Human Experience of Health and Illness-Vanderbilt Nursing School
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
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| What is Cardiac Output? | Volume of blood being pumped by the heart in 1 minute
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| What does decreased CO do to tissue perfusion? | decreases tissue perfusion
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| What is shock? | SYSTEMIC abnormal cellular metabolism occurring when tissues are not getting enough oxygen to maintain the cellular function
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| Decreased Cardiac Output can lead to Ischemia, Hypoxia, Anaerobic metabolism and necrosis. Describe each. | Ischema- not enough blood getting to a part of the body (heart attack, stroke)
Hypoxia- not enough O2 to meet cell needs
Anaerobic metabolism- produces lactic acid, not enough energy b/c no ATP (requires O2), Na/K pumps fail, pH changes
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| How can you calculate Cardiac output? | Stroke volume X Heart Rate
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| If John's CO is low, what could his body do to compensate? What negative effect could this have on his body if it compensates too much? | Increase heart rate (Tachycardia)
Can lead to decreased diastolic filling->decreased stroke volume-> decreased CO
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| What is stroke volume? What determines stroke volume? What is the typical stroke volume? | how much blood is ejected from the left ventricle during each contraction. Typically ~70mL,
affected by Heart rate, preload, after load, and contractility
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| What is Starlings Law? | increase in ventricular volume increase muscle fiber length and tension -> enhanced contraction and improved stroke volume TO A POINT
If you have too much filling and too much stretch then you don't have enough contractility so heart will fail
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| What is afterload? | resistance experienced by the ventricles during systole (pumping of blood out of heart)
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| How does vasoconstriction affect afterload and cardiac output? | increases velocity of blood flow, to a point
may decrease cardiac output
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| How does vasodilation affect afterload and cardiac output? | decreases velocity of blood flow, decreases afterload, increase Cardiac output
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| What is preload? Why does this matter for CO? | volume of blood within the ventricles. Inadequate preload means inadequate stroke volume which means inadequate cardiac output
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| Your patient is taking a negative inotropic medication. How might this affect his CO? | (-) inotropic drugs decrease the force of contractility of the heart, decreasing the CO
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| What is blood pressure? How can you calculate it? | force of the volume of blood against the vessel wall
CO x afterload
or
Hydrostatic pressure x resistance
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| If your patient has a high systolic BP, what is happening in the heart? | the left ventricle of the heart is generating a lot of force to push the blood into the aorta with each contraction
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| If your patient has less pressure against the arterial walls during the relaxation phase of the heart, what would you expect of their BP? | low diastolic pressure
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| Your patient's BP is 120/80. What is her pulse pressure? | PP= SBP-DBP
PP=40
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| As babies age, their HR, RR, and BP tend to do what? | HR and RR decrease towards Adult normals
BP increases
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| Your patient has an increase HR and is believed to be in shock. He has lost a lot of blood or is dehydrated. What type of shock is he probably in? How do you treat? | Hypovolemic shock (loss of volume)
treat with IV fluids stat
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| What is a normal ejection fraction for the left ventricle? | 55-75%
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| Your patient is in apparent shock. His has just had a heart attack and his heart valves are not closing appropriately. What type of shock is this? How do you treat? | Cardiogenic shock
treat by increasing heart pump effectiveness
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| How do you know if your patient is in cardiogenic shock due to systolic failure? How do you know if your patient is in diastolic failure? | ejection fraction drops below 40% (normally 55-70%)
ejection fraction remains higher than 40% because blood is being pumped out, it just isn't getting in
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| Your patient is experiencing anaphylaxis. What type of shock are they in? Why? How do you treat? | anaphylaxis leads to vasodilation which leads to loss of vascular resistance so they are in Distributive shock.
Treat with vasoconstriction and volume expansion
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| Your patient's heart is blocked by a massive clot. What type of shock is your patient likely in? How do you treat it? | Obstructive shock because the heart cannot fill properly, treat by fixing the problem, increasing preload and decreasing afterload in hopes of getting blood out
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| Your patient presents to the ED with increased sympathetic NS responses, mild vasoconstriction, and increased heart rate. What stage of shock are they probably in? | Initial compensatory
the body is trying to make sure enough blood gets to all parts of the body by
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| Your patient presents to the ED with sympathetic stimulation and anaerobic metabolism in non vital organs. They are not peeing anymore. What stage of shock are they probably in? | Non-progressive compensatory shock, the body is still trying to save itself by prioritizing the body parts, starts the renin-angiotensin-aldosterone cascade so kidney's can keep working
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| Your patient presents to ED w/, absolutely no urine output, extreme weakness, vomiting and possibly altered mental status due to hypoxia of vital organs. Their metabolism is now mostly anaerobic so their blood pH low. Stage of shock? | Progressive uncompensated shock, body is shutting down
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| YOur patient is very confused, keeps passing out, has a weak, thready pulse, their organs are shutting down, and they are probably going to die. What stage of shock are they in? | Refractory irreversible shock
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| A patient presents to the ED. They are pale, blue, sweaty, combative, confused, vomiting, and nauseous, and have cool skin. You determine that they need fluids immediately. Why? | They are in hypovolemic shock and need fluids to replace the fluid loss immediately
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| Your patient is in shock. How is his body going to compensate with the sympathetic nervous system? | Vasoconstriction to increase venous return
Tachycardia and increased force of contraction
Hypotalamus tells you to drink
Posterior pituitary releases ADH
Adrenal cortex releases Aldosterone
Adrenal medulla releases epinephrine to ^BP and afterload
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| Why is decreased renal perfusion considered a compensatory mechanism of the Sympathetic nervous system if a patient is in shock? | kidneys stop getting blood, release renin which converts angiotensinogen to angiotensin 1 then 2 which tells the adrenal cortex to release aldosterone which tells the body to hold Sodium (which makes the body hold water) which can increase blood volume
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| Why might you pass out or feel dizzy if you lose a lot of blood? | Baroreceptors and vagus nerve reflex recognize that not enough blood is getting to your brain so it wants you horizontal so resistance is reduced
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| If your patient has extra aldosterone and ADH in their blood, how long has their body been compensating for shock? | a long time because those are the long term responses
if they are just dizzy and have vasoconstriction, they've been compensating for a short time
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| Why is it a problem if your body compensates for shock for too long? | ^ HR causes increased workload of heart, inadequate O2 supply can lead to decompensation (heart failure, MI)
Aldosterone, ADH, and RAA can lead to fluid volume overload (systemic or pulmonary edema, congestive heart failure)
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| A patient is in shock and suddenly has a problem breathing. What do you check for? | Pulmonary edema from fluid volume overload
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| What are the signs and symptoms of SHOCK? | S-skin is cool, clammy, blue, decreased pulse, >3 sec cap refill
H- HR increased
O-oxygen Tachypnea
C-consciousness, anxiety, irritability, confusion, coma
K- kidney- no urine
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| What can you do for a patient in shock? (VIP) | V-ventilation,
decrease O2 demand with rest and warmth, alleviate pain
maintain open airway, semi-fowlers
I-infusion
appropriate I&O, assess GI tract prior to giving PO, elevate legs, administer IV fluids
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| What can you do for a patient in shock? (VIP) | P-pharmacology
avoid IM injections (body deprioritizes muscles and skin)
administer oxygen
give inotropic medications (increase FOC)
chronotripic medications (slow heart)
vasoactive medications (vasoconstriction/vasodilation)
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| What are crystalloids? Colloids? (For IV fluids, shock patients) | Crystalloids- similar to body concentration, normal saline
Colloids- have big proteins in them, blood products, Albumin
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| How do you know if your shock interventions are working? | Skin-cap refill improves
HR- returns to baseline
O- Respirations-restful respirations
C-onsciousness- LOC back to baseline
K-idneys- making urine again
GI -normoactive bowel sounds
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| Patient shows up in nonprogressive shock. What do they look like? | increase HR, decreased urine
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| Why are you acidotic in hypovolemic shock? | lactic acid production resulting from decreased O2 deliver and increased anaerobic metabolism
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| Client comes to ED after car accident. Suspect internal bleeding. What INITIAL manifestation of hypovolemic shock might you see? | INCREASED HR, then increased respirations, then cool pale skin, then decreased urine
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| What is plasma? What is included in the plasma? | extracellular fluid, rises to top, clear yellow
albumin-maintains osmotic pressure
globulins-transport antibodies
fibrinogen-blood clotting
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| What cells are found in the blood? Primary function? | WBC- immune response
RBC- O2 and CO2 transport
Platelets- clotting
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| Where are RBC made? How long does an adult RBC live? What are immature RBC called? Mature? | made in red bone marrow
120 days
immature- reticulocyte
mature-erythrocyte
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| What is oxygen dissociation? | the concept that hemoglobin is combined loosely with O2 so that when O2 levels drop, HGB readily releases O2
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| What is hemoglobin A? | Major type of adult hemoglobin
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| Where are platelets created? Where are they found in the body? How long do they live? Function? | made in bone marrow, found circulating in body (20% stored in spleen), 1-2 weeks life span, clotting with activation of clotting cascade
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| What function does the kidney, spleen and liver have in blood formation? | Kidney- produce erythropoietin (growth factor to mature RBCs)
Spleen- destroy old RBC, stores platelets, breaks down hemoglobin
Liver- produces blood clotting factors, stores extra iron
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| Why are you concerned that a patient might have uncontrolled bleeding if their liver is damaged? | the liver produces blood clotting factors. Without the liver, you will have improper clotting
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| What is hematocrit (aka Packed Cell Volume)? | the % of red blood cells in the total blood volume, amount that sinks to the bottom, (~42%)
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| If you have decreased oxygenation due to low levels of RBC's, what might you expect to be elevated on a blood test? | high levels of erythropoietin to encourage maturation of stem cells into RBCs
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| What is anemia? | reduced number of functioning RBCs
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| What is mean corpuscular/cell volume (MCV)? | measures RBC cell size
well fed person has normal size RBC
small RBC indicate malnourishment
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| What is mean corpuscular hemoglobin (MCH) or Mean corpuscular hemoglobin concentration (MCHC)? | looks at the color of the RBC due to amount of hemoglobin
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| You send blood to the lab for a CBC on your patient. What are the expected findings? | RBC- 4.2-6.1 million/ul
Hgb- Female- 12-16 g/dl
Male- 13-18 g/dl
Hematocrit- Female- 37-47%
Male- 42-52%
WBC- 5000-10,000/mm3
Platelet- 150,000-400,000/ mm3
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| If your female patient has a CBC with the following results, what (if anything) are you concerned about? RBC- 4.5 million/ul Hgb- 13 g/dL Hct- 35% WBC- 4500/mm3 Platelet- 200,000/mm3 | Hct- low (expected 37-47%)
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| When looking at the RBC indices of your patient's blood test, what do you expect of the MCV, MCH, and MCHC? | Mean Corpuscular Volume- 80-95 fL
Mean corpuscular hemoglobin- 27-31
Mean corpuscular hemoglobin concentration- 32-36 g/dl
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| If your patient's blood work comes back and says they are microcytic and hypochromic, what does that mean? | Microcytic indicates a low mean corpuscular volume (MCV) <80 fL
Hypochromic indicates a low mean corpuscular hemoglobin concentration (MCHC) <32 g/dl
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| If your patient's blood work comes back and the MCV is 97 fL and the MCHC is 40 g/dl, what do you say about the results? | the MCV is high (expect 80-95 fL) so you call it macrocytic
the MCHC is high (expect 32-36 g/dL) so you call it hyperchromic
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| Why do you look at a reticulocyte count? What is normal range? If your patient has increased levels, what could this indicate? Decreased? | expect- 0.5-2.0%
looks at bone marrow function
High- may reflect response to blood loss or anemia
Low- indicates inadequate RBC production
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| If your patient has a reticulocyte count of 0.3%, what do you know? | they are not producing enough RBCs
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| What is different about fetal hemoglobin and hemoglobin A? | fetal hemoglobin has a higher affinity for O2
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| Your infant patient is diagnosed with physiologic anemia. What do you tell the parents? | this is totally normal, it results in infants around 6-12 weeks because the RBCs of infants live about 70 days (instead of 120). The hemoglobin level drops as the RBC's die and stimulates erythropoietin and RBC production and Hemoglobin A
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| In infants, you can expect to see (higher/lower) lab values, whereas in the aging population, you can expect to see (higher/lower) lab values for blood volume, hemoglobin, RBC, WBC? | Infants- higher
Aging- lower
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| Anemia is not a disease, but a sign of a disease. What blood tests can you order and expect to see if a person is anemic? | Low hematocrit
Low RBC
Microcytic
Hypochromic
Low hemoglobin
Increased reticulocyte
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| Your patient has sickle cell disease. What type of anemia do they have? | hemolytic anemia (increased cellular destruction)
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| Your patient has an iron, b12 and folic acid deficiency. What is likely causing their anemia? | decreased production of RBC
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| A patient complains of suddenly tired all the time. They are having a hard time doing their ADLs. When you check their vitals, you notice they have an increased heart rate and, orthostatic hypotension, and their O2 sat is 92%. What might be wrong? | Anemia
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| What is the most common cause of anemia in toddlers and young children, adolescents, and pregnancy? | Iron deficiency
during pregnancy due to increased blood volume, w/o increased iron
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| An adult patient presents to the ED with signs and symptoms of anemia (fatigue, tachypnea, elevated HR, decreased SPO2). What should you check for? | GI bleeding, most common cause of anemia in adults
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| World wide, what is the most common type of anemia? What are the major causes? How can you treat? | Iron deficiency anemia
-blood loss, dietary insufficiency, malabsorption of iron, increase in iron ultilization (infancy, adolescence, pregnancy)
Treat with increased dietary intake (leafy greens, red meat, eggs, raisins, kidney beans) or (supplement
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| If you have low iron or folic acid, what do you expect on the CBC? | Decreased RBC production b/c prevents DNA synthesis, cells are small and pale
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| A patient has aplastic anemia. What does that mean? What causes? | the bone marrow is not making enough new blood cells, so you see a reduction in all blood cells (RBC, WBC, and platelets)
Causes? toxins
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| If a patient's blood shows that they have hemoglobin S instead of hemoglobin A, what does this indicate? How long do RBCs with Hemoglobin S live for? What does this cause? | Sickle cell disease
Hgb S cells live for 12-15 days, leading to chronic anemia
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| Your patient has sickle cell disease. You are teaching them how to avoid a sickle cell crisis. Your teaching includes... | Avoid becoming dehydrated or low on oxygen, avoid infection, alcohol consumption, pregnancy, extreme temperatures, strenuous exercise, stress, anesthesia, and high altitudes
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| In a patient with sickle cell disease, you would expect their hematocrit to be (lower/higher), reticulocyte count (decreased/increased), and WBC (decreased/increased). | Hematocrit- decreased b/c of short lifespan of RBC
Reticulocyte count- increased, trying to replace RBC
WBC- increased due to chronic inflammation
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| What is the most common sign of sickle cell anemia? | Pain due to obstructed blood flow
Acute- chest, back, abdomen, extremeties
Chronic- can require high doses of opiodis
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| A patient comes in with a sickle cell crisis. How should you treat it? | Oxygen to alleviate hypoxia which causes sickling
Pain meds
Hydration via IV
Rest
Treat infection
monitor vital signs and PVS
Maybe blood transfusion
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| What is thalassemia? What does it look like in blood tests? How do you treat it? | a genetic defect in hemoglobin synthesis, fewer RBC and less hemoglobin
RBC are misshapen, small (microcytic) and pale (hypochromic)
treat with blood transfusions
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| Briefly describe thrombocytopenia, the causes, treatment, and prognosis. | an autoimmune disorder where spleen destroys platelets, triggered by infection, seen in children and women 20-40
bleeding and large brusing common
Treat with platelet transfusion and prevent trauma
Prognosis is great: 75% spontaneously recover
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| What is the function of BNP (B-type naturiuretic peptitde)? | BNP is excreted by the cardiac ventricles if there is too much preload in the heart. It blocks the effects of aldosterone so that the kidneys will excrete sodium and water in hopes of decreasing the preload of the heart
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| How do they kidneys affect fluid balance? | If the kidneys are not getting enough blood, they release renin which ultimately causes angiotensin II to cause thirst, vasoconstriction, secretion of aldosterone from the adrenal cortex (hold salt and water) in hopes of increasing BP
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| What role does the posterior pituitary play in fluid balance? | releases ADH in response to hypothalamus being thirsty (too much solute, not enough water), so the kidneys are told to hold water
also causes vasoconstriction to increase BP
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| What does aldosterone do? | released by the adrenal cortex in response to Renin and angiotensin II, tells kidneys to hold salt(and water), to increase BP
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| If your patient has a specific gravity of 1.200, what does that indicate? What does it look like? | Specific gravity is the density of urine compared to water (expect 1.005-1.030) increased means dehydration or SIADH, urine is concentrated
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| If your patient has a specific gravity of 1.000, what does that indicate? What does it look like? | Urine is dilute due to increased fluid intake, diuretics, or diabetes insipidus, urine is clear
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| Describe the difference between: Diffusion Filtration Osmosis | Diffusion- movement of particles
Filtration- movement of water due to hydrostatic pressure, gradient of SOLVENTS
Osmosis- passive movement of water based on concentration gradient of solutes
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| If you have a high concentration of solutes on the left side, what will osmotic pressure force the water to do? | Water will go towards the left side because the solutes are pulling the fluid
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| If you have a high hydrostatic pressure within a capillary bed, what happens? | Fluid is pushed out of the vessel into the interstitial space
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| Your patient is on an isotonic IV (normal saline). What does this mean? What can this do to the cells? | the solution has the same osmolarity as normal body fluids (person needs fluids and solutes)
Maintains normal concentration of solutes and water in cells
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| Your patient is on a hypotonic IV (.45% Sodium Chloride). Why? What can this do to the cells? | They are dehydrated, but don't need any extra solutes. This pulls water into the cells
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| Your patient is on a hypertonic IV (Total Parenteral Nutrition). Why? What can this do to the cells? | They need fluids, but need more solutes (sugar, protein, etc) than fluid to maintain proper osmolarity of the body. This pulls water out of the cells
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| What impact will anaerobic respiration have on the sodium-potassium pump, and ultimately the cells/ | Na-K pump will shut down because not enough ATP to keep them going, causes Na+ to go into the cells (which pulls water and can make cells explode) and K+ to exit the cells
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| You take a daily weight on your patient and determine that they have lost 5% of their body weight since yesterday. What fluid volume deficit would you say they have? | Mild- 2%
Moderate- 5%
Severe- 8%
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| What patients are at risk for Hypovolemia (fluid volume deficit)? | Elderly b/c decreased renal capacity to reabsorb
Infants- increased insensible fluid loss and decreased renal concentrating ability
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| A patient can have isotonic, hypertonic, or hypotonic fluid volume defecit. Describe each. | Isotonic- equal loss of Na+ and water (sweating)
Hypotonic- greater loss of free water (diarrhea)
Hypertonic- greater loss of Na+ (burns, kidney fail)
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| Your patient has Diabetes Insipidus. What does that mean? What do you need to be aware of? Treatment? | they have an ADH deficiency so they pee lots of dilute urine (low specific gravity) and are very thirsty. low BP, tachycardia.
Treat with Desmopressin (synthetic ADH)
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| You suspect a patient has a fluid volume deficit. What do you expect them to look like? What could the labs look like? | dry mucous membranes, disorientation (from decreased CO), slow cap refill, decreased skin turgor, decreased urine output, concentrated urine, postural hypotension
All cell components appear elevated because there isn't enough fluid to dilute them
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| If your patient has relative fluid overload, what does that mean? | They appear to have excess fluid because the fluids have shifted out of the blood stream into the intravascular space
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| What is iatrogenic fluid volume excess? | The patient has too much fluid in their body due to a medical intervention such as too high IV or encouraging too much PO intake
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| What is psychogenic polydipsia? Where do you see it? | Frequent in elderly, psychiatric disorder of compulsive water drinking (10-15 L/day!)
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| What is SIADH? What causes it? How do you treat it? | Syndrome of Inappropriate Antidiuretic Hormone, caused by too much ADH (cancer, tumor etc)
causes fluid volume overload and small urine output (eventually pushes fluid into lungs)
Must treat cause of it
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| If a patient has Kwashiorkor, why are their bellies swollen? | They have enough calories to survive but not enough protein in the body to keep the fluids where they need to be
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| You suspect your patient has a fluid volume excess. What do they look like? What do the labs look like? | Edema
Hypertension
Bounding pulses
Flushing
Low O2 and Crackles (from fluid in lungs)
JVD
Tachypnea
Pink frothy sputum as surfactant is washed out
Increased daily weight
Low cell counts and elecrolytes, high BNP
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| In a typical person, you would expect to see most of the Na+ (intracellular/extracellular) and most of the K+ (intracellular/extracellular). | Na+- extracellular
K+- intracellular
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| What patients are at risk for electrolyte abnormalities? | Elderly, dehydrated, immobile (can't access electrolytes)
burn patients
nausea/vomiting
malnourished
Kidney failure (kidneys regulate)
diuretics
meds that alter fluid/electrolyte
ANYONE IN HOSPITAL
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| What is hypernatremia? How can this affect the body? | decreased ratio of water to sodium in extracellular fluid (>145 mEq/L)
too much Na+ or not enough H2O
Increased cellular excitability
Can kill the brain by pulling water out of brain cells into extracellular fluid
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| Your patient is lethargic, weak, irritable, having seizures, has dry oral mucosa, elevated body temperature and is thirsty. What do you suspect? How do you treat? | Hypernatremia or dehydration
Increase water/decrease Na+ slowly PO
Give Hypotonic or Isotonic solutions as needed (hypotonic have more water, less sodium)
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| What is the normal range for sodium? | 135-145 mEq/L
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| What is Hyponatremia? What does this cause? | too much water, not enough sodium in extracellular fluid <135 mEq/L,
reduced excitability of cells
cellular swelling
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| Your patient comes in to the ED complaining of nausea, diarrhea, weakness, abdominal cramps and diminished DTR's. You notice that they constantly drink water. What do you suspect? How do you treat? | Hyponatremia, treat with sodium replacement, slow water intake, aquaphoresis and vasopressin
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| A patient has a Potassium level of 6.1 mEq/L. What do you expect? How do you treat? | They are hyperkalemic, cells are easily excited, difficult to regulate appropriately
The patient has muscle twitching, nausea, diarrhea, irregular heart beat
Restrict K+ intake, force K+ into cells (Insulin)
Remove K+ from body (dialysis)
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| A patient has acidosis of the blood due to respiratory distress. How will the body try to regulate? How do you treat? | The H+ will be pushed into the cells, but the K+ will be pushed out of the cells to maintain a charge causing hyperkalemia of the blood
Treat the acidosis (excess H+) with Sodium Bicarbonate to correct Hyperkalemia
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| If a patient is hypokalemic, what happens to the cells? What can cause this? | cells are less excitable, diuretics, wound drainage, NG suction cause actual hypokalemia
TPN and Alkalosis, hypotonic IVS can cause relative hypokalemia
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| If a patient has alkalosis because they are hyperventilating, how will the body try to compensate? | Not enough H+ in blood stream, body shifts H+ out of cells and pulls K+ into cells to compensate. Causes Hypokalemia of the blood
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| If a patient has hypokalemia, what do they look like? How do you treat them? | weak, decreased tendon reflexes, irritable, confused, lethargic, decreased peristalsis, irregular heart beat because harder to reach threshold potential
Treat- Oral K+ supplements, IV administration
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| If a patient is Hypercalcemic, how does the body respond? | Heart, skeletal/smooth muscles, and nerves are less sensitive to stimuli
Kidney stones
Calciphylaxis (calcium deposits)
Tired, weakness, constipated, nausea/vomiting, excess clotting, hypertension, like hypokalemia
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| How do you treat hypercalcemia? | Discontinue calcium supplements
Give calcium binders
Hemodialysis to dialyse off unbound (small amount) portion of calcium
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| Citrate is a chemical used in blood donation to keep the cells from sticking together. What potential danger does this cause for patients with electrolyte imbalances? | Contributes to hypocalcemia because it binds with calcium
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| You put on a blood pressure cuff and notice Trousseau's sign (hand spasm). What does this indicate? | Hypocalcemia
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| Your patient is in renal failure. What would you expect of their calcium and phosphate? | Hypocalcemic and hyperphosphatemic
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| What white blood cells are typically responsible for phagocytosis (soldier cells)? They mature in the bone marrow. There can be mature (segmented nucleus) or immature (banded nucleus) cells. | Neutrophils
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| These WBCs are released from the bone marrow and mature in the spleen to machrophages. THey are part of the immune response. Serve as messenger cells to tell the immune system it needs more neutrophils. | Monocytes
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| These WBCs release chemicals (heparin to inhibit blood clotting so WBCs can reach infection, Histamine to vasoconstrict to keep blood in capillaries, and Kinins to dilatearterioles and let plasma leak into interstitial spaces) | Basophils
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| This WBC will be elevated if you have an allergic reaction or a parasitic infection. | Eosinophils
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| This WBC directs the immune system. They are born in the bone marrow and have memory for immunity. They produce antibodies. | Lymphocytes
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| What are the 2 types of Lymphocytes? What does each do? Which is most common? | B lymphocytes- antibody production
T lymphocytes- cell mediated immunity (75% lymphocytes)
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| CBC labs show a left shift. What does that mean? | There are lots of immature neutrophils being released from the bone marrow
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| The inflammatory response occurs in 3 predictable stages. What are they? | Vascular/Cellular response
Cellular Exudation
Tissue Repair
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| What happens during stage 1 of the inflammatory response? | Vascular/cellular response,
Vasodilation brings nutrients to injured area (redness/warmth)
Increased capillary permeability, stuff leaks into the interstitial space (pain, edema, loss of function)
Injured cells release cytokine ask neutrophils help!
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| What happens during stage 2 of the inflammatory process? | Cellular exudation-
WBC migrate through capillary walls
Neutrophils phagocytosis
Exudate forms at site (pus made of dead cells)
Platelets and fibrinogen form matrix to prevent spread
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| What happens during stage 3 of the inflammatory response? | Tissue repair
scab and scar formation
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| What are the cardinal manifestations of localized inflammation? | Swelling
Heat
Redness
Pain
Loss of function in body part
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| How do B and T cells work? | B cells are in the blood- covered in specific antibody receptors, immediate response
T cells are in the thymus- mature in response to call of B cells, help the B cells multiply and then release antibodies to destroy other antigens
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| What are the 4 stages of infectious disease? | Incubation- time between exposure and symptoms
Prodromal- nonspecific SS
Illness- specific SS to illness
Convalescence- acute symptoms disappear
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| What is the hallmark of most infectious diseases? What causes this to occur? | Fever
Phagocytosis releases pyrogens which produce fever by increasing thermoregulation in hypothalamus
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| Your patient has a fever. They want to know if they should take a fever reducing medication. Tell them the benefits and harmful effects of fever/ | Benefit- increased WBC production, enhanced phagocytosis, drowsiness
Harm- discomfort, restlessness, increased O2 need, Increased caloric need, dehydration
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| Who is at risk for infection? | Premature infants (don't get antibodies in last 3 mos
Children
Older adults (less likely to have B and T lymphocytes mature, less likely to make new antibodies)
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| Your patient's CBC w/ diff shows that they have 20,000 WBCs. What might this indicate? | Infection
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| What does RICE mean (think edema from infection). | Rest
Ice
Compression
Elevate
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| What should happen to your WBCs to indicate that an infection is being cured? | WBC trending down (fewer WBCs in CBC with diff)
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| What are ventilation, diffusion, and perfusion? | V- moving air through respiratory tract
D- exchanging gas between alveoli and blood
P- transport O2 and CO2 in blood to and from cells
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| Respiratory Regulation is controlled via CNS controls in Medulla and pons. The central chemoreceptors (in aorta) respond to (CO2/O2) while the peripheral chemoreceptors respond to (CO2/O2). | Central- CO2 (pH of blood)
Peripheral- O2
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| If your patient's BP decreases, how would you expect their respiratory rate to be affected? How would you expect a fever to affect the RR? | Increase Respiration
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| Your patient has COPD. What respiratory manifestation might you expect? | Hypoxia and Hypercapnia
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| What percentage of O2 is bound to the hemoglobin? what percentage is dissolved in the plasma as free gas? | Bound- 97%
Free- 3%
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| Your patient has an SpO2 reading of 60%. What do you do? | Request an SaO2 from the arterial blood gas from a respiratory therapist because SpO2 readings are not reliable below 70%
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| Carbon dioxide is found in your blood in 3 ways. What are they? | Dissolved in plasma (7%- partial pressure gas)
Combined with water as carbonic acid (70%)
Coupled with hemoglobin (23%)
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| Your patient is breathing 10 times per minute. What do you call this? | slow breathing- bradypnea
expected (12-20 breaths/minute)
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| What is tidal volume? Inspiratory reserve? Expiratory reserve? Residual Volume? Respiratory dead space? | TV-normal inspiration/expiration (500 mL)
IR- extra deep breath beyond TV (3000 mL)
ER-extra forceful expiration after TV (1100 mL)
RV- air left in lungs after ER (1200 mL)
dead space- no gas exchange (trachea, nose, pharynx)
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| Your patient is hypoventilating (taking shallow breaths). What does their O2 and CO2 look like? | Low O2
High CO2
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| Your patient is in shock or has a pulmonary embolis. What does this do to perfusion? | Ventilation without adequate perfusion so the air is not being carried in the blood
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| What would cause a ventilation perfusion mismatch where perfusion was good, but ventilation was not? | shallow respirations, atelectasis, pneumonia
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| What is pulmonary hypoxic vasoconstriction? | the lungs are compensating for collapsed alveoli by redirecting blood flow to working alveoli so that the body gets oxygenated blood
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| What clients are at risk for alteration in gas exchange? | Post op patients
Pulmonary diagnosis
Tobacco use (pack per day x years smoked)
Airway occlusion
Decreased CO
Older adults
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| Why are older adults at risk for alteration in gas exchange? | chest wall stiffens = reduced ventilation capacity
respiratory muscle atrophy
loss of elastin, risk for alveolar collapse
decreased response to hypoxia
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| What is the first symptom of hypoxia? Secondary? | First- decreased mental activity
secondary- tachypnea, difficulty speaking, decreased SpO2, tachycardia, fatigue, cyanosis, ischemia
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| You are treating a patient with impaired gas exchange with an incentive spirometer. What should your goal be? | more than tidal volume
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