(from Greek pathos, meaning "disease")

deals with the study of the structural and funcitonal changes in cells, tissues and organs of the body that cause or are caused by disease 

deals with the cellular and organ changes and the effect that these changes have on total body function. 

it focuses on the mechanisms of the underlying disease process 

Biologic agent: bacteria, virus

physical forces: trauma, burns, radiation

chemical agents: poisons, alcohol

nutritional excesses/deficits: hypertension, diabetes

risk factors: factors that predispose to a particular disease

    - congenital vs acquired 

sequence of the cellular and tissue events that take place from the time of initial contact with an etiologic agent until the ultimate expression of a disease 

• the fundamental structure/form of cells or tissues
• microscopic and macroscopic changes of the disease 

• symptom: subjective complaint that is noted by patient (pain, shortness of breath)
• sign: manifestation that is noted by observer, objective (heavy breathing, pale face)

compilation of signs and symptoms 

- removed risk factors (ex- obesity is a risk factor, primary prevention would be to introduce an exercise program)

-folic acid for pregnant women, immunizations 

- detects disease early when pt is asymptomatic 

- ex: pap smear for women, colonoscopy 

- clinical interventions to prevent further deterioration

-ex: chemotherapy for cancer, antibiotics for infection 

- stress affects normal cell function 

- either your body adapts to maintain function or 

-failure to maintain function results in cell injury which could cause maladaptive changes or cell death. 

*decrease in cellular size 

- disuse: plaster cast

-denervation: muscles of paralyzed limbs 

-loss of endocrine stimulation: menopause (lack of estrogen, reproductive organs get smaller)

- malnutrition and decreased blood flow: cells decrease size and energy requirements as means of survival

*increase in cell size 

- results from increased workload of an organ that can not adapt through mitotic division (ex- heart and muscle) 

*increase in the number of cells 

- occurs in tissues with cells capable of mitotic division (epidermin, glandular tissue)

- hormonal: breast enlargement during pregnancy 

- compensatory: when part of liver is removed there is regeneration 

*replacement of one mature cell by another 

- substitution of cells that are better to survive under certain circumstances

-ex: adaptive substitution of stratified squamous epithelial cells for ciliated columnar epithelial cells in the trachea of a smoker (creating more mucous for dried out/ not as elastic trachea)

*abnormal changes in the size, shape and organization of mature cell 

- strong precursor of cancer 

- start of most diseases

- loss of function results from cell injury and cell death 

- occurs when cell is unable to maintain homeostasis 

-mauy be reversible or irreversible 

- mechanical forces: split and tear tissue, bone fractures, falls, injury to blood vessels 

- extreme temperature: heat (heatstroke), cold (hypothermia)

- electrical forces: disruption of neural and cardiac impulses

- ionizing radiation

-ultraviolet radiation: affect at atom level

-nonionizing: ultrasouns, microwave, thermal injuries like burns 

- drugs: alcohol, street drugs

- lead toxicity: risk factors are children, low socioeconomic status, living in older homes 

- range from submicroscopic viruses to the larger parasites

- electrically uncharged atom/group of atoms having unpaired electron

-may be initiated within cells by absorption of extreme UV light, iron uptake, growth and enzymatic metabolism of chemicals and drugs

- damage caused by: lipid peroxidation (destruction of polyunsaturated lipids- membrane damage), alterations of proteins, alterations of DNA, damage to mitochondria. 

- lack of sufficient oxygen to the cell 

- caused by: decreased oxygen in air, respiratory and cardiovascular diseases, ischemia, anemia

* most common: ischemia- lack of oxygen in tissue, neural can last 4-5 min, heart can only last up to min without oxygenated blood. 

** Apoptosis 

- programmed cell death, eliminates aged/injured cells 

- controls tissue regeneration

-normal physiologic process: embrionic process 

-pathologic process: alzheimers, parkinsons 

- cell death in an organ or tissue that is still part of a living person (amputation) 

-gangrene: mass of tissue undergoing necrosis, dry or wet,

-gas gangrene: infection of tissue by anaerobic bacteria

- normal physiologic process that is universal and inevitable

- time dependent loss of structure of function, gradual result of "wear and tear" 

- genetic blueprint of individuals 

- 23 pairs of chromosomes, 46 total 

- DNA divided into sections called genes

-each codes for particular protein (enzymes)

control the synthesis and function of each cell or tissue of body 

- 22 autosomes from each parent (44) and one sex chromosome from each parent (46 total) 

-copies of a gene

-homozygous: copies are alike

-heterozygous: copies are different 

-carrier: you are heterozygous for a recessive trait and don't show it 

-hemizygous: you have only one copy of a gene 

precise genetic info carried in the chromosomes of offspring

- physical presentation of genetic information 

(having green eyes)

- male/female offspring affected equally 

- one of the parents is usually affected 

- if one of the parents is heterozygrous affected, the children have a 50% chance of being affected. 

-if both parents are heterozygous affected, the children have a 75% chance of being affected

- no such thing as being a carrier 

- male/female offspring affected equally 

- if both parents are unaffected but are carriers, children have 1/4 chance of being affected

- if both parents are affected, all of their children will be affected

- if one parent is affected and the other not a carrier, all of their ofsping will be unaffected but will be carriers 

-if one parent is affected and the other is a carrier, each of the offspring wil have 50% chance 

- caused by genes located on sex chromosomes

-also called X linked

- female has XX, male has XY

- if have abnormal trait will have 1 affected parent 

- if a father has xlinked dominant disorder, all daughters and none of the sons will be affected 

- if a mother has an xlinked dominant disorder, there is a 50% chance that her children will be affected 

- may be lethal in males, family hx of miscarriage and predominance of female offspring. 

- primarily affected people are males with unaffected parents 

-all daughters of an affected male will be carriers

-sons of affected males are unaffected and can't transmit disease

- unaffected males of a female carrier don't transmit the disease 

-conncetive tissue disease

-affects men/women equally, 1 in 20,000 people 

- inherited autosomal dominant trait 

-pathogenesis is related to the dysfunction of the gene that codes for fibrillin I, major component of elastic fibers

- joint hypermobility (circus contortionist)

-sprinal deformity 

-heart: mitral valve prolapse

-vascualr: aortic valve disease, weakness of aorta leading to dissection 

- defect in amino acid metabolism 

-inability of the body to convert the essential amino acid phenylalanine to tyrosine-a precursor to melanin

-accumulation lead to mental retardation 

-rx: diet restriction of phenylalanine (low protein diet)

- accumulation of glcolipids in the brain neurons & retina

- deficiency of hexosaminidase A enzyme 

-mental retardation and motor problems 

-blindness

-seizures

-death occurs by 2 to 5 years 

* most common in retina (cherry red spot on macula)

- chloride transport decrease

- mutation in gene CFTR which is required to regulate compinents of sweat, digestive fluids, and mucus 

-abnormal transport of chlorid and sodium across the epithelium 

- respiratory infections- difficulty breathing 

- sweat test 

- alterations in structure one or more chromosomes with rearrangement/deletion of chromosome part

(radiation/chemical exposure or viral infections)

- abnormal number of chromosomes (failure of chromosomes to separate during oogenesis/spermatogensis) 

Trisomy 21

- chromosomes 21 has 3 copies instead of 2

- phenotype: protruding tongue, flat nasal bridge, small ears

-mental retardation, heart problems

-advise for pregnant mom: under 35 triple screen, check for alpha fetoprotein. over 35 amniocenteses, chorionic villi sampling 

- amniocenteses risk for miscarriage so many women don't do it 

- partial/ total inactivation of X chromosomes

- have 45 chromosomes, 22 pairs of autosomes and 1 sex chromosome, usually the X

- present in 1 in 2,500 live births

- often results in spontaneous abortions 

- diagnosed through genetic testing 

- range from no clinical manifestations to moderate (depends on degree of inactivation/deletion of X)

- short statue and webbing of neck

- lack of secondary sex characteristics 

- absent ovaries, amenorrhea

- associated with CHD

- may have signs of mental retardation 

- error in fetal development that results in structural or functional deficit- caused by environmental stimuli  (xrays, viruses, drugs, alcohol)

-effect dependent on: timing and dose of exposure, maternal health and nutrition, paternal health and chemical exposure

T: toxoplasmosis

O: other- hepatitis B and herpes zoster

R: rubella (german measles)

C: cytomegalovirus (CMV)

H: herpes simplex 

all teratogenic 

can cause microcephaly, hydrocephalus, eye/hearing prob

maintain the body's normal fluid and composition 

- water is the most common substance in the body (46-60% of adult total body weight)

- all fluid outside the cell (1/3 of body water) 

- intravascular fluid: plasma 

-interstitital: fluid between cells "third space", blood, bone, and connective tissue water 

- 2/3 of body water

- refers to fluid within the cell 

-contains solutes such as oxygen, electrolytes, and glucose

-metabolic processes take place here 

- ECF: sodium and chloride 

- ICF: potassium and phosphate 

- as people get older the body fluid proportion decreases

- less body fat, greater body fluid

- women have smaller % fluid in relation to total body weight than man and more fat 

- electrolytes

-minerals

-cells 

- body secretions and excretions also contain electrolytes

- imbalance of electrolytes can occur 

osmolarity: osmolar concentration in 1L solution 

osmolality: osmolar concentration in a kg of water 

*** because 1L of water weighs 1kg, the terms are often used interchangeably 

275-295 mOsm/kg

- a measur eof the osmotic concentration of blood serum, which can be affected by serum sodium, chloride, proteins and glucose concentrations 

the power of a solution to draw water across a semipermeable membrane 

- isotonic: same osmolality as ICF

-hypertonic: will draw fluid out of the cell 

-hypotonic: water is drawn into the cell 

-urine

-through the skin as perpiration and through the lungs as water vapor in the ait

-intestines and feces 

- average daily urine output: 1500ml

-" lungs: 300ml

-"skin: 500 ml

- feces: 200 ml

TOTAL: 2500 ml 

- normally fluid intake and fluid loss are balanced

- average adult needs 2500 ml per day of fluid intake 

- thirst mechanism is primary regulator of fluid intake 

- fluid intake is triggered by: osmotic pressure of body fluid, vascular volume, angiotensin II, hemorrhage, psychological factors 

water balance 

- goal is to have enough "effective circulating volume" to perfuse tissues

- mechanisms to increase volume: thirst, ADH, RAAS

mechaism to decrease volume: Atrial Natriuretic Peptide

ADH synthesis and storage--> osmoreceptors sence increased osmolality--> posterior pituitary releases ADH   --> ADH increases renal water reabsorption ---> osmolality returns to normal 

- increased thirst--> increased fluid intake --> increased water retention--> increased circulating fluid volume--> decreased plasma osmolality--> decreased ADH and thirst

- increased ADH secretion--> decreased water excretion--> increased water retention --> increased circulating fluid volume --> decreased plasma osmolality--> decreased ADH and thirst 

regulation of aldosterone secretion by the renin-angiotensin-aldosterone (RAA) pathway 

- aldosterone helps regulate blood volume, blood pressure, and levels of Na+, K+ and H+ in the blood 

***see chart*** 

dehydration, Na deficiency or hemmorage--> decrease in blood volume--> decrease in BP--> juxtaglomerular cells of kidneys secrete RENIN--> kidneys convert angiotendinogen from the liver to angiotensin I---> angiotensin I moves to the lungs where the ACE(hormone) converts it to angiotensin II--> angiotendin II is potent vasoconstrictor which increases BPuntil it returns to normal but also has an effect in the adrenal cortex which regulates release of aldosterone--> aldosterone reabsorbs sodium/water and excretes potassium and H+ into urine --> increased blood volume--> also increases BP 

ANH chart 

increase in total body sodium 

- increase in total body sodium--> increased drinking and osmotic shift of water out of cells --> increased plasma volume--> increased atrial stretching detected by atrial endocrine cells --> increased ANH release --> action on glomerulus to increase GFR (increasing plasma volume) and action on proximal tubule to decrease sodium reabsoprtion. 

- ANH: atrial naturaletic hormone: tries to get rid of fluid 

- atrial natriuretic peptide: stored in cells of atria and ventricles, opposes renin-angiotensin system, decreases blood pressure and volume 

- B-type natruretuc peptide: stored mainly in ventricles, levels correspond with heart failure, increase GFR due to vasodilation 

- concentration of particles in the plasma 

- **normal value: 275-295 mOsm/kg

- increased serum osmolality indicates FVD

-decreased serum osmolality indicated FVE 

- solute concentration of the urine 

- normal value is 500-800 mOsm/kg

- above 800= FVD

- below 500= FVE 

- ICF: 40% of body weight in adult; fluid within cell 

- ECF: 20% body weight in adult

- two main subdivisions in ECF: plasma and interstitial

-one minor subdivision: transcellular compartment 

- normally 1% of ECF

- found in CSF and peritoneal, pleural, pericardial cavaties, joint spaces 

- transfer of water b/t vascular and interstitial compartments 

 - cap filtration pressure: pushes water out of cap into interstitial space

- cap colloidal osmotic pressure: pulls water back into cap

-interstitial/tissue hydrostatic pressure: opposes movement of waater out of caps 

- interstitial colloidal osmotic pressure: pulls water out of cap into interstitial space 

- movement of water through capillary pores b/c of mechanical rather than osmotic force.

- 30-40 mm Hg at arterial end

- 10-15 mm Hg at venous end 

- 25 mm Hg in the middle 

- Capillary Hydrostatic Pressure: pressur pushing water out of the capillary into interstitial space 

^{capillary colloidal osmotic pressure} 

(capillary oncotic pressure)

-osmotic pressure generated by plasma proteins that are too big to pass through cappilary pores

- albumin- main one

-proteins attract fluid INTO the capillary

Starling's Law of the Capillaries 

interstitial 

- filtration is determined by the difference b/t the forces favoring filtration and those opposing it 

-  interstitial hydrostatic pressure: pushing water into capillary 

- interstitial oncotic pressure: pulling water out of capillary 

-very low pressures and are essentially equal, thus normally exert little influence on fluid movement in/out of caps 

Starling's law of the capillaries

capillary 

- capillary hydrostatic pressure & cap oncotic pressure not the same 

- at arterial end of cap, cap hydrostatic pressure (pushing water out of cap) EXCEEDS cap oncotic pressure (pulling water in)- net fluid movement is from cap into tissue, carrying nutrients with it 

- at venous end, cap hydrostatic pressure is LESS than cap oncotic pressure- net fluid movement is INTO the cap from tissue, carrying wastes with it. 

- at arterial end +10 

- fluid exits capillary since capillary hydrostatic pressure is greater than capillary oncotic pressure 

- no net movement of fluid since capillary hydrostatic pressure = capillary oncotic pressure 

- venous end -7

-fluid re-enters capillary since capillary hydrostatic pressure is less than capillary oncotic pressure. 

- excessive fluid in interstitial space

-evident when interstitial volume has been increased by 2.5-3L 

- can account for up to 10 lbs in weight

- generalized edema: anasarca 

1. increase in capillary hydrostatic pressure 

2. decrease in capillary oncotic pressure (anything that descreases protein levels will lead to edema)

3. lympth node obstruction 

- accumulation of fluid in the transcellular space 

-similar to edema, contributes to body weight, but not to fluid reserve or cuntion 

1. age 

2. climate

3. diet

4. stress

5. illness

6. medical treatments

7. medications 

8. surgery 

-two types: isotonic and osmolar 

- isotonic imbalance: water and electrolytes are lost or gained in equal proportions 

- osmolar imbalance: loss or gain of only water, thus osmolarity of the serum is altered. 

- isotonic fluid loss 

- body loses both water and electrolytes from the ECF in similar proportions 

-referred to as hypovolemia 

- loss of water and electrolytes from: vomitting, sweating, polyuria, diarrhea, bleeding, abnormal drainage or wound loss

- insufficient intake due to: anorexia, nausea, inability to access fluids, impaired swallowing, confusion, depression 

- complaints of weakness and thirst

- weight loss: mild, moderate, severe

-fluid intake less than output 

- decrease tissue turgor

-dry mucous membranes, sunken eyeballs, decrease tearing

-postural hypotension 

- results from h20 loss without the proprtionate loss of electrolytes

-results in increased serum sodium level and concentration

-results in intracellular dehydration 

-h20 is drawn out f the cells and into the blood 

-causes impaired cellular function (cell shrinkage)

- inadequate fluid intake: NPO, decreased thirst mechanism 

-watery diarrhea in children

diabetes insipidus

-increased solute intake: highly concentrated parenteral feedings, hyperglycemia

- involves greater losses of electrolytes

-results in decreased serum sodium level and concentration 

-h20 is drawn into the cells and out of the blood (cell swelling) 

- elderly and newborns 

-clients who have decreased responce to thirst

-clients whose kidneys have a decreased ability to concentrate urine

-diabetes insipidus: decreased ADH secretion 

- isotonic fluid excess

-body retains both water and sodium in similar proportion to normal ECF

-referred as hypervolemia 

- excess intake of sodium-containing intravenous fluids 

-excess ingestion of sodium in diet or medications (antiacids such as alka-seltzer)

-impaired fluid balance regulation related to: CHF, renal failure, cirrhosis of the liver

- weight gain

-fluid intake greater than output

-moist mucous membrane

-inc BP and central venous pressure

-crackles

-distended neck and peripheral veins 

- results from h20 gain without the proportionate gain of electrolytes such as sodium

-decreased serum sodium level and osmolality 

- too much ADH; sydrome of inappropriate ADH hormone 

- excessive intake of water (polydipsia)

- excessive ADH secretion due to SIADH

- electrolytes maintain fluid balance

- contribute to acid-base regulation 

-favilitate enzyme reactions 

-transmit neuromuscular reactions: Na and Cl are not stored int he body, K and Ca stored in cell and bone 

- electrolytes affected by almost any disease 

most abundant cation ECF 

- normal serum sodium 135-145 mEq/L

- major contributor to serum osmolality 

-control and regulates water balance 

-Cl and water are reavsorbed with Na from the kidney tubules 

-sodium is found in many foods such as bacon, ham, processed cheese 

-inverse relationship with potassium (usually) 

- decreased sodium in the blood plasma 

- causes h20 to move out of the vascular space into the interstitial space and then into the intracellular space 

- hyponatremia--> hypoosmotic 

- results from osmotic shift of water from ICF to ECF (eg, hyperglycemia) 

- most common

- caused by water retension 

- plasma sodium below 135

- serum osmolality below 275 

-urine specific gravity below 1.010 

- excessive sweating and loss of sodium

-GI suction

-extreme intake of salt free fluids

-adrenal insufficiency 

-head injury, stroke

-diuretic therapy 

- fatigue, muscle cramps, weakness: early 

-abdominal cramps

-nausea, vomitting, diarrhea

-headache

-confusion and lethargy 

-convulsions and coma 

- last two are worst/most severe hyponatremia: NEURAL symptoms 

- excess sodium in the blood plasma 

- increased extracellular osmotic pressure causes fluid to move out of the cells into ECF

- cell becomes dehydrated 

-plasma sodium exceed 145

- specific gravity of urine about or higher than 1.030 

- thirst

-dry mucous membranes

-rapid, weak pulse

-dry skin 

-oliguria

-headache, disorientaiton 

-seizure and coma if severe 

- normal serum chloride is 98-106 

-essential for the production of hydrochloric acid in the stomach 

-functions to maintain the osmotic pressure in the blood 

-reavsorbed in the kidney secondary to sodium 

-involved in acid-base balance in the body 

- usually when Cloride levels are abnormally high or low, there is a corresponding increase or decrease in postassum and sodium levels

-clinical signs and symptoms are those expected with potassium and sodium 

- major cation of ICF 

-normal range is 3.5-5

- primarily intracellular 

-insulin promotes entry of postassium into cells 

-regulated by EC/IC shift- insulin 

-regulated in kidneys by 2 mechanisms: exchange with sodium in the tubules, and secretion of aldosterone 

- below 3.5

- vomitting and gastic suction 

-diarrhea

-increased urine production

-prolonged sue of potassium wasting diuretics 

-poor intake of potassium in diet 

- muscle weakness and leg cramps 

-fatigue 

-anorexia and N+V

- decrease bowel sounds 

-cardiac arrythmias

-EKG changes (prolonged PR interval, flattened T wave)

- less than 3.5 mEq/L

- ABG's show increased pH and HCO3- 

- EKG shows flattened T waves and depression of the ST segment 

- avocado, carrots, tomatoes, raisins/dates, bananas, cantaloupe, orange juice, milk 

- crushing injury

-kidney disease

-adrenal insufficiency 

-infection

-increase intake of postassium 

- potassium sparing diuretics 

- gastrointestinal hyperactivity 

-cardiac arrhythmia 

-muscle weakness

-paresthesisas

-numbness in extremity 

-K+ above 5

-EKG changes and irregularity 

- normal range 8.5-10.5 mg/dL

- store in bone, excreted by kidneys 

- functions: cation found in ICF, regulated by PTH, vitamin D and calcitonin, transmission of nerve impulses, contraction of cardiac muscle, formation of bones and teeth, coagulation process 

- etiology: poor absorption (GI, pancreatitis, vitamin D), renal failure, hypoparathyroidism, hyperphosphatemia (inverse relationship with phosphate)

- clinical presentation: tetany, +trosseau sign, +chvostek sign, prolonged ST and QT, laryngeal stridor, hypotention-arrest 

- blood pressure cuff is placed around the arm and inflated to a pressure greater than the systolic BP and help in place for 3 minutes

- if carpal spasm occurs, test is positive 

- relax facial muscles

- stand directly in front and tap facial nerve either just anterior to earlobe and below zyogatic arch or between the zygomatic arch and the corner of mouth 

- a postive responce varies from twitching of the lip at the corner of the mouth to spasm of all facial muscles, depending on severity 

- etiology: increased bone release- immobility, fractures

hypophosphatemia, malignancies, hyperparathyoidism, increase GI absorption 

-clinical manifestations: decreased LOC, EKG changes, shortened ST segment, AV blcoks, renal calculi*, bone pain, fractures*, calcifications 

- normal range: 1.8-3 mg/dL

- functions: second most abundant intracellular cation, contracts the myocardium, influences trasnport of Na/K across cells, role in metabolism of carbs/proteins 

- history of chronic alcoholism 

-vomitting and diarrhea

-malnutrition

-enterostomy drainage

-prolonged administration of Mg free solutions 

- insomnia

-hyperactive reflexes

-positive chvostek's sign 

leg and foot cramps 

-positive trousseau's sign 

- tetany

-convulsions

-cardiac dysrthymias 

- renal disease

- diabetes acidosis 

-antacids

-lab level above 3

- S&s: PVC's lethargy 

-respiratory failure/death 

- normal range: 2.5-4.5 mg/dl

- functions: anion found highest in ICF, bone and teeth formation, nerve and muscle activity, acid base, stores metabolic energy 

- etology: renal failure, excess intake (overadministration IV, PO, laxatives), hypoparathyroidism, hypocalcemia 

-clinical presentations: hypereflexia, S/S of hypocalcemia, phosphate deposits in joints 

- etiology: inadequate intake, malabsorption symdrome, hyperparathyroidism, renal phosphate wasting 

-calinical presentations: dyspnea, muscle weakness, confusion, decreased cardiac contractility 

sodium: 135-145 mEq/L

potassium: 3.5-5 mEq/L

chloride: 98-106 mEq/L

calcium: 8.5-10.5 mg/dl

magnesium: 1.8-3 mg/dl

phosphate: 2.5-4.5 mg/dl

serum osmolality 275-295

- hematocrit (HCT): measures the volume of whole blood that is comprised of RBCs

-increases with severe dehydration and hypovolemic shock

- decreases with severe overhydration 

-normal values: men 40% to 54% women 37% to 47% 

HgB normal values: 12-18g/ 100ml of blood 

female: 12-16, male 14-18 

- decreased levels of HgB are found with severe hemorrhage 

- usually hematocrit is 3x the hemoglobin 

acid: substance that releases hydrogen ions (H+) 

bases/alkalis: have a low hydrogen ion concentration and can accept hydrogen ions in solution 

-pH: reflects the hydrogen ion concentration of the solution 

- body cells are extremely sensitive to their environment 

-slight changes in pH can affect normal cell functioning 

-pH refers to the measurement of relative balance between acids and bases in solution 

- three types: neutral, acid, alkalotic 

-as acid is added to solution, pH will go down

-denote H+

- pH lower than 7 (7.35 in blood) 

- as bases are added to solution pH will go up

-accept H+

- higher than 7 (7.45 in blood) 

- human blood is considered slightly alkalotic 

-normal pH is between 7.35-7.45

-normally maintains ratio of 1 acid to 20 bases

- primary acid is Co2

-praimary base is HCO3 

- chemical buffers systems in body fluids: neutralizing excess acids/bases

-lungs: control elimination of CO2

-kidneys: eliminate H+ and reasorb and generate HCO3

- acidosis: H+ diffuses into cells and drives out potassium, elevating potassium concentration in ECF

-alkalosis: H+ diffuses out of cells and K+ diffuses in 

- eliminating or retaining Co2 by the lungs also regulates acid/base balance 

-CO2 and H2o ---> H2CO3 (carbonic acid)

- response is rapid, occur within minutes by altering the rate and depth of respiration 

- carbon dioxide is a powerful stimulator of respiratory system 

PaCo2 : partial pressure carbon dioxide 

respiratory regulation 

-paCo2 represents partial pressure of carbon dioxide in arterial blood

-normal level is 35-45 mmHg 

- increasing ventilation increases pH by eliminating Co2 

-decreasing ventilation decreases pH by retaining CO2 

-an acute rise in pCO2 is a powerful stimulant to respiration 

-ultimate long-term regulator of acid-base balance 

-slower to respond byt their responce is more permanent and selective 

-maintian acid-base balance by excreting or conserving bicarbonate and hydrogen ions 

-when pH decreases, H+ ions are excreted, and bicarbonate acid ions are formed and retained 

-when pH incrreases, H+ are retained, and bicarbonate acids are excreted

normal serum bicarbonate: 22-26 mEq/l 

- respiratory acidosis

-respiratory alkalosis

-metabolic acidosis

-metabolic alkalosis 

- pH normal: 7.35-7.45

-acidosis: less than 7.35

-alkalosis: greater than 7.45

-PaCo2 normal 35-45 (respiratory component)

-bicarbonate normal: 22-26 (metabolic component) 

- decreased bicarbonate with low pH 

- caused by: increased metabolic acids, inability of kidneys to excrete acid, excess loss of bicarbonate via kidneys/GI, increased chloride 

-body compensates by breathing faster to get rid of co2 

- overproduction of acids: diabetic ketoacidosis, starvation ketoacidosis, anaerobic metabolism, overdose of salicylic acid or ferrous sulfate

-renal failure, uremia 

-severe body loss of bicarbonate: diarrhea, pancreatic secretions lost via pancreatic fistulas, excessice acetazolamide or ammonium chloride, renal failure 

- increased bicarbonate with elevated pH 

-caused by: increased bicarbonate administration, excess loss of acid via kidneys/GI, increased bicarbonate levels by contraction of ECF via hypokalemia and hypochloremia 

- body compensates by slower breathing to retain Co2

- excess base loading: antacids, ringer's lactate

-loss of acid: gastric suctioning, vomitting, thiazide/loop diuretics

-contraction of ECF: decrease in ECF due to vomitting/NGT suction leads to loss of CL and reabsorption of Na and bicarbonate 

- increase in CO2 with decreased pH

-caused by: acute disorders of ventilation, chronic disorders of ventilation, increased carbon dioxide production 

- acute disorders of ventilation: impaired function of respiratory center in medulla, lung disease, chest injury, weakness of respiratory muscles, aiirway obstruction

-chronic disorders of ventilation: COPD, pulmonary fibrosis 

breathing is supressed, holding co2 in the body 

- decrease in CO2 with increased pH 

- caused by hyperventiliation, central stimulation of respiratory center, stimulation of peripheral pathways to repiratory center

-common with patients having panic attacks 

- central stimualtion: anxiety, pain, pregnancy, febrile states, sepsis, encephalitis, salicylate toxicity 

-hypoxemia: stimulation of chemorecptors in carotid bodies due to high altitudes 

-hyperventilation: anxiety 

- results when 2 or more primary acid-base disorders are presnt simultaneously 

-pH may change more dramtically in directino of acidosis or alkalosis depending on specific disorders involved 

-examples: renal failure + narcotic-induced respiratory depression = metabolic acidosis and respiratory acidosis 

-COPD + diarrhea= respiratory acidosis + metabolic acidosis 

- body's attempt to return the ratio of acid to base back toward 1:20 to maintain the pH between 7.35-7.45 

- patient is not considered to be compensated unless pH is within normal range 

-if changes in that direction are noted either in PaCO2 or HCO3 with minimal changes in pH, the patient is considered to be partially compensated. 

- normal values:

pH: 7.35-7.45 (below 7.35 acidosis, higher 7.45 alkalosis)

PaCO2: 35-45 mmHg (below 35 alkalosis, above 45 acid) 

HCO3: 22-26 (below 22 acidosis, above 26 alkalosis)

PaO2: 80-100 mmHg 

O2 salt: 95% or greater 

1. look at pH (last name first) acidosis or alkalosis 

2. first name next, look at CO2 and bicarb levels... whichever matches last name is first name: respiratory or metabolic 

1. type one: IgE mediated, immediate 

2. type 2: IgG, IgM mediated 

3. type 3: immune-complex mediated 

4. type 4: t-cell mediated, delayed 

-immidiate reaction after antigen exposure

-examples: hay fever, anaphylaxis (systemic), asthma 

- all IgE-mediated 

- steps:

1. exposure to antigen 

2. production of AB (IgE) against the antigen 

3. IgE coats the surface of mast cells (-minimal systemic effects with first exposure)

4. upon subsequent exposire to the antigen: degranulation of IgE-coated Mast cells and release of histamine, prostaglandins, leukotrienes ---> vasodilation, edema, mucous secretion, bronchospasm, epithelial damage, leukocyte infiltration 

-life threatening type 1 hypersensitivity reaction 

-systemic release of histamine, prostaglandins and leukotrienes

-marked hypotension

-marked bronchospasm

-marked edema

-angioedema

-itching

-GI cramps 

- mediated by IgG or IgM

-result in destruction of targeted cell

-ex: blood transfusion mis-match

-myasthenia gravis: makes antibodies against ACH receptors, muscles can't contract: paralysis 

-graves disease: antibodies made against thyroid cells, attach to cells & act like stimulators: hyperthyroidism 

type 3 immune-complex mediated disorders

-accumulation & deposition of insoluble antigen-antibody complexes

-may occur: following widespread bacterial or viral infection or with autoimmune diseases such as systemic lupus erythematosus 

- immune system making too many antibodies.. antigen complexes deposit in walls of blood vessels.. neurtrophils come to destroy antigen stuck to blood vessel, kill it by releasing toxins which also damage normal tissue 

- widespread deposition of AG-AB complexes in tissues, blood vessels and kidney 

-result in vasculitis, joint pain, renal damage, pain, fever, rash, lymphadenopathy 

-autoimmune disorder: female predominance of 10:1, genetic predisposition with certain MHC genes 

-b cells produce antibodies against multiple cell components: DNA, blood cells, ribosome, microtubules 

- wide range of targets= wide range of symptoms 

-"great imitator" 

- can effect multiple tissues 

-can spread widespread tissue damage (wolf bite?)

-characterized by exacerbation & remission 

-treat with NSAID's, corticosteroids, immune suppressing drugs 

-delayed hypersensitivity reaction: 24-72 hours after exposure 

-mediated by tcells and not antibodies 

-ex: contact dermatitis, latex allergy, poison ivy, tuberculin skin test? 

example: latex. 

someone can have a type 4 sensitivity to latex by contact dermititis by wearing them and have type 1 by breathing in the cornstarch molecules from the latex 

-epinephrine: bronchodilator and vasoconstrictor 

-hydrocortisone: antiinflammatory, blocks IgE interaction with mast cells 

-above must be given by IV for immediate effect 

- epinephrine NOT norepinephrine because nor has no beta 2 effects (no bronchial effects) 

1981: "gay related immunodeficiency sydrome"

1986: Human Immunodeficiency Virus (HIV)

2000: 60 million cases of HIV worldwide 

- contact with blood and body fluids

- sexual most common

-IV drug use 

-infected blood products 

-maternal-fetal transmission 

- must use "host cell" replication machinery "obligate parasite"

- RNA virus: double strand of identical RNA 

-"retrovirus:" must have its RNA genome copied into DNA in order to be replicated 

-center of virus is composed of protein capsid 

-surrounded by second layer of protein: viral shell 

-enveloped virus covered by lipid bilayer 

-peplomers or "spikes"= organs of attachment made of glycoproteins gp120 and gp41

-use human CD4 as sites of attachment (found on helper T-cells)

- reverse transcriptase: copies RNA into DNA- needed since body cannot do on its own 

-HIV integrase: integrates the HIV genome into the host cell 

HIV protease: necessary for HIV maturation 

1. using plus strand RNA as a template, a complementary DNA strand is made... produces hybrid RNA-DNA double strand 

2. RNA strand is degraded--> single strand of DNA

3. ssDNA is duplicated, producing dsDNA encoding the same info as the viral genome 

1. binding 

2. fusion

3. revere transciption 

4. integration

5. transcription 

6. translation

7. new virus assembly & budding

8. maturation 

- (Zidovudine) acts by inhibiting reverse transciptase 

1. primary infection

2. chronic asymptomatic (latency)

3. overt AIDS 

- 2-4 weeks 

-acute, flu like syndrome 

-very high "viral loads" - in the first month of so very large amounts of virus in the blood replicating quickly, level of helper t cells dropping 

-(aggressive treatment here may yield the best long term outcomes) 

- median time 10 years

-few overt signs or symptoms

- persistent lymphadenopathy possible

-viral load drops 

-CD4 cells are gradually dropping at this point (not obvious)

-disease spreading within from immune cell to immune cell

- CD4 cell counts < 200 cells/microliter

-can lead to death in 2-3 years without treatment 

-viral load rises

-overt symptoms: opportunistic infections, cancers, virus may enter CNS 

- varies from person to person 

-typical progressors

-rapid progressors

-slow progressors

-long term non-progressors (have mutation in chemokine receptors-CCR5 32-bp deletion- and makes it so that it can't bind correctly (Maraviroc)

- opportunisitc infections: take opportunity of impaired immune system to infect you

-cancers: kaposi sacroma (skin/oral cavity), burkitt's lymphoma 

-many viruses that usually aren't very harmful can cause seriosu reactions in AIDS patients because they can't fight them off 

HIV is major factor in resurgence of TB 

candida 

- late stage manifestation 

-direct HIV effects on the brain

-motor& mental impairment 

-amnesia 

-personality disorders 

-doesn't usually occur with treatment 

-similar effects as altheimers and parkinsons 

- fusion inhibitors (fuzeon t-20)

-Nucloside analogues, non-nucleoside RT inhibitors: reverse transcriptase (zidovudine (AZT), NEvirapine)

-protease inhibitors: maturation (ritonavir, saquinavir)