Docsity
Docsity

Prepare for your exams
Prepare for your exams

Study with the several resources on Docsity


Earn points to download
Earn points to download

Earn points by helping other students or get them with a premium plan


Guidelines and tips
Guidelines and tips

FINAL EXAM REVIEW SHEET-Essentials of Pathophysiology-Questions With-Answers Latest Update, Exams of Nursing

FINAL EXAM REVIEW SHEET-Essentials of Pathophysiology-Questions With-Answers Latest Update Tested And Verified 100 Correct Score

Typology: Exams

2022/2023

Available from 10/28/2022

DOCSGRADER001
DOCSGRADER001 🇺🇸

4.6

(7)

999 documents

1 / 63

Toggle sidebar

Related documents


Partial preview of the text

Download FINAL EXAM REVIEW SHEET-Essentials of Pathophysiology-Questions With-Answers Latest Update and more Exams Nursing in PDF only on Docsity! 1 FINAL EXAM REVIEW SHEET-Essentials of Pathophysiology-Questions With-Answers Latest Update Tested And Verified 100 Correct Score Respiratory system includes: Nose and nasal cavity, Pharynx, larynx, trachea, Bronchi and their smaller branches, Lungs and the air sacs called alveoli, Hypoxemia - deficient oxygen in bloodstream / Hypoxia - a decrease in tissue oxygenation Hypercapnia – excessive carbon dioxide levels in blood / Dyspnea – shortness of breath Tachypnea – rapid respirations, >20 breaths per minute 1. Review the difference between primary and secondary brain injury • Primary brain injury - occurs as a direct result of the initial insult Example – Stroke, concussion • Secondary injury - refers to progressive damage resulting from the body’s physiologic response to the initial insult Example – brain swelling secondary to stroke • Critical factor in determining the neuronal cell fate after injury - degree of adenosine triphosphate (ATP) depletion 2. Review causes of intracranial pressure; how does it lead to impaired neurological function? Increased Intracranial Pressure (ICP) • Volume of cranium composed of three elements: o Brain tissue o Cerebrospinal fluid (CSF) o Blood • Normal ICP 0 to 15 mm Hg • Increased ICP can occur with space-occupying lesions, edema, or with obstruction or excessive Increased Intracranial Pressure (ICP) • Leads to impaired neurological functions due to: • Compression of brain tissue • Inability of the cranium to expand in adults – bones of skull fused in adulthood • Reduced blood flow to the brain from increased pressure • production of CSF 3. What are signs of increased ICP? • Clinical manifestations 2 o Headache, vomiting, and altered level of consciousness (drowsiness) o Blurry vision o Pupil responsiveness to light becomes impaired o Altered respiratory patterns and unresponsive to stimulation o Patient may become unable to move, verbalize, or open the eyes 4. Review the Glasgow coma scale, what is it used to assess? Standardized tool for assessing LOC in acutely brain-injured persons Numeric scores given to arousal-directed responses of eye opening, verbal utterances, and motor reactions Mild (>12), moderate (9 to 12), to severe (<8) Motor response is the most powerful predictor of patient outcome Decorticate posturing, abnormal flexor Decerebrate posturing, abnormal extension Traumatic brain injury (TBI) leading cause of death and disability in United States • Most head injuries incurred in transportation-related accidents, falls, firearms, and sports accidents • Severity of TBI is classified by the Glasgow coma scale (GCS) as: • Mild - GCS score 13 to 15 • Moderate - GCS score 9 to 12 • Severe - GCS score 8 or below • Primary injury • Usually caused by a sudden and violent blow or jolt to the head (closed injury) or a penetrating (open injury) head wound that disrupts the normal brain function • The injury can bruise the brain, damage nerve fibers, and cause hemorrhaging 5 Encephalitis o Inflammation of the brain commonly caused by West Nile virus, western equine encephalitis, and herpes simplex virus o Typical presentation includes fever, headache, malaise, muscle pain, rash seizure, confusion, stupor, and coma o Diagnosis - CT, MRI, lumbar puncture o Treatment - supportive with control of symptoms, including antipyretics, antiviral, steroids, antiseizure, fluid resuscitation 7. Review the different types of seizures. How are seizures diagnosed? • Generalized seizure - whole brain surface is affected during the seizure • Absence (petite mal): occurs in children, staring spells that last only seconds • Myoclonic: single/several jerks of limbs, upper body • Atonic (drop attack): loss of muscle tone, can cause falls • Tonic-clonic (grand mal): jerking of many muscles • Focal (Partial) seizures - abnormal electrical activity restricted to one brain hemisphere • Status epilepticus - continuing series of seizures without a period of recovery between episodes • Can be life-threatening Diagnosis ❖ Electroencephalograms (EEG) - assess electrical patterns of brain regions ❖ Laboratory studies - identify metabolic/nutritional deficits, infections, and exposure to toxins ❖ Lumbar puncture – rule out CNS infections ❖ CT, MRI to aid in identification of structural causes 8. Review the etiology of cerebral palsy. Is cerebral palsy reversible ? o Etiology o Prenatal infections o Mechanical trauma to the head before, during, or after birth o Exposure to nerve-damaging poisons or reduced oxygen supply to the brain o Treatment varies according to the nature and extent of brain damage o No cure o Muscle relaxants, anticonvulsant drugs, orthopedic surgery, casts, braces, and traction 9. What causes Parkinson’s disease? What does this condition affect? • Progressive loss of dopamine producing neurons within the brain • Dopamine deficiency associated with motor impairment Clinical manifestations o Difficulty initiating and controlling movements results in slow muscle movement, tremor, and rigidity o Tremor occurs at rest, hand tremors exhibit pill-rolling movements o General lack of movement, loss of facial expression, drooling, propulsive (shuffling) gait, and absent arm swing 6 10. What are the major mechanisms of spinal cord injury? How do we treat if we suspect someone has a spinal cord injury? Usually traumatic, a result of motor vehicle accidents, falls, penetrating wounds (such as a gunshot), or sports injuries Cord may be compressed, transected, or contused Mechanisms of injury Hyperflexion, hyperextension, compression Secondary injury may result from hemorrhage, swelling, ischemia, inflammation Treatment Appropriate stabilization of spinal vertebrae May be accomplished surgically with internal fixation or with external fixation and bracing High-dose methylprednisolone may be used to decrease secondary injury Intensive rehabilitation is required to maximize function 11. What happens with oxygen and carbon dioxide levels in the blood and lung with hypoventilation? Hyperventilation? Hypoventilation 7 Air delivered to alveoli is insufficient to provide O2 and remove CO2 Hypoventilation causes hypercapnia (high carbon dioxide) and hypoxemia (low O2 in blood) Causes of hypoventilation - morphine, barbiturates, obesity, myasthenia gravis, obstructive sleep apnea, chest wall damage, paralysis of respiratory muscles, surgery of the thorax or abdomen Hyperventilation Rapid ventilation Increase of air entering the alveoli leads to hypocapnia (carbon dioxide exhaled at a quicker rate than the body cells produce) Causes - pain, fever, anxiety, sepsis, high altitude, and brainstem injury Acute Respiratory Failure o State of disturbed gas exchange resulting in: o low PaO2 (<60 mmHg) o PaCO2 >50 mmHg o pH less than 7.30 (acidosis) o Causes - central nervous system problems, neuromuscular diseases, chest wall and diaphragm dysfunction, pulmonary diseases, airway problems Clinical manifestations of acute respiratory failure include: Hypoxemia, hypercapnia, headache, dyspnea, confusion, ↓ LOC, agitation, dizziness, restlessness Early signs - rapid, shallow breathing Late signs - cyanosis, nasal flaring, retractions A patient has acute respiratory failure. Which lab findings will the nurse expect to find? Alkalosis and hyperventilation Hypoxemia and hypercapnia Alkalosis and high potassium Elevated sodium and acidosis 12. Be able to identify normal versus abnormal ABG values and example of causes for metabolic acidosis/alkalosis , respiratory acidosis/alkalosis . ABG- Measured by pH ▪ Normal blood serum pH: 7.35–7.45 ▪ Body fluids, kidneys, and lungs help maintain balance ▪ Subtle changes can cause serious effects ▪ Three systems work to maintain acid–base balance - the buffers, respiratory system, and renal system ▪ Manages pH by altering carbon dioxide excretion 10 14. Review conditions that affect the lungs such as: asthma (extrinsic, intrinsic, exercise-induced), mycobacterium tuberculosis, COPD, cystic fibrosis, ARDS, pneumonia Asthma : Etiology Airway inflammation, airway obstruction Increased airway responsiveness to a variety of stimuli Occurs in 7% to 14% of U.S. population Most common chronic disease of children Extrinsic – allergic asthma 1/3 to 1/2 of asthma cases Pediatric onset An IgE-mediated response is common Treatment - pharmacologic therapy, allergen-specific immunotherapy, and environmental control Intrinsic – non-allergic Develops in middle age with less favorable prognosis No history of allergies Triggers include upper respiratory infections, air pollution, emotional stress, smoke, exercise, and cold exposure Allergen-specific immunotherapy and environmental control not helpful Exercise-induced asthma Common in children and adolescents 11 Bronchospasm often occurs within 10-15 minutes after the end of exercise, usually resolves in 60 minutes May be a compensatory mechanism to warm and moisten the airways Running, jogging, and tennis are the most common stimulators Clinical manifestations Wheezing Feeling of tightness of chest Dyspnea Cough (dry or productive) Increased sputum production (thick, tenacious, scant, and viscid) Hyperinflated chest Decreased breath sounds mycobacterium tuberculosis (Pulmonary tuberculosis (TB) Causes Mycobacterium tuberculosis Acid-fast aerobic bacillus Infects lungs and lymph nodes Infection Inhalation of small droplets containing bacteria Droplets expelled with cough, sneeze, or talking Classifications Primary (usually clinically/radiographically silent) May lie dormant for years or decades Reactivating May occur many years after primary infection Impaired immune system causes reactivation HIV, corticosteroid use, silicosis, and diabetes mellitus have been found to be associated with reactivation Pathogenesis Entry of mycobacteria into lung tissue Alveolar macrophages ingest and process microorganisms 12 Microorganisms destroyed or persist and multiply T cells and macrophages surround organisms in granulomas Pathologic manifestation is Ghon tubercle or complex Clinical manifestations: Low-grade fever, Chronic cough with purulent or bloody sputum (hemoptysis) Night sweats, Fatigue. Weight loss Diagnosis Sputum culture Chest x-ray TB skin test (Mantoux or PPD test) No able to distinguish between current disease or past infection False-positive PPD with other mycobacterial infections or bacille Calmette–Guérin (BCG) vaccine Treatment Administer multiple drugs (antibiotics) to which organism is susceptible Rifampin, isoniazid, ethambutol Therapy is for 9 to 12 months for active disease Therapy shorter in persons exposed with no active disease COPD 15 High dose antibiotics (bacterial infections) Acute Respiratory Distress Syndrome (ARDS) Etiology Damage to the alveolar-capillary membrane Causes widespread protein-rich alveolar infiltrates (pulmonary edema) and severe dyspnea Associated with a decline in the Pao2 that does not respond to supplemental oxygen therapy Mortality rate 30% to 63% Pathogenesis Atelectasis and decrease in lung compliance from lack of surfactant Fibrosis Pulmonary edema Disruptions in O2 transport and utilization Severe hypoxemia Causes Severe trauma Sepsis (>40%) Aspiration of gastric acid (>30%) Fat emboli syndrome Shock 15. What are signs of ARDS? Clinical manifestations include: Dyspnea, labored and shallow respirations Productive cough with frothy sputum Crackles or rales Hypoxia, cyanosis Fever Hypotension Tachycardia Restlessness, confusion, lethargy, and anxiety 16 16. What is a tension pneumothorax, how is it treated? Etiology Accumulation of air in the pleural space Air enters pleural space, lung collapses, and ribcage springs out Open “sucking” chest wall wound Air enters during inspiration but cannot escape during expiration Decreases venous return and cardiac output Clinical manifestations Tension pneumothorax is an emergency situation Severe tachycardia Hypotension Tracheal shift to contralateral (opposite) side Neck vein distention Subcutaneous emphysema Treatment Management depends on severity of problem and cause of air leak Lung collapse Chest tube placement with H2O seal and suction to remove air from pleural space Oxygen 17. What is Virchow’s Triade? How do these factors increase a patient’s risk for developing a pulmonary embolus? ✓ Virchow’s triad - factors causing thromboemboli formation include: ✓ Venous stasis/sluggish blood flow ✓ Hypercoagulability ✓ Damage to the venous wall (intimal injury) ✓ Common risk factors - immobility, trauma, pregnancy, cancer, heart failure, and estrogen use Pneumonia Etiology Inflammatory reaction in the alveoli and interstitium caused by an infectious agent Organisms enter lung, multiply, and trigger pulmonary inflammation Inflammatory cells invade alveolar sacs 17 Alveolar air spaces fill with exudative fluid Consolidates and difficult to expectorate (cough up) Causes Aspiration of oropharyngeal secretions composed of normal bacterial flora or gastric contents (25% to 35%) Inhalation of contaminants Contamination from the systemic circulation Viral Can be classified as hospital acquired or community acquired High risk Elderly Those with a diminished gag reflex Seriously ill Hospitalized patients Hypoxic patients Immune-compromised patients Clinical manifestations Severity of disease and patient age cause variation in symptoms Crackles (rales) and bronchial breath sounds over affected lung tissue Chills Fever Cough, purulent sputum Diagnosis Chest x-ray Parenchymal infiltrates (white shadows) in involved area Sputum C&S Sputum from deep in lungs Treatment Antibiotic therapy Based on sensitivity of culture 20 *Tip: When applying the method for ABG interpretation, remember to keep the R and O together and the M and E. NOTE: BICARB What does Respiratory Opposite mean? The CO2 (remember carbon dioxide represents the respiratory system) and pH will be OPPOSITE of each other…one will be elevated while the other will be decreased…this means it’s a respiratory disorder. CO2 ⬆, pH ⬇: Respiratory acidosis CO2 ⬇, pH ⬆: Respiratory alkalosis What does Metabolic Equal mean? The HCO3 (remember bicarb represents the metabolic system) and pH will be EQUAL…either both will be elevated or decreased….this means it’s a metabolic disorder. HCO3 ⬇, pH ⬇: Metabolic acidosis HCO3 ⬆, pH ⬆: Metabolic alkalosis Before solving ABG problems, you must commit to memory the following lab values: Blood pH: Normal: 7.35-7.45 Acidosis: <7.35 Alkalosis: >7.45 CO2 (carbon dioxide): Normal: 35-45 mmHg Acidosis: >45 mmHg Alkalosis: <35 mmHg HCO3 (bicarbonate): Normal: 22-26 mEq/L Acidosis: <22 mEq/L Alkalosis: >26 mEq/L Now, let’s apply the ROME method and solve practice ABG problems: Problem 1: pH 7.28, CO2 50, HCO3 24 Setup ROME: R: ⬆ (CO2 is 50 and acidotic) O: ✔ 21 M: NORMAL 22 E: pH: ⬇(pH is 7.28 and is acidotic) Answer: CO2 ⬆, pH ⬇= Respiratory acidosis, uncompensated: this is a respiratory problem and the pH is abnormal (acidotic)…the metabolic system (HCO3) is normal and is not at this time trying to compensate…if it was the bicarb would be abnormal (alkalotic) in an attempt to increase the pH to normal range. Problem 2: pH 7.30, CO2 40, HCO3 18 Setup ROME: R: NORMAL O: M: ⬇ (HCO3 is 18 and acidotic) E: ✔ pH: ⬇(pH is 7.30 and is acidotic) Answer: HCO3 ⬇, pH ⬇: Metabolic acidosis, uncompensated: this is a metabolic problem and the pH is abnormal (acidotic)…the respiratory system (CO2) is normal and is not at this time trying to compensate…if it was the carbon dioxide would be abnormal (alkalotic) in an attempt to increase the pH to normal range. Problem 3: pH 7.42, CO2 26, HCO3 18 Setup ROME: R: ⬇ (CO2 is 26 and alkalotic) O: ✔ M: ⬇ (HCO3 is 18 and acidotic) E: pH: ⬆ (pH is 7.42 and is NORMAL but alkalotic*) *You need to ask yourself what side of “normal” is the pH on? 7.40 is the absolute normal for pH…any value greater than 7.40 is considered on the alkalotic side, while any value less than 7.40 is considered on the acidotic side. Answer: CO2 ⬇, pH ⬆: Respiratory alkalosis, fully compensated: this is a respiratory problem and the pH is normal (on the alkalotic side of normal)…the metabolic system (HCO3) is ABNORMAL and on the acidotic side, so it is compensating. Since the blood pH level is back to normal, there is full compensation. However, if the blood pH was abnormal it would be partial compensation. 25 Third, you want to ask yourself do we have compensation? You're either going to have no compensation where would be uncompensated or you're going to have partial compensation or you're gonna have full compensation. I’m going to show you how to solve those problems with all three different scenarios so before you even try to solve an arterial blood gas problem you have to have this table committed to memory because you're going to pull from your memory bank for these values and apply it to whatever method you're using to solve the ABG problem. so let's quickly go over this 02:32 table pH a normal blood pH is 7.35 to 02:37 7.45 anything less than seven point 02:41 three five is considered acidotic 02:43 anything greater than seven point four 02:46 five is considered alkalotic 02:48 then carbon dioxide co2 a normal level 02:51 is thirty five to forty five anything 26 02:54 greater than 45 is acidotic and anything 02:57 less than 35 is alcoholic then we have 03:00 hco3 a normal level a bicarb is 22 to 26 03:05 and anything less than 22 is acidotic 03:08 and anything greater than 26 is 03:11 alkalotic 03:12 now let's look at the acronym roam our 03:15 stands for respiratory oh four opposite 03:18 m for metabolic and E for equal and I 03:21 like to keep the are in the Oh together 03:23 and the M and the e together to help me 03:25 keep my information separated so one the 03:28 world does respiratory opposite mean 03:31 well what value represented respiratory 03:33 27 that was our carbon dioxide level or a 03:35 co2 so whenever your carbon dioxide 03:39 level is high and your blood pH is low 03:42 hence their opposite its respiratory 03:46 acidosis when your co2 level is low but 03:50 your blood pH is high and can their 03:53 opposite its respiratory alkalosis now 03:56 what does metabolic an equal mean well 03:59 metabolic was represented with bicarb 04:02 hco3 so whenever your hco3 is low and 04:07 your blood pH is low hence they're equal 04:11 because they're both low its metabolic 04:13 acidosis when your bicarb is high and 04:16 your blood pH is high they're equal 04:19 because they're both high its metabolic 30 05:36 normal with our metabolic level now 05:41 let's apply Rome we have opposite going 05:45 on our respiratory systems high pH is 05:47 low so according to row 05:51 we have respiratory acidosis so we're 05:56 gonna write that out that's the story 05:58 acidosis so we've answered our first two 06:01 questions we figured out that we have a 06:03 respiratory problem and we figured out 06:05 that we have acidosis going on but our 06:08 third thing we need to figure out is do 06:10 we have compensation and this is where 06:13 you have to look further at your problem 06:16 I mean you know whatever method you're 06:17 31 using you have to dive a little bit 06:20 deeper with it so first of all ask 06:23 yourself do we have compensation going 06:25 on at all well whenever you have 06:27 compensation going on full compensation 06:29 that means the body has fully 06:31 compensated its corrected itself our 06:34 blood pH should be normal 06:38 is not normal so whatever you're solving 06:40 these problems and you see a normal 06:42 blood pH level you should be thinking 06:44 full compensation but we don't have that 06:46 so we can rule that out 06:47 now do we have partial compensation 06:49 going on maybe or are we completely 32 06:51 uncompensated for so partial 06:54 compensation would be another system 06:57 that is trying to balance it out for 07:00 instance we have a respiratory problem 07:02 we've determined that well if we had 07:04 partial compensation our metabolic 07:06 system should be abnormal because it 07:09 should be trying to throw itself until I 07:11 can alkalotic state so we can bring this 07:14 will actually increase this blood pH 07:16 back because remember they're trying to 07:18 balance each other out like how I talked 07:20 about at the beginning we don't even 07:22 have that our metabolic system is still 07:25 35 compensated but are we partially 09:03 compensated so our system that should be 09:06 helping balance this out because we 09:08 already have a metabolic problem should 09:10 be a respiratory system an arrest or a 09:12 system right now is normal so it's not 09:15 trying to make itself out normal to help 09:17 balance this acidotic blood pH out so we 09:21 don't have any compensation going on so 09:24 we have metabolic acidosis and 09:27 compensate it our next problem says that 09:31 our blood pH is 7.4 to our co2 or carbon 09:36 dioxide levels 26 and our bicarb is 18 09:39 so let's look at our blood pH normal 09:42 levels 7.35 to 7.45 we're at 7.4 to so 36 09:46 we're normal so right now if you're 09:49 thinking about compensation you should 09:51 be thinking oh I bet we have full 09:53 compensation I bet you're right but 09:55 we've got it this Herman is this arrest 09:57 for a problem or metabolic problem so 09:59 whatever we're looking at this blood pH 10:01 we're normal but what side of normal are 10:05 we on our wheel in the acid oxide normal 10:07 or the alcoholic side normal and to help 10:09 you do that remember that the absolute 10:11 normal blood pH is 7 point 4 0 so 10:15 anything greater than that would be on 10:18 the alcoholic side of normal and 10:19 37 anything less than that would be on the 10:21 Asus acidotic side so we're at 7 point 4 10:24 2 so we're on the alkalotic side so 10:28 we're just gonna put its elevated and 10:30 just fit alkalotic to help us remember 10:33 that now let's look at respiratory those 10:37 represented in carbon dioxide and we are 10:39 at 26 a normal level is 35 to 45 so we 10:44 are on the low side so we're gonna put 10:47 low and it's alkalotic so and then our 10:54 metabolic is 18 normal is bicarb is 22 10:58 to 26 so we are on the low side so we're 11:04 going 11:04 lo and we are on the acidotic side 11:08 because it's less than 22 so using the 40 12:39 normal but what side of normal is it on 12:41 absolute normal is seven point four zero 12:44 so it's seven point three seven so it's 12:47 lower than that so we're on the Asus 12:49 acidotic side of normal so we're low and 12:54 we're just going to put acid to help us 12:56 remember 12:57 okay respiratory normal carbon dioxide 13:01 is thirty five to forty five we're at 13:02 thirty two so we are low and we're on 13:07 the alkalotic asad so we're going to put 13:10 alcoholic here our bicarb is seventeen 13:14 normals 22 to 26 13:17 we are low so we are going to put low on 13:22 41 the metabolic part of our acronym and 13:24 what side of low are we on 13:26 we're on acidotic side so we're just 13:30 going to write a sit here now using the 13:33 row method when we look at our pH which 13:36 is on the low side and we look at our 13:38 metabolic it's also low so they're equal 13:41 so this is where we're at we have 13:43 metabolic acidosis and we are fully 13:53 compensated our blood pH is back to 13:57 normal but our respiratory system 14:01 because remember these two systems 14:02 balance each other up also when I'm 14:04 normal on the alcoholic side to help 14:06 balance those acidotic conditions we are 42 14:10 having so we are now fully compensated 14:12 our next problem says that the blood pH 14:14 is 7.5 one carbon dioxide is 47 and our 14:18 bicarb is 32 so let's analyze the blood 14:20 pH normal blood pH is 7.35 to 7.45 so we 14:25 are elevated because we're at 7 point 5 14:27 1 so it's increased and it's alcoholic 14:33 hey our respiratory system which is 14:35 represented with carbon dioxide is 47 14:39 normal carbon dioxide level is about 35 14:42 to 45 so we are on the high end so we 14:45 are elevated and it's acidotic and our 14:53 bicarb which represents the metabolic is 14:55 at 32 normal bicarb is 22 to 26 so we 15:00 45 this metabolic alkalosis okay so that 46 19. What are causes of anemia? Complications of anemia? Goal in treatment? 20. Review the following conditions of the blood including causes: polycythemia, thrombocytopenia, disseminating intravascular coagulation (DIC). How do we treat DIC? 21. What hormone plays a role in RBC production? What organ produces this hormone? 22. Review the difference between Hodgkin’s vs Non-Hodgkin’s lymphoma. How are these cancers diagnosed? 23. Review modifiable versus nonmodifiable risk factors for hypertension. How is hypertension managed/treated? What medications are often prescribed to manage HTN? What are complications of hypertension if left unmanaged? 24. Review the steps of the renin-angiotensin-aldosterone system in managing blood pressure. 25. What is coronary artery disease? 26. What is atherosclerosis? How does plaque formation begin? 27. Review the difference between stable versus unstable angina 47 28. What diagnostic tool is used to identify acute coronary syndrome? 29. Review the following terms: afterload, preload, cardiac output 30. Review the differences between left-sided versus right-sided heart failure, know signs/symptoms for each. 31. Review the signs and symptoms of shock. Review the causes of different types of shock including: anaphylactic shock, cardiogenic shock, hypovolemic shock, obstructive shock, septic shock (distributive shock) 32. What are complications of shock? 33. What are the stages of hemostasis? What medications can affect hemostasis? 34. What is hemophilia? What is the treatment for hemophilia? Quick Quiz Which characteristic best describes a malignant tumor? Virchow’s Triad includes all of the following EXCEPT 3 (Te) oO v6 6 Damage to arterial wall EN rel Symptoms of ARDs include all the following EXCEPT v1 2 6 Coenen en ek: hart Cntr) 5 | 50 End game End game Thrombocytopenia is caused by all of the following EXCEPT . O vi 0 a waz es ls 2 ao End game @ Overproduction of platelets Which of the following ABG values is outside of the normal range? 2 rn End game >a: cose 51 Decorated — OoMnt a ite sata Mann > Paice Fe FH Shere Yes Nig Vide Ptepne! Meee Hels ge Desitop Bonin @ so eer pares Doan nrc. aed ox camel EG | Btn rp anaes ciyantianrgitdersi998 Bro Tf] sa 26 OF CuO OTS ey oavene BY miieonrcrern. Qmensensrssin Bi rackgtereees Phim. inde @sakince Weta B Sees ue erase Non Hodes Lunnahoma le clagnosed bythe presen of aed srombergcelsina bind emearbamle meg ec: GePmtion ¥15 =e 2 __ Oa exrsilstnene tines [a crenn Tans “probes Geondicp eosekcp Documents OES evour ane 9/15 & kahootit n” Eee ms JD Unmute ~ Ge Stetvien ~ Share Photos Screenshot (5726),png ee oe €5¢@ [0 am SS voaviers impitvmne oma St A soe BB peipenatener Qrericentees tnt Kinng eens log sass (Yt me All of the following are presenting symtoms of left-sided HF except ZF Unmute - BStartvdao ~ ("1Share SeIAI=) @. Y Participants 3) = @" 8 oO ne ezle Lutner ACO april eapwood AMO pdsy Malpiea 2S 9 eureia sine 8 © pittary Palomine 2 chat Game PIN: 7566864 | ° °e = eee ¥ Partikipants 122) 2 saverh er eet Tors Micole Luther AG apri caynoos aM Oo 8S pureia Sainz Sallary Salone Partciparss = * " chat ’ . | ® € igame ‘ ¢ , 5 55 Which of the following leads to serum hyponatremia? ~~ ey @ SIADH QDexoweteemeesser | Crees fo Hide ven tor eon * . " i Seach fe mn - rp Ceistetoms gy « ©) FG [Ge rmmsrdestemetnncigonabitgtndeontce ins = © #4] O serch dng@ = i a. Go vere ‘ Brcmvitce BUwonitoniyrens Qerecnctiim. & tningesboneek. EB ppm. tag ase WY odes ter 3 howe rs AC & april eaywood a 8 aS apr sheer oompasnee nen ae ter re 5 n a B® semsrse © cee 3 Urmute ~ Bi statvdac ~ I Share @ 2 Typrhereto-search Qeviertinrbsiyy | Ore ans a ® trarat ‘a svat liptos © Participants (27) * Teorey . cs te seta se Gayo i" Cae | (0 cealnters gy : C2 FG [0B minrnndininivniasreietees es» & a] 2 sont kwae = Sia , ee es oe 8 . april caywood Oo # Disorders that cause hypoventilation would lead to which pH Imbalance? ° ° © 180 pawn sam © ttn Paorine « omen 2 i ‘aia © OO cece a kz la a . BM ar ce esses ape Gisor oelienea thelere eee v¥ oon Ae i © 4 , ZO S ZUnmte > eStetwolen © share @ wags | ©) ease 2 Type rere te search Desovievacmestings Oost ag info de sou er File Eat share View Auto @ Video Partiipart Mewsing Help $F vores ta cml ms © Panipat 7, x - ete ens sete sunt tem teen se 8 search ero trent 7 ©) 2 O [BB hseipantahor rujgmeblectigd seid: © wy], seach EROS Ey Nubian Maven ME sinieyrerm. Q tennis, Hrsg tained. Wiaiontsram. © pn dene W Neate ir. 2 bed © 2 wHterpot o 8 Inkl potents with malignancies of the blac and lymhold tase may be nyrngromatic OD 5% weiasaie " ll Ee EF O Brtsry Palorins 9 ae ° EEE 2 U coe @ kw Cea vie x Endgame ens 426° solace pit <v seul bum Tos | vaso oeet ¥ B/I2 & kahoot.it Game FIN: 5687935 | ne ° S Unmute - @Stetvden » shee B e Ei raricpars OD chat BD teach Module 9- blood disorders 57 é ee Fig Gd Stam Vew AucioM video Particvant Meeting Hep Ps oo Feena-Pri re cr e \ Parpas 28 « | ome me m sai Q Search, CEERS : epee er Dvn Min tenga Qa Ot. @ Resi tlewcent, EB cteuksinr th Sabtoue W Nain tnt \dantifythe ASC imbatznce: © <8 iesveca o 8 9° Ocidesise) oe : 1 | : wt [Pleo secs srieparts ©) Chat 3 ~ ZUrmuw + Bisivdes ve she Fo 8 TA Qeccowitwe Meets — Orders ey ies tet Son -o0 Seat, oF Deop ~ Patkpans 25) a Bouwiae, ‘Cecalis Nowra apni czywooe sural se = Lestany velemine “a " anak eo EE] (pe mabmn rn cenit (253 CG [0 0 etpatmtintymsistsansnsses is o & $7] 2s Enae = hese ume , @ CUHOMOT Ee om vencd BB nmpeiicamircrao GQ rscmicenvrscei ES ruringretewneces &Z amprisoemecracmm Login We caetwee W) seatecerne anor 3 Host arom @) Eo ries ole Which ofthe felowing isan exarele ofasymetor? Bede - hie vl UO wrttaryPalorins ® Son ee 70 ees a... ‘ Sree | = ES ao os om . Ia cen Tans =a ve fo Spx oben bjestie ; econtens cabjestine Geondicp eid eosekcp sjestive Documents 1 Doe onde aves BE Buns ums J Unmute ~ Fe Stetvien ~ Share tS) @ winsgaits | © ct som Acxovienecmetings OMeerag info =e Wen 3a cee ecg 1 9 Setia Tors © CQ [© aims 1p kab 2.2 arabosk ud 258301 T th) 0 sen sume esle Luther ae 2 vlomns ‘ ee Oo svn sie ‘ cia are Z Unie < Bi stetvdew ¥ Estee S See P Type rere te searey Addison’s- adrenal insuff. (lack of cortisol) 61 Dc ce Wicinen Meetings OoMert vg lr ke Rm Rar Seat oe cerned irene fearon 2 Seah a ceceliatd ure G1 Cece Toes s oe ACY april eaywood a ee eee g be O wrttary Palomine e a |CO aaa © D cece 4 OOo kz lu ore: 438 20 Ronee) . Terry J Unmute ~ Fe Stetvien ~ Share Ak Sams som Oy D. Wpe eee seen an 1 Qeaewtertininn OMewtwhie AueMense > SaaS | > wo Gee aru 5 5 Sh: EEE ro et 0 turds tones ‘ mem. Ke ROTO Ml [a ntpaemsceneyeranmenmacnset — all ams : 19 Gemma env Kiem Qtr, heer Aer. Bist Ne © sou came ‘ ‘ofthe folowing are signs acute respirator fale EXCEPT Bo . c) oO 1 oO E&) ©) coe ‘ == 2 foe ao | oe 2 wpe here to search 62 Dimensional Analysis Review: https://rasmussen.webex.com/webappng/sites/rasmussen/recording/78976728f25f4d6580fe4 01844c54f00/playback I&O Review: https://rasmussen.webex.com/rasmussen/ldr.php? RCID=dbdccb60a31f4b7da20a42c5bee5ec71