Patho Exam 1 Study PDF
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This document is a study guide for the Patho Exam 1, covering a broad range of topics including cellular structures and functions, metabolism, transportation, and tissue information. Includes important clinical information about diseases, and is useful for students of medicine and healthcare professionals to review key concepts.
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Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e process and packages protiens Golgi Apparatus synthesis of proteins...
Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e process and packages protiens Golgi Apparatus synthesis of proteins Ribosomes Makes ATP. Takes nutrients (eg glucose) and oxygen to create the energy, which drives up cellular respiration Mitochondria synthesis and transportation of protiens. synthesis of lipids Smooth and Rough ER DNA in the nucleus is transcribed into mRNA, which leaves the nucleus through the pores and goes to the cytosol. Here, it's How does DNA become Protien read by a ribosome (which is composed of protein and rRNA). To produce amino acids, the ribosome works w/ tRNA (which delivers each amino acid to the production) to form a protein Mircotubules part of the cytoskeleton (the 'bones' and 'muscles' of the cells) 1. movement 2. conductivity 3. metabolic absorption (all) 4. secretion The Eight Cellular Functions 5. excretion (all) 6. respiration (all) 7. reproduction 8. communication All cells have the same DNA information but express themselves why do cells express in different ways? in different ways based on their location, environment, etc. 1 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e Anabolism: the usage of energy to build molecules fatty acid + fatty acid + ATP = Lipid "Add" Catabolism: breaks down molecules that create energy protein = amino acid + amino acid + ATP "Cut" Energy Metabolism Anaerobic metabolism The metabolism that takes place in the absence of oxygen Aerobic metabolism Metabolism that can proceed only in the presence of oxygen. Passive Transport (doesn't use energy; goes down the concentra- tion gradient) substances diffuse across the plasma membrane (eg CO2, Oxy- gen, Alcohol) No protein involved Passive Diffusion Passive Transport (doesn't use energy; goes down the concentra- tion gradient) A membrance protein facilitates with the diffusion facillitated diffusion Passive Transport (doesn't use energy; goes down the concentra- tion gradient) Osmosis The movement of *water* down it's concentration gradient 2 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e Uses energy and a membrane pump; goes agaisnt the concen- tration gradient (up). active transport Tissue that covers the outside of the body and lines organs and cavities. epithelial tissue binds tissue and organs together adipose, cartilage, bone and blood connective tissue specialized cells neurons and glia Nerve tissue composed of myocytes striated, cardiac, smooth Muscle tissue Atrophy 3 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e decrease in cell size (thymus gland, gonads, disuse atrophy) increase in cell size due to mechanical stimuli (eg myocyte enlargement due to hypertension) Hypertrophy Hyperplaysia increase in number of cells (eg liver, start of cancer) change from one type of cell to a different cell type (such as chron- ic irritation of cigarette smoke causing ciliated pseudostratified Metaplaysia epithelium to be replaced by squamous epithelium). It is reversible if the causative factors are removed. the abnormal change of a cell in organization, size, and shape. Dysplasia *Not a true adative change* benign tumor does not spread but may become malignant malignant tumor metastasis (spreads) in situ tumor pre-metastasis. has not spread yet -Physical -Radiation -Chemical -Nutritional Imbalances (low or high) -Hypotoxic injury: cell injury or death due to the lack of oxygen due Call Injury and Ceath Causes to many causes (eg blockage, ischemia [ig lack of blood]) -Free Radial Injury: cell damage caused by free radicals (caused by radiation, diet, mitochondria, smoking, pollution). These radi- cals, ROS (reactive oxygen species), atk the cell causing oxidative stress that impairs cell function self destruction of a cell Physiologic process eg destruction of cells during embroyonic process, endometral cells during menses, breast tissue regres- Apoptosis sion after breastfeeding Pathologic process eg too much apoptosis (alzheimers/oarkisons) or too little apoptosis (cancer, autoimmune disorders) unprogrammed cell death due to a change in the enviornment (eg lack of nurtients) Necrosis Always Pathological Involves Inflammation Chromosomes 4 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e a threadlike structure of nucleic acids and protein found in the nucleus of most living cells, carrying genetic information in the form of genes. All cells in the body have 23 *pairs* chromosomes, except in the How many chromosomes do the egg and sperm have? egg and sperm that have 23 chromosomes two identical alleles for a trait Homozygous having two different alleles for a trait Hetrozygous 22 of the 23 pairs of chromoses. Autosomes X and Y chromosomes. 1 pair of chromosomes of the 23Autosom Sex chromosomes XX female XY male Single-gene -Autosomal Dominant -Autosomal Recessive Genetic Disorders -X-linked dominant or recessive (recessive is more common) Multifactoral 5 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e Chromosomes disorders Single-gene Male/female offspring are affected equally No carriers (either have it [Bb, BB] or don't [bb]) Ie Marfan Syndrome automsomal dominant Autosomal, dominant inheritance Long *thin limbs* Connective tissue affected High arched palates and occasional cleft palate but little orofacial malformations Clients shouldn't do physical activity Primary causes ocular, skeletal, and CV anomalies Marfan Syndrome the children have a 50% chance of being affected If one of the parents is heterozygous affected? If both of the parents are heterozygous affected the childern have a 75% chance of being affected Single-gene Autosomal recessive Includes carriers Male/female offspring are affected equally Ie cystic fibrosis, PKU,t tay-sachs autosomal recessive If both parents are unaffected but are carriers for the trait? 6 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e each offspring has a 25% chance of being affected 50% of being a carrier If both parents are affected? all of their children will be affected If one parent is affected and the other is not a carrier? all of their offspring will be unaffected but will be carriers If one parent is affected and the other is a carrier each of the offspring will have a 50% of being affected A genetic disorder that is present at birth and affects both the respiratory and digestive systems. Sinuses, lungs (mucus build up), skin (sweat glands), liver/pan- creas (blocked), intestines, reproductive organs test sweat to find out if patient has disorder (elevated chlorides) Preventative Cystic Fibrosis an inherited disorder of protein metabolism in which the absence of an enzyme leads to a toxic buildup of certain compounds, causing intellectual disability. Patients are also usually lighter skinned with fair hair bc pheny- lalanine is supposed to convert to tyrosine =, which is a precourser to melanin. Phenylketonuria (PKU) Diet resitrtion (meats, eggs) a fatal genetic disease that causes fatty material to build up in the nerves, brain, and retina due to failure of lysosome function Brain damage -> lower IQ and motor problems Tay-Sachs Cherry spot on the retina Blindness, seizures, and death occurs by 2-5 years Only screening 7 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e Single-gene caused by genes located in the sex chromosomes sex-linked inheritance (sex-linkage) X-linked or Y-linked X-linked diseases/disorders usually affect males, females are usually carriers. And are recessive Males with X-linked recessive disease Cannot transmit the affected gene to sons but can to all daughters sons of female carriers have 50% risk of being affected Female carriers w/ X-linked recessive disease Daugthers of female carriers have 50% rish of being a carrier caused by 1. alterations in the structure of chromosome(s) ie radiation/chemical exposure and viral infection Chromosomal Disorders 2. Abnormal # of chromosomes ie failure of chromosomes to separate during oogenesis/spermio- genesis Chromosomal disorder caused by the presence of all or part of a third copy of chromosome 21. Instead of 46 chromosomes, there are 47 Risk increases w/ maternal age and for exposure to environmental factors Advice to pregnant people: 35 weeks amniocentesis, chorionic villi sampling Down Syndrome (Trisomy 21) small ears, flat nasal bridge, heart problems, protruding tongue A chromosomal disorder usually in females in which a sex chro- mosome is missing, making the person XO instead of XX, or part of one X chromosome is deleted. 45 chromoses instead of 46 Diagnosed through genetic testing Often results in spontaneous abortions Lack of secondary sex charactertistics (eg breast) Absent ovaries, amenorrhea, sterile Normal intellgence but difficultly driving, nonverbal problem solv- 8 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e ing, math Heart problems Turner Syndrome transports fasses, nutrients, and waste Help generate the electrical activity needed to power body func- Fucntions of the body fluids tions Plays a part in the transformation of food into energy To main parts: Intracellular (40% of tbw) and Extracellular (20% of tbw) Extracellular is divided into: TBW (total body water) a. Interstitial b. Intravascular (plasma and lymph fluid) c. Trancellular (fluids contained in various body spaces like CF, urine, sweat, synovial, etc.) As adults Does TBW is lower when we are childern or adults? Rationale: as we age, tbw decreases bc of renal decline, dimin- ished thirts perception, and decreased free fat mass & muscle mass fluid inside cells Intracellular (ICF) High concentration of K everything other than fluid inside the cells Extracellular ECF High concetration of Na Osmolarity definition concentration fluids shift from area of less concentration to area of greater If ICF or ECF changes in concetration concenration using active transport Kidenys, heart, lungs, adreanal glands, parathyroid glands, and Organs involved in fluid-electrolyte balance (6) pituitary gland Kidneys excretes or retains electrolytes to maintian balance Lungs regulates O2 cocentration provides blood to the other organs to allow them to conduct their Heart functions secretes *Aldosterone*, which causes sodium & water retention Adrenal glands while potassium is excreted Regulate blood calcium and phosphorus levels Parathyroid glands ^ calcium in blood v phosphorus secretes *Antidiuretic hormone (ADH)* -> makes body retain wa- Pituitary gland ter, no pee leads to the excretion of every electrolyte in the urine, except Diuretic calcium the tendency of H2O to move into one solution from another Osomtic forces through osmosis Net filtration forces favoring filtration minus forces opposing filtration Capillart Fluid exchange 9 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e Starling Forces Filtration to reabsorption capillary hydostatic pressure (plamsa-pushing) interstitial oncotic pressure (uses protien. btw cells-pulling) Forces favoring filtration capillary oncotic pressure (uses protien. plamsa-pulling) Forces opposing filtration Interstitial hydostatic pressure (btw cell-pushing) accumuation of fluid in interstitial Edema localized vs generalized vs pitting increase in capillary hydrostatic pressure increase in capillary permeability Edema is caused decreases in plasma oncotic pressure Lymph destruction daily weight visual assessment methods for assessing edema measurement of the affected portion application of finger to assess for pitting antidiuretic hormone Pituitary gland increase water reabsorption into the plasma ADH Heart - like during heart failure Natriuretic peptides ANP BNP increases excretion of Na by the kidneys renin angiotensin aldosterone system ^ h2o and sodium while v k and ^ vasoconstriation RAAS Isotonic Alterations there is not change in concentration when there is any loss or gain Hypertonic Alterations 10 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e Related to sodium gain or water loss. Results in hypernatremia (sodium levels above 145). Water movement from the ICF to the ECF (Intracellular dehydra- tion) - decreased osmolality Hypotonic Alterations - hyponatremia (sodium levels under 135) - water excess in ECF equal loss of fluids and solutes caused by an inadequate intake of Isotonic Dehydration eletrolytes and fluids more water loss then electrolyte loss Hypertonic Dehydration extracellular compartment excessive perspiration hyperventilation ketoacidosis Hypertonic dehydration causes prolonged fevers diarrhea diabetes insipidus (pee alot, thirsty bc there is insiffiucnt ADH) loss of more electrolytes than water Hypotonic dehydration extracellular compartment chronic illness, renal failure (eg kidney disease), chronic malnu- Hypotonic dehydration causes trition HR BP Assessment of Fluid Loss Venoud volume/filling Capillary Refill Rate Known as *hypervolemia* and results from excessive fluid in the extracellular fluid compartment *(No fluid shifts)* Isotonic Overhydration Causes circulatory overload and interstitial *edema* Rare but caused by excessive *sodium intake*. Hypertonic Overhydration Fluid is drawn *from* the intracellular fluid compartment, the ex- tracellular fluid volume expands and the intracellular fluid volume contracts. Known as water intoxication; the excessive fluid moves into the intracellular space and all body fluid compartments expand. Hypotonic Overhydration Electrolyte disturbances occur as result of dilution 135-145 mEq/L Primary determinent of plasma osmolotity Na essemtial for nerve impulses, muslce contraction and the move- Y is Na important ment of glucose and amino acids Too little Sodium hyponatremia 5.0 mEq/L hyperkalemia Mild atks: *membrance cell depolarization, initially increased neu- romuscular irritability* increased intake shift of K+ from ICF to ECF decreased renal excretion Hyperkalemia causes hypoxia acidosis *Addison diseases* renal problem which involves the accumula- tion of K and the excretion of H2O and sodium BLANK Hypwekalemia effects on EKG NEEDS COMPLETOPNS 12 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e 8.5-10.5 Calcium exist as protein bound, complexed and ionized (most) 1. Necessary for structure of bones and teeth 2. blood clotting 3. hormone secretion why is calcium important 4. cell receptor function 5. Contraction of muscles 6. Plasma membrane stability 7. Plasma membrane permeability maintains the Ca concentration of the ECF If ca is low, PTH is activated and calcium is mobilized from the bone if ca is too hight, PTH is inhibited as ca is stored in the bones parathyroid hormone (PTH) acts to sustain normal plasma levels of calcium and phosphate by Vitamin D increasing thier absortption from the GI Na-K inverse relationship Ca-Phosphate lipiduria, vit d deficiency nephrotic syndrome manifestions and risk factors risk factors: lupus, kidney diseases, DM, infections (eg HBV, HCV, HIV, Malaria), *NSAIDs* hematuria and some proteinuria in the urine treatment: corticosteroids and cyclophosphamide, plasmaphere- sis may be helpful Nephritic syndrome - renal insufficiency occurs when renal function is impaired to 25% the normal function Classification of renal failure - acute (prerenal, intrarenal, and postrenal) and chronic -end-stage renal failure (ESRF) -sudden decline in kideny function w/ a decrease in glomerular filtration and urine output with accumulation of nitrogenous waste Acute renal failure products as demonstrated by an elevation in plasma creatinine and BUN -can be reversable Prerenal: sudden and severe drop in BP (shock) or *interruption of blood flow* to the kidneys due to injury or illness Intrarenal: *direct damage* to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply Postrenal: sudden *obstruction* of urine flow due to enlarged prostate, kidney stones, tumor, or injury types of Acute renal failure Most common cause of ARF inadequate kidney perfusion (less than 25% of CO), diminished Prerenal AKI forces favoring filtration and drop or stop of GFR leading to oliguria reversible w/ reestablishment of adequate flow Cardio-vascular disorders: Heart failure, Myocardial infarction, Cardiac tamponade: decreased CO Hypovolemia/Hemorrhage Prerenal etiology Burns Dehydration Diuretic overuse Trauma or tumor Intrarenal AKI 19 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e Acute tubular necrosis ATN -> direct damage to the kidneys by inflammation, toxins (contrast media), drugs (NSAIDs), infection (glomerulonephritis, pyelonephritis), or reduced blood supply (hy- potension) occurs with urinary tract obstructions that affect the kidneys bilat- erally Postrenal AKI -bladder obstruction, tumors, calculi -anti-cholinergic drugs (urinary retention) -autonomic nerve dysfuction oliguria pathohysiology Postrenal AKI the backup pressure will compress the kidneys, may lead to in- trarenal failure Initiation The phases of AKI Oliguria Recovery no to little s&s Initiation phases AKI reduced perfusion or toxicity w/ kidney injury envolving maintenace phase, from weeks to months -oliguria -elevated BUN and serum creatinine -metabolic acidosis -edema, HTN, CHF -electrolyte imbalance (^ K, ^ Phosphate, V Ca, V Na) Oliguric phase AKI recovery phase Polyuric Phase glomerular functions returns, but tubules canont concentrate the filtrate Daily weights Assess serum electrolytes acute renal failure nursing interventions *Signs of hypocalcemia, hyperkalemia and hyponatremia* Monitor intake and output Provide special skin care to prevent breakdown The progressive inability, over months to years, of the kidneys to respond to changes in body fluids and electrolyte composition with an inability to produce sufficient urine Chronic renal failure CKF Results in gradual tissue destruction and loss of kidney function and affects nearly all organ systems Associated with *HTN, DM, SLE*, intrinsic kidney disease patho Chronic renal failure 20 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e gradual loss of nephron units no s&s until more than 75% of nephrons are lost -eventually the kidneys are unable to excrete metabolic waste and regulate fluid and electrolyte balance normal GFR (which measures the kidney function) us 120 ml/min Stage 1 normal GFR >90 ml/min Stg 2 mild gfr 60-89 ml/miin Stages of CKF Stg 3 moderate gfr 30-59 ml/min stg 4 severe gfr 15-29 ml/min stg 5 end stage gfr cast, too tight, impair circulation or edema -> blood vessels are constricted too much development of fat emboli (fat from the marrow; fat globules are released into the bloodstream) Pain Pulse Pallor 6 P's Paresthesia Paralysis Polar Cold Intracapsular (femoral head is broken within the joint capsule) -Femoral head and neck receive decreased blood supply and heal slowly Extracapsular (fracture is outside the joint capsule) -Fracture can occur at the greater trochanter or can be an in- tertrochanteric fracture Fractured Hip Yes. Are women more at risk for hip fracture? If so, why? Low estrogen during menopause makes elder women the most of risk abduction compression devices/stockings as it lowers the risk of blood clots lay on the side of the unaffected leg Interventions Hip fractures A condition in which the body's bones become weak and break easily. osteoporosis predisposes to bone fractures (pathologic fractures) osteoclast > osteoblast -lose a 1-2 in per year 24 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e - Endocrine dysfunction (Parathyroid hormone, cortisol, thyroid hormone, and growth hor- mone) - Medications Potential causes osteoporosis - Vitamin D deficiency - Underlying diseases - Low physical activity - Abnormal BMI -genetic -anthropometric: pale skin, small stature, women, less weight higher risk -dietary - high phosphorus low calcium risk factors of osteoporosis -hormonal -lifestyle -concurrent illnesses, meds, steriods (blocks the building of bone) -postmenopausal osteoporosis (estrogen deficiency, remodeling imbalance) Kyphosis (mid), Lordosis (lower), Dowager hump (upper) Manifestations of Osteoporosis Pain, bone deformity loss of height weight-bearing exercise Lifestyle Osteoporosis adequate dietary calcium adequate vitamin D Estrogen replacement -suppresses cytokines that induce osteoclast activity HRT Hormone replacement therapy the risk outweigh benefits of the bone benefits: cancer, CV dis- ease, thromboembolism infection of the bone (staphy); very difficult to cure Occurs mostly in childer 3-12 Exogenous - need portal of entry Endogenous - infection travels from one area in the body to another Osteomyelitis - organism lodges in bone, multiplies and initiates inflammatory response Pathophysiology Osteomyelitis - pus accumulates - leads to necrosis and death - new bone formation develops around the necrotic bone Osteomyelitis treatment 25 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e antibiotics, debridement, surgery, and *hyperbaric oxygen thera- py* arthritis caused by loss of cartilage cushion covering bones in joint most common in bearing weight joints; results in bone rubbing against bone -asymmetric just cus my left wrist has it, does not mean my right is affected -ESR and CRP increased show infection -Worse in the afternoon Osteoarthritis (OA) Overuse -Osteophytes grow outward and alter the bone contours and joint anatomy: bouchard (DIP) and heberden nodes (PIP) -sYNOVITIS (inflammation of the synovial membrane) and joint effusion Pathophysiology OA Exercise, Weight loss, and RICE. Treatment OA NSAIDs Braces chronic systemic disease characterized by *autoimmune* inflam- matory changes in the connective tissue throughout the body rheumatoid arthritis RA Woman more 3:1 Worse in the morning Synovitis—marked inflammation, cell proliferation Pannus formation—granulation tissue spreads ->thicken synovial tissue. leads to the distruction of catilage and bone. Pathophysiology RA Cartilage erosion—creates unstable joint Fibrosis—calcifies and obliterates joint space Ankylosis—joint fixation and deformity develop if untreated. Boutonniere deformity 26 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e RA flexion of PIP joint and hyperextension of DIP joint RA flexion DIP joint and hyperextended PIP joint Neck swan deformity RA results in ulnar deviation of the fingers at the MCP joints Ulnar drift raised, firm, nontender, overlying skin moves freely [occur with RA] subcutaneous nodules -morning stiffness lasting for at least 1 h to over 6 weeks -swelling or effusion of 3 or more joints over 6 weeks Diagnosis RA -symmetric arthritis -nodules -joint dislocation Balance between rest and moderate activity Heat and cold applications Physical and occupational therapy NSAIDs Glucocorticoids for severe inflammation Treatment RA Analgesia for pain Disease-modifying antirheumatic drugs, such as gold salts, methotrexate, hydroxychloroquine Biologic response-modifying agents, such as infliximab, rituximab, anakinra GOUT 27 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e a type of arthritis characterized by deposits of uric acid crystals in the joints -primary: inability to clear purine metabolic -secondary: from diet Big toe 'podagra' but can happen in other areas (ankle, knee) Medications Dietary restrictions -> less or no red meat, alcohol, organ meats, high levels of uric acids Male increased age GOUT Rish Factors alcohol, red meat and fructose drugs Deposits of monosodium urate monohydrate *tophi* 1000x more likely to develop renal stones than the general popu- Gout contiue lation trauma is the most common aggravating factor Tophaceous gout joint changes become permanent Normal osmalrity 275-295 7.35-7.45 pH of the body - by the lungs as CO2 gas (eliminate by breathing faster) Acid can be eliminated by - by the renal tubules (retain more bicarbonate) - by regulating secretion of H+ into urine what is the ratio btw bicarbonate and carbonic acid to maintain pH 20 (base) : 1 (acid) It will retain or eliminate CO2 (H2CO3) to regulate the pH within normal limits (hypoventilation or hyperventilation) ^ breathing v co2 v breathing ^ co2 respiratory system (acid-base balance) renal system (acid-base balance) 28 / 30 Patho Exam 1 Study Study online at https://quizlet.com/_fmcs1e the kidneys will retain or eliminate both HCO3 and H+ ions as needed (controls rate of excretion of these ions). its a slower system than the respiratory system When pH increases (alkalosis) --> kidneys retain H+ and excretes HCO3 When pH decreases (acidosis) --> kidneys excrete H+ ions and retains HCO3 draw blood from the arteies How to check someone for acidosis or alkalosis? ABG - arterial blood gas noraml range 35-45 mmHg PaCO2 -partial pressure of carbon dioxide in arterial blood ph: 7.35-7.45 PaCO2: 35-45 mmHg ABG Interprpretation Normal Values HCO3: 21-28 mEq/L PaO2: 80-100 mmHg O2 Sat: 95-100% alkalosis: >7.45 PH (acidosis,alkalosis) acidosis: 28 Bicarbonate ABG Acidosis: Hypoxia* Cyanosis Primary stimulation of CNS: anxenty, fear, salicylate toxicity hyperventilation Respiratory alkalosis causes Stimulation of peripheral pathways to respiratory center hypoxemia Numbness, tingling in face, hands, or feet Respiratory Alkalosis S/S LOC, Lightheaded hyperventilation The body's attempt to restore pH balance through respiratory or compensation in ABGs metabolic adjustments, with partial or full compensation over time. compensated or partially compensation Practice ABG ph: 7.3 Resitatory Acidosis PaCO2: 50 HCO3: 24 Practice ABG ph: 7.49 metabolic alkalosis PaCO2: 44 HCO3: 32 Practice ABG ph: 7.26 Metabolic acidoss PaCO2: 40 HCO3: 13 Practice ABG ph: 7.10 Mixed acidosis PaCO2: 50 HCO3: 15 Practice ABG ph: 7.54 respitory alkalosis PaCO2: 20 HCO3: 26 Practice ABG ph: 7.33 Metabolic acidosis PaCO2: 25 Partial compenstaion HCO3: 20 Practice ABG ph: 7.28 mixed acidosis PaCO2: 54 HCO3: 20 Practice ABG ph: 7.52 Metabolic alkadalosis PaCO2: 48 Partial compenstation HCO3: 36 30 / 30