Kidney is the most efficient regulator 
* Postassium adaptation
* **SLOW CHANGES tolerated better than acute**

Roles of Potassium

* Transmission and conduction of nerve impulses 
* Normal cardiac contraction 
* Skeltal and smooth muscle contraction 
* Acid base balance

Hyper__ka__lemia

* Serum K+

Etiology of Hyperkalemia 

* Increased intake 
* K+ leaves the cells into blood
* Decreased renal excretion of K+ 
* Insulin deficiency 
* Large infusion of stored blood 
* Cell trauma 

Clinical Manifestations of Hyperkalemia

* **Nueromuscular excitability increases (repolarizing quicker)** 


* Tingling of lips and fingers 
* Restlessness 
* Tall, peaked T waves on ECG
* Severe attacks 
* Muscle attacks 
* Loss of muscle tone 
* Flaccid paralysis-paralyzed 
* Cardiac dysrhythmias (irregular rhythm)

Hypo__ka__lemia

* Serum K+ >5 mEq/L
* Slower action potential 

Etiology of Hypokalemia

* Decreased intake 
* Increased entry of K+ into cell 
* Acid base balance 
* Increase in aldosterone 
* Insulin overuse 
* Increased loss of K+
* NG suctioning 
* Burns 
* Vomiting and Diarrhea 
* Use of non K+ sparing diuretics

Clinical Manifestations of Hypokalemia

* **Neuromuscular excitability decreases** 
* **Skeletal muscle weakness** 
* **Loss of smooth muscle tone** 
* **EKG=prolonged PR interval, flat T wave, prominent U wave**

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Roles of Calcium 

* Transmission and codunction of nerve impulses 
* Normal cardiac contraction 
* Skeletal and smooth muscle contraction 
* Acid base balance

Hyper__ca__lcemia 

Serum Ca²+ >10.5 mg/dL

Etiology of Hypercalceima 

* Insufficient dietary 
* Inadequate intestinal absorption 
* Blood administration 
* Renal disease 
* Vitamin D Deficiency 
* Decrease in PTH

 Clinical Manifestations of Hypercalcemia 

* Neuromuscular irritability (spasms, cramps)
* Hyperactive reflexes 
* Tetany 
* Positive Trousseau sign 
* Positive Chvostek sign (cheek)
* Cardiac dyrhythmias 

Hypo__ca__lcemia 

Serum Ca²+

Etiology of Hypocalceima

* Vitamin D overdose (activates calcium) 
* Prolonged immobilization 
* Some cancers (COMMON CAUSE)
* Hyperparathyroidism (COMMON CAUSE)

Clinical Manifestations of Hypercalceima 

* Muscle weakness 
* Cardiac dysrhythmias, bradycardia, cardiac arrest 
* Bone pain osteoporosis 
* Pathological fractures 
* Kidney stones 
* Non-specific: fatigue, weakness, lethargy, nausea, constipation 

Roles of Magnesium

* Acts as a cofactor in intracellular enzymatic reactions
* Increases neuromuscular excitability 
* Neromuscular junction 

Hypomagnesemia 

Serum Mg

Etiology of Hypomagnesemia 

* Alcohol abuse 
* Urinary losses (renal tubular dysfunction, loop diuretics) 
* Malnutrition 

Clincial Manifestations of Hypomagnesemia 

* Positive Chvostek 
* Positive Trousseau signs 
* Tachycardia 
* ALtered LOC
* Muscle Cramps 
* Hyperactive deep
* Tendon reflexes 
* Tetany 
* Convulsions 

Hypermagnesemia 

Serum Mg >2.1 mEq/L

Etiology of Hypermagnesemia 

* Milk of Magnesia 
* Renal Disease (renal insuffciency or failure) 
* Increased intake 

Clinical Manifestations of Hypermagnesemia 

* Loss of reflexes 
* Muscle weakness 
* Bradycardia 
* Respiratory distress 
* Excess nerve function 

Roles of Phosphate 

* Provides energy for muscle contraction 
* Component of RBC’S 
* Acid Base regulator 

Hypophosphatemia 

Serum PO43-

Etiology of Hypophosphatemia 

* Mg and aluminum antacids 
* Alcohol abuse 
* Diuretic use

Clinical Manifestations Hypophosphatemia 

* Phosphate low, calcium is high 
* Mild cases
* Asymptomatic 
* CNS depression (confusion, coma) 
* Muscle weakness 
* Numbness 
* Convulsions

Hyperphosphatemia 

Serum PO43- 3-4.5>mg/dL

Etiology of Hyperphosphatemia

* Acute or chronic renal failure 
* Hypoparathyroidism 
* Chemotherapy 
* Long term use of laxatives or enemas containing phosphates

Clinical Manifestations of Hyperphosphatemia 

* Phosphate high, calcium is low 
* Tetany 
* Muscle cramps 
* Paresthesia 
* Seizures 

1st line of defense-

innate (natural, native) immunity (NONSPECIFIC)

Physical defense

  Skin, GI, GU, and Respiratory tracts

Mechanical defense

o   Sloughing of cells,

o   Coughing

o   Urination

o   Vomiting

o   Muscle and cilia

biochemical barriers

o   secrete saliva,

o    tears,

o    earwax,

o    sweat,

o   pH levels

o   mucus

o   normal microbiome

2nd line of defense

inflammatory response; nonspecific

o   Variety of materials

o   Infection, tissue necrosis, trauma,

o   physical or chemical injury,

o   foreign bodies

o   immune reactions

o   ischemia

local manifestations

Redness, heat, swelling, pain, loss of function

vascular responses

o   Vessel dilation

o   Increased vascular permeability and leakage

o   WBC cell adheres to the inner wall of the vessels and migrates

o   Blood clot walls off, or plugs damaged tissue

3rd line of defense

adaptive (acquired, specific) immunity

Mast cells

cellular bags of granules located in loose connective tissue close to blood vessels; chemical release in two ways: degranulation and synthesis

·      Skin, digestive lining, and respiratory tract

Contain histamine, cytokines, and chemotactic factors

Basophils

found in blood and probably function the same way as mast cells. Chemical release in two ways: degranulation and synthesis.