Medsurge 2 Final Exam Study Guide

Medsurge 2 Final Exam Study Guide Most people did not end up doing as well on the final as the other tests but good luck and it wasn’t terrible! Fluid and Electrolyte Balance- 8 Fluid Volume Deficit (alone or with electrolyte imbalance) o A decrease in intravascular, interstitial, and/or intercellular fluid in the body o Causes: excessive fluid loss, insufficient fluid intake, or failure of regulatory mechanisms and fluid shifts within the body o Types: Hyperosmolar Description o Blood becomes hypertonic o The water moves out of the cells to dilute the extracellular tissue causing the cells to shrivel and become dehydrated o Not enough water can cause hypovolemia Causes o Decreased fluid intake (gery doesn’t recognize thirst) o Increased water loss (diabetes insipidus) o Hyperosmolar dietary intake (like TPN) o Build up of solutes due to disease (cancers associated with bone metastases) o Sequestration of body fluids (edema, pleural effusion, ascites) Isotonic Description: loss of WATER AND SOLUTES from extracellular spaces (balanced loss) Causes o Hemorrhage, excess sweat, GI loss (N/V, NGT, ileostomy), wound drainage o Signs and Symptoms Skin: dry, flushed, poor turgor Mouth: dry, sticky mucus membranes Eyes: sunken eyeballs, tears decrease CNS: weak, restless, confusion, increased pulse pressure (systolic decrease and diastolic increase) CV: orthostatic/postural hypotension, tachycardia Other: thirst, water, weight loss Urine: decreased UOP Labs: Isotonic: normal Hyperosmolar: BUN, creatinine, hematocrit, urine osmolarity and specific gravity all increase o Treatment: fluid replacement and rehydration Hyperosmolar: If normotensive, hypotonic solution If hypotensive, isotonic solution Isotonic: isotonic solution (bc only volume is decreased) o Nursing Care Assessment: meds causing fluid loss, illness, access to fluids Physical assessment: weight, VS, bp!, UOP Careful I & O: watch for 30 mL/hour o Nursing Diagnosis Deficient fluid volume Ineffective tissue perfusion Risk for injury Fluid Volume Excess - Typically results from conditions in which Na and water are retained - Types (Hypotonic and Isotonic): o Hypotonic causes: Renal failure- decreased UOP due to failure/disease Pump failure CHF or renal perfusion deficit Oral hydration overload- too much water at once (enema, psych issues) SIADH- water retention issues (weight gain, no edema), dilutional Na (seizure risk) No edema, low Na, give meds to prevent seizures Na >120 is a major concern o Isotonic Causes: Increased venous pressure (obstruction due to DVT) Increased aldosterone (cushings- NaCl and water reabsorption; cirrhosis- decrease in metabolism of aldosterone) Decreased capillary oncotic pressure 1. Loss of protein (burn, liver disease, nephrotic syndrome) o leads to outer extremity edema Increased interstitial oncotic pressure: blocked lymphocytes o Symptoms Skin: dependent edema, tight cool skin CNS: lethargy and confusion Respiratory: SOB, cough, crackles, increased breathing rate, frothy sputum, decreased O2 stat, dyspnea at rest CV: full pulse, distended veins, tachycardia Labs 1. Isotonic- normal 2. Hypotonic- decreased Na, Hct, osmolarity, BUN, specific gravity Types of edema Increased hydrostatic pressure in blood causes fluid to shift into tissues o Pitting (ankle/dependant)- CHF or pregnancy o Pulmonary- blood not pumping out fast enough and stays in lungs o Ascites- liver scarring prevents portal blood from going into liver so ascites is seen Edema caused by electrolyte imbalance o Cerebral edema (fluid shifts to brain and causes swelling and seizure risk) o Low protein edema- nonpitting, low albumin if poor nutrition or malnourished (so increase dietary protein) Often seen in burn victims o Edema caused by lymphatic problems- either nodes are removed or can’t filter properly Treatment of fluid volume excess Diuretics (K sparing or not sparing) Fluid restriction- divided throughout the day (plan) Sodium restriction- no added Na and remove high Na foods from diet Elevation of HOB/FOB depending on symptoms Lymphedema Nursing Care Health assessment: history, recent weight gain, diet (Na), complaints of SOB at rest, coughing, edema Physical assessment: weight, VS, lung sounds, UOP, consciousness Nursing Diagnosis Fluid volume excess Risk for impaired skin integrity Impaired gas exchange IV Fluids FLUID CLASSIFICATION Isotonic Lactated Ringers (LR): a balance electrolyte formula, commonly used for surgical patients. Hypotonic 0.45% Normal Saline (1/2NS): Treats cellular dehydration and promotes waste elimination by kidneys. Hypertonic 5% Dextrose and 0.45% Sodium Chloride (D51/2NS):Draws fluid into the vasculature from interstitial and intracellular compartments. NAME AND COMMON USES OF FLUIDS Normal Saline (0.9%NS): used for vascular volume expansion and fluid resuscitation. 5% Dextrose (D5W): Can become free water when dextrose metabolizes; expand intracellular and interstitial fluids. 3% Sodium Chloride (3%NS): Prevents seizures from severe hyponatremia. 5%Dextrose and Lactated Ringers (D5LR): Electrolyte formula used for patients with draining wounds. 5% Dextrose and Normal Saline (D5NS): provides calories to prevent catabolism when NPO Total Parenteral Nutrition (TPN): Used when patient is NPO more than 5 days or have extensive caloric needs (burns, GI surgery) TPN (Total Parenteral Nutrition) central line o Large bag of hyperosmolar solution o Provides items necessary to sustain life (fat, protein, glucose, vitamins, electrolytes) o Not a tube feeding- use patient’s gut instead if it works Indications: Patient can eat but not getting enough (burn, anorexia) Bowel system off limits Not for those who can be fed enterally Administration: Give via central line Hanging TPN: q day at night, change bag/tubing with each TPN Nursing Care: Hang new bag exactly when ordered Discard old bag including any fluid in it BS q 6 hours PINCH so 2 nurse check before administration If old back out and no new bag available, hang D10 until the new bag comes (24 hr limit) to sustain patient Complications Hyperglycemia (check bloodsugar at least qid) Sepsis: infection in blood stream due to sugar in TPN and central line (change bag and lines accordingly) Fluid overload due to increased osmolality of solution (monitor sx of overload: LS, BR, and edema)  Electrolyte Imbalance: Sodium, Normal Range= 135-145 - primary regulator of volume, osmolality, and distribution of extracellular fluid - helps in maintaining neuromuscular activity - imbalance affect osmolality of ECF and water distribution between fluid compartments - Low sodium= water drawn into cells of the body, causing them to swell - High sodium= water drawn out of the cells, causing them to shrink - Hyponatremia o Causes: Diuretics Kidney Disease Adrenal insufficiency Vomiting Diarrhea GI suctioning Excessive sweating o Symptoms BP decrease (fluids shift to intracellular space shock) Muscle cramps Weakness Headache (from brain edema) Brain edema: lethargy, stupor, coma o Treatment If dilution is the cause, restrict intake and give diuretics  - Hypotensive hyponatremia: give normal saline Patient has CNS symptoms: give 3% saline &/or mannitol Loop diuretics- caution if BP too low! No thiazide diuretics because they pull water and Na off o Nursing Care High Na diet (if it is a true loss) Monitor neuro status and pad rails Weigh daily Accurate I&O Monitor VS Monitor electrolytes Hypernatremia: hypertonic dehydration, water drawn out of cells cell dehydration o serious in brain cells because if they shrink they can tear and cause permanent neuro damage o Causes: Fluid loss (wound drainage, NGT to suction) Medication (cortisone, PCN) Increased intake of salt Hyperosmotic tube feeding o Symptoms Excessive thirst Lethargy, weakness, irritability Coma, seizures, death Weight gain Dry mucous membraines o Treatment Hypotonic fluids 0.45% NS or 5% dextrose (D5W) becomes hypo when glucose is metabolized Diuretics (thiazide!) to get rid of Na with urine o Nursing Care Fluid replacement Assessment of neurological function Safety precautions Electrolyte Imbalance: Potassium (Normal Range: 3.5-5.3) - primary intracellular cation - vital in cell metabolism, cardiac and neuromuscular function - maintenance of nerve impulses, normal cardiac rhythms, and muscle contraction - Hypokalemia o Causes Inadequate intake Excessive loss (renal, intestinal, skin)  Redistribution between the ICF and ECF (diabetic ketoacidosis) Secondary loss from medications (diuretics, corticosteroids, some abx) GI/GU loss like urine, diarrhea, or suctioning o Symptoms Confusion, lethargy Dysrhythmias, irregular pulse, ECG abnormalities, cardiac arrest N/V, diarrhea Fatigue, muscle cramps, muscle weakness, parathesia Paralytic ileus due to decreased muscle activity in smooth muscle When section of bowel falls asleep and food doesn’t make it past that point o Treatment Meds: IVF with K added, oral/parenteral supplements Potassium rich foods: banana, orange, avocado, spinach, potato, tomato, meat, seafood, milk, yogurt o Nursing Care Urine output: monitor for decreased/normalizing UOP Monitor patients taking digoxin- hypokalemia potentiates dig toxicity Evaluate serum labs Dilute potassium given intravenously! Never IV push! Also K can irritate the vein Hyperkalemia o Causes ICF to ECF redistribution (burns, acidosis, chemo) Total body excess from increased intake Renal retention from failure (ARF or CRF) o Symptoms Oliguria (if r/t renal failure) Intestinal colic diarrhea from hyperactive bowel EKG changes- peaked T wave and wide QRS Muscle twitching, weakness, irritability o Treatment Kayexalate: binds K to feces Insulin with D50: shifts K back into cells Dialysis Low potassium diet o Nursing Care High serum levels need to be called ASAP Assess heart sounds and pulse irregularity Monitor heart via ECG monitor; ask if potassium is above 6 and not ordered Monitor muscle tone and deep tendon reflexes - Electrolyte Imbalance: Calcium/Phosphorus: Normal Range: 8.5-10 - distinct relationship between calcium and phosphorus (inverse) - Calcium regulated by PTH and Calcitonin o PTH increases when calcium levels fall o Calcitonin secreted by thyroid gland when Ca levels are high - Hypocalcemia o Causes Decreased intake- poor nutrition or decrease in vitamin D Decreased absorption- from loss of parathyroid gland o Risk factors Parathyroidectomy Older adults, especially women Lactose intolerance Alcoholism o Symptoms Numbness and tingling, especially around the mouth Tetany: spasms/cramping of hands/feet Deep tendon reflex hyperactivity Trousseau’s sign: hand flexes when BP cuff on 2-3 min Chvostek’s sign: lip contracts when the facial nerve is tapped Laryngeal spasms o Treatment Oral or IV calcium (tums, Ca salts at bedtime with full glass of water) Ca gluconate injection if tetany Calcium rich diet (dairy, canned salmon, broccoli, spinach, tofu) o Nursing care Health history: current manifestations Physical assessment: musculoskeletal and respiratory status Monitor airway and respiratory status and report stridor! (from pharyngeal spasms) Tetany: provide safe, quiet environment with raised rails and oral airway at bedside - Hypercalcemia o Causes High dietary intake of calcium or vitamin D Diseases that cause Ca to be released (lung, kidney, bone cancers) Fractures or long term immobility cause Ca to be released Thiazide diuretics increase Ca reabsorption in renal tubules and cause Ca to be released o Symptoms GI: N/V, diarrhea, anorexia MS: weakness, fatigue CNS: lethargy, confusion, personality changes CV: dysrhythmia, EKG changes o Treatment IVF: normal saline to enhance Ca extrantion Loop diuretics flush out Ca Calcitonin with immediate need (quickly absorbs Ca into bones) o Nursing care Physical assessment: bowel sounds, muscle strength, LOC Increase mobilization to drive Ca back into bones Encourage fluids       Surgical- 8 Unexpected Complications o Malignant hyperthermia Acute life threatening complication of certain anesthetic drugs, causes rapid temperature increase that is potentially fatal Rapid release of Ca ions trigger increased metabolic rate Genetic autosomal trait that triggers metabolic error Symptoms Tachycardia first End tidal C02 rises without response to ventilation Muscle rigidity and skeletal muscle contraction Hypercalcemia, hyperkalemia, hyperphosphatemia Metabolic acidosis cell death CHF, DIC, compartment syndrome, or cardiac arrest Rapid rise in temperature Treatment Surgery stopped immediately O2 via rebreather Dantrolene (muscle relaxer) given Sodium bicarb (alkaline to counteract the acid) Chilled saline IV (to decrease body temp) Ice packs/hypothermia blanket CV monitoring/meds Start labs and blood gases monitored frequently Insert foley to monitor OP (for heart and kidney function) o Hemorrhage and Shock Cause: blood loss and hypovolemia Symptoms: VS changes, oliguria, skin (ashy/pale and cool), restlessness (due to drop in O2), tachycardia and low BP Treatment: Trendelenburg or leg elevation, call MD, activipate blood and IV fluid Open IV clamp so fluids pump into body ASAP o Caution: need to know pt’s history in case of fluid volume overload if given too much fluid Later complications     o Wound dehiscence/evisceration Cause Bacteria to site, poor wound healing due to excess fat Ruptured bowel form appendix= common site for this Symptoms Drainage, abscess first, patient feels stitches “pop”, swelling, obvious once dressing removed Prevention: avoid lifting/straining and cough/sneeze with pillow Treatment/Interventions Bedrest, cover site with sterile gauze, take VS, call MD Priorities should this occur: 1. Cover site with sterile soaked gauze 2. Bed rest position 3. VS and call MD o Ileus- intestines cease peristalsis due to air from surgery or anesthetics; gastric secretions don’t empty and progress properly Cause: air exposure, manipulation, anesthetics, paralytics Symptoms: abdominal pain, N/V, distention, no BS past ileus, unable to pass gas Treatment: NPO, ambulation, IVF, mylicon (chew it to produce gas), no straws, possible NGT Informed Consent o Legally mandated o No consent, no surgery o Protects patient and ensures permission Nature and reason Who is performing and present during Risks/alternatives related to: Procedure Anesthetic Desired outcome of surgery o Legal Implications Witnessed by licensed person Voluntary Written in understandable terms for patient Explanation of risks/benefits/alternatives/outcomes Opportunity for questions Who does the consent protect? Everybody o Process of consent MD explains and patient gives verbal consent MD writes order RN obtains signature What if patient changes their mind? You stop o o  o What if surgery is delayed? Consent lasts 30 days as long as pt does not leave the hospital Who gives consent? Mentally/physically competent 18 years of age unless emancipated minor: court petitioned married legal next of kin or surrogate emergency- just do it Consent is not legal if: The patient is confused (hard to define) Tremendous pain Sedation, alcohol, or pain meds within 4 hours When is it required? Use of anesthetic/unconscious sedation Any invasive procedure Verbal consent may need written consent Forcing the patient to do something is assault Legal and ethical issues Can student sign consent? No Does an “X” count? Yes Phone consent if family is out of state Emergency override o      Diabetes- 6 Type 1 Diabetes o Most often occurs in childhood and adolescence o Characterized by hyperglycemia and ketosis o Beta cells in the islet of Langerhans in the pancreas are destroyed and insulin is no longer produced o Classified as autoimmune or idiopathic o Risk Factors: Genetic predisposition (markers often found in most type 1 pt) Environmental factors- trigger autoimmune response that causes antibodies to destroy beta cells Viral: mumps and rubella Chemical: smoked and cured meat Type 2 Diabetes: childhood (obesity) and middle aged adults o Condition of fasting hyperglycemia despite endogenous insulin o Occurs at any age but typically seen in middle aged and older adults o Most common form of diabetes o Cellular resistance to insulin’s effects exists o Risk Factors Family history Obesity Physical inactivity Race/ethnicity HTN, high cholesterol, and high triglycerides  Hyperglycemia: elevation of BS > 250 (really anything above 110 but concern arises @ 250) Etiology- too much food, not enough meds, exercise decrease, or illness Symptoms o Polyuria Bc blood becomes hypoosmolar, draws water into blood, kidneys get increased blood flow o Polydipsia Thirsty because of frequent urination o Polyphagia Not as much in type 2 o Glucosuria o Weight loss (in type 1) o Malaise o Fatigue Treatment- diet, exercise, medication regimens: (insulin/OHA) o Control BS from the beginning of the day o Patient does not always need SSI after DC o If not treated, serious complications arise Hypoglycemia: BS: 50-60 (frequent episodes can lead to brain cell death) Etiology o Food: not enough meals or spaced too far apart o Exercise: too much, need to eat before o Medication: too much and no way to turn it off once given Peaks and most likely times to be hypoglycemic NPH o Peaks at 9-12 hours o Typically given at 0700 o Most likely to be hypoglycemic around 4-5 pm Regular and Humalog o Peaks at 2-4 hours o Most likely to be hypoglycemic right after lunch if given before breakfast 70/30 or 75/25 has dual peaks Symptoms o Early: irritability, hunger, weakness, can’t concentrate, confusion o Late: shaky, nervous, tachycardia, cold, sweat, seizures with rapid drop Diabetic Ketoacidosis (DKA) In type 1 because there is no insulin and the body cannot use glucose so it starts to burn fat and protein BS is > 300 Fats breakdown into fatty acids that cause metabolic acidosis Typically seen at diagnosis, with illness, or if Type 1 patient stops taking insulin (noncompliance) Can be weeks or days before it develops Is rarely fatal if treatment is sought out Symptoms o Hyperglycemia >300 o Dehydration o Fever o Acidosis o Kussmaul respirations o N/V and abdominal pain o Kussmaul respirations o Rarely fatal is treatment is sought out DKA 4 metabolic problems occur: o 1. Hyperosmolarity from hyperglycemia and dehydration o 2. Metabolic acidosis o 3. Extracellular volume depletion from osmotic diuresis o 4. Electrolyte imbalance during osmotic diuresis Treatment o Requires immediate attention o Fluid replacement PO and IV (if unconscious) Need 8-10 mL fluid to replace lost from polyuria and vomiting Initial fluid will be NS bolus to restore kidney function and BP IV insulin drip Separate from IVF to lower BS and reverse acidosis Insulin stops conversion of fat into fatty acids Type of insulin used for drip: regular, never NPH Stopping the insulin drip when BS reaches 250 and use SSI o Dextrose then added to prevent too rapid of a drop in BS You never piggy back insulin drip! Acidosis and high potassium go together and eventually potassium enhanced fluids may be added only if RF and BP have been corrected o Glucagon- injection that causes release of glycogen by the liver Mainly for children who ignore symptoms of hypoglycemia Give to unconscious who can’t swallow Patient and family members taught to give injection when hypoglycemia is detected The glucagon reserve will run out so it can’t be done twice IM injection that causes the hepatic glucose stores to be released into the body for energy SE: N/V (from major sugar rush) PO and IV nourishment after to replenish store in liver   Dawn phenomenon Cause: growth hormone and cortisol releases between 0500 and 0900 this normally causes you to wake up cortisol is a glucocorticoid and causes hyperglycemia in those not getting enough insulin Symptoms: o Early morning hyperglycemia o No previous hypoglycemia Treatment o Check BS at 0200 o Anticipate 0200 BS to be normal o Prepare to change insulin regimen (possible NPH at supper)   Somogyi effect (too much insulin in the evening) Cause: insulin induced hypoglycemia triggers a compensatory increase in catecholamines, glucagon, cortisol, and GH liver releases stored sugar hyperglycemia occurs in early AM Symptoms o Hypoglycemia caused by the hyperglycemia o Common for brittle diabetics o Happens at night so it is easily unnoticed Treatment o Decrease in NPH at supper o Check BS at 0200 and anticipate it to be low o Ensure the patient eats a bedtime snack Pain/Nausea- 2 Epidurals (can still walk if low dose) o Mechanism of action: med infused into dura of spinal cord and then to subarachnoid space Spinal cord opioid receptors o Uses: post op, labor, chronic cancer Settings similar to PCA Ordered in set doses and frequency Typically anesthesiologist or neurologist determine these o Expected side effects Urinary retention Micturition reflex inhibited Symptoms: retention, low UOP Precautions: I&O, monitor bladder distention     Interventions: I&O cath/Foley (most already have) Loss of sensation (ambulation= a challenge) Itching o Unexpected side effects Allergy: itching with hives Infection: poor sterile technique or bactermia Spinal headache: puncture causes CSF leak Symtoms o 24 hours post insertion o elevation of HOB exacerbates (so don’t) Precautions o Minimum HOB elevation first 24 hours (30 degrees or less) Interventions/Treatment o Lower HOB o Notify MD if symptoms observed o Replace IVF Respiratory depression Caused by subarachnoid space erosion from the catheter or simply a side effect of the anesthetic Precautions: HOB elevation, close VS monitor, sensory and motor function assessment Interventions: possible reposition with MD, O2, intubation, ventilation assistance o Nursing Responsibilities Ensure proper settings VS q 30 minutes first 2 hours, then q 4 hours Dual verification Established IV access Naloxone/Narcan for reversal AMBU bag- have ready Foley removal and dressing changes (do Foley last) Catheter DC Assessment Managing Specific Pains o Preemptive analgesia (stop it early) o Addiction Only 1% of population gets addicted to pain meds from the hospital Cannot hold paints from a potential drug addict Higher tolerance (addicts)- harder to control their pain o Elderly- need less medication o Brain injury- make sure MD has seen patient and permitted pain meds Cannot give much because medication can mask a decline in neuro status (give tylenol, NSAID, etc.) o Specific pains Kidney stone- give a ton of pain meds fast Appendix- nothing for pain until diagnosis and plans are made Pain meds could mask a rupture o Placebos Natural or endogenous production of endorphins Relives 1/3 of population first time used due to endorphins o Uncontrollable pain- high loading dose until the pain is controlled Exception to the start low go slow Hematology- 5 Blood Transfusion Components o Albumin Low: peripheral edema Pulmonary edema: Albumin transfusions Due to Lasix not working in fluid elimination So, crackles turning into clear breath sounds would be a positive indicator Plasma expander to raise BP by pulling water from tissues Severe burns, cirrhosis (rapid fluid shifts) Assess allergies Consent needed o Fresh frozen plasma (FFP) Patient missing clotting factors or have prolonged (higher) PT and PTT levels Clotting factors normally made in the liver Hemophilia: prolonged PT and PTTs Coumadin and safe levels Gonna have to make sure PT is lower normal for them due to the bleeding risk during surgery o White Blood Cells Oncology units use these the most (chemo decreases WBC) Bone marrow stimulating medication: neupogen Less likely to cause a reaction than a WBC transfusion Immunocompromised/chemotherapy o Platelets 50,000/20,000 marks 50,000= too high (bleeding risk) 20,000= too low (risk for spontaneous brain bleed) Often given prior to surgery even if platelets are at a low normal Multiple bags pooled ABO blood type not important for platelets Single donor platelets- from actual recipient (less likely to have a reaction), multiple rounds of “donation” Apheresis: platelets removed and RBSs returned to platelets o Packed Red Blood Cells Treats anemia and increases volume HGB/HCT <8/24 ABO compatibility Typed and cross matched “washed” or irradiated- removed antigens/WBC to decrease chance for a reaction each “unit” of blood= roughly one increase in Hgb 3 day hold limit, then returned back into pool Cell saver- so patient gets their own blood back o Blood is collected from the patient draining and made back into blood during the surgery Risk Factors for Specific Anemias o Iron Deficiency Anemia Most common type of anemia Supply of iron not optimal for RBC production Body is normally efficient at recycling iron Small amounts are always lost in stool so iron intake is necessary Causes: Chronic bleeding is usual cause (heavy periods) Inadequate dietary iron Malabsorption syndromes Increased requirements (like pregnancy/breast feeding) o Folic Acid Deficiency Anemia Similar to B12 in that it is needed for cell synthesis and normal maturation; needed for cell division to make DNA Causes Inadequate intake Alcoholics- absorption because suppress folate metabolism Geriatrics- folate metabolism suppressed Drug addiction Pregnancy- most at risk because baby using too much of what they need Malabsorption disorders like celiac or chromes o Aplastic Anemia Caused by injury to the pluripotent stem cell that is the precursor cell (meds, chemicals, viruses) Characterized by pancytopenia (shortage of all types of blood cells) or bone marrow failure Patient will also have thrombocytopenia and neutropenia o Anemia of chronic disease Immune activation keeps EPO from stimulating bone marrow Associated with: RA, DM, HTN, ESRD Antigen antibody reactions cause inflammation of bone marrow and this blocks synthesis of new RBCs o Hemolytic anemias Characterized by lysis (premature destruction) of cells that can occur in the circulatory system Bone marrow activity increases in response so the cells produced are immature Causes can be intrinsic (originating from disorders within the RBC) or extrinsic (outside the cell, like hepatitis or meds) o Sickle Cell Anemia (intrinsic) Hereditary and chronic hemolytic anemia Characterized by episodes of sickling or abnormal crescent shaping of the cell Autosomal recessive trait Significantly shortens life span Predominantly found in African American population Causes of crisis: anything that stresses RBCs (hypoxia, stress, infection, too much exercise) o Vitamin B12 Deficiency Anemia Inadequate B12 impairs cells division and maturation As a result, macrocytic (larger) cells form but are immature, misshapen, and weak when they go into circulation They are not capable of carrying the right amount of oxygen and they have short lifespans Deficiency is a result of not consuming enough or the body not being able to absorb it properly (pernicious anemia= type of B12 deficiency lacking intrinsic factor in GI mucosa Also a problem for people with gastric bypass surgery B12 specific symptoms Smooth, sore, beefy red tongue Diarrhea Parasthesias: because B12 is important for neuro functioning Proprioception: inability to tell your position in space (depth perception) Brittle nails AMS from deficiency (Altered Mental Status) Shilling Test Determines B12 deficiency Radioactive B12 given orally Amount excreted in the urine is measured Impaired absorption= none in urine Vascular- 5