Exam 3 Study Guide Patho Study Guide PDF

**EXAM 3** **10-20 GFR start doing dialysis** - Causes of high BUN (blood urea nitrogen). Look into that. What might cause a BUN to rise. - Decreased GFR - Dehydration - Extremely muscular persons - High protein diet - Goog: urinary tract obstruction - A...

**EXAM 3** **10-20 GFR start doing dialysis** - Causes of high BUN (blood urea nitrogen). Look into that. What might cause a BUN to rise. - Decreased GFR - Dehydration - Extremely muscular persons - High protein diet - Goog: urinary tract obstruction - A blood urea nitrogen (BUN) test measures the amount of urea nitrogen in your blood. Levels of urea nitrogen is one marker on how well your kidneys are working. This is a simple test done by drawing blood out of your body through a vein in your arm. - Comparing & contrasting acute kidney injury vs. chronic renal failure. - Acute kidney failure comes on quickly, often curable. Chronic kidney failure comes on slowly and generally leads to long-term dialysis. **[Acute Kidney Injury (AKI) (Acute Renal Failure)]** - Prerenal - Renal ischemia, hemorrhage, shock - Intrarenal - Nephrotoxic drugs (NSAID's, aminoglycosides, radiopaque dyes) - Infections - Excess hemoglobin, myoglobin, purine breakdown - Postrenal - Nephrolithiasis, prostatic hyperplasia - Treatment - Must address underlying cause **AKI Can Be Divided Into Four Phases** 1. - 2. - 3. - 4. - **[Chronic Renal Failure (progressive gradual loss of kidney function)]** - - - - - - - - - - - - - Look into concepts of renal disorders. (We talked about pre renal, inter renal, and postrenal). Know what those are and what causes them, as well as what they can cause. - Prerenal - Decreased blood flow and perfusion to the kidney: Hypovolemia, heart failure, shock - Intrarenal - Actual injuries to the kidney: infection, drug, trauma - Postrenal - Obstruction of urine outflow from the kidneys - Obstructive uropathy - Prevents urine outflow from the kidney - Hydronephrosis - Urine back up into kidney - *Examples:* - Kidney stone - Prostate gland hyperplasia - Understand pathophysiology of gout. What are some complications, what's building up in the body, what could happen because of that build up. - Gout. [Uric acid (byproduct of protein metabolism) accumulates and crystals may be deposited] in subcutaneous tissue ("tophi") and synovial fluid. Hyperuricemia triggers inflammation - Primary: Metabolic disorder of purine metabolism (genetic defect in renal excretion or uric acid production). Secondary: Alcoholism (esp beer or hard liquor), certain drugs, chemo, etc (box 39-1) - Patient presents with redness, warmth, swelling of joint, possible fever. Joints are extremely sensitive. Often affects toe joints, also hands, wrists, elbows - May cause nephropathy and nephrolithiasis - Avoid organ meats, red wine, aged cheese/steaks, shellfish, etc. Diet high in meat- cooked or processed, organ meats, shellfish\...Purines: uric acid - UTIs. Who is more susceptible to UTIs vs their counterpart. Looking at are young women more susceptible than young men? Are older men more susceptible than younger men? That sort of thing. Looking at who compared to their counterparts are more susceptible to a UTI. - **UTI is very uncommon in young, adult males, thus should be investigated as to cause.** (Thus, females more susceptible to UTIS) - **Know adrenal glands and their several disorders. What are the signs and symptoms for each hyper and hypo function of the adrenal and pituitary glands? What do their symptoms and labs look like? Treatment? ** **Cushings: (hyperadrenalisim):** - Hypercortisolism. Cushing Disease: pituitary tumor that excretes lots of ACTH\> adrenals to produce excess corticosteroids. Cushing Syndrome: caused by hyperactive adrenal gland. Glucocorticoid (corticosteroids) therapy can also cause Cushings - Symptoms: High BG, low K, high NA, hypervolemia, immune suppression, osteoporosis, etc - Fat redistribution: Central obesity, "Moon Face" rose colored puffy face, "Buffalo Hump", darkening of skin behind neck line and under breasts, purple stretch marks - [May need to remove pituitary or adrenal tumor removal, and/or drugs to reduce steroid production] **Adrenal Insufficiency (Addison\'s Disease)** - - - - - - **[Hypopituitarism]** Deficiency of one or more anterior pituitary hormones Panhypopituitarism---Decreased production of all anterior pituitary hormones. - Growth hormone deficiency affects bones (increased osteoclastic activity),cartilage and other tissues. - Vision change can be first sign. Severe hypotension, weakness, weight loss. - Treatment: - Lifelong hormone replacement Therapy (HRT) - Androgen therapy for virilization (male sex characteristics); gynecomastia can occur - Estrogens and progesterone - SQ Growth hormone injections at night to mimic normal release. Watch BG! - DIABETES INSIPIDUS: Posterior pituitary insuff = lack of ADH aka central DI (or nephrogenic, kidney don't respond to ADH) **[Hyperpituitarism]** - - - - - S/s depending on what hormone is increased: Visual changes due to increased pressure in optic chasm, HA, s/s increased ICP, Osteopenia (in women ST antiandrogens), galactorrhea and gynecomastia, reduced sexual function, infertility, cardiac hypertrophy, etc. - Excess ACTH overstimulates the adrenal cortex causing overproduction of gluco/mineralocorticoids and androgens (excess cortisol leads to Cushing\'s Disease & Diabetes). - Too much TSH also a possibility! - Hypo/Hyperadrenalism. Hypo/hyperpituitarism. Treatment. - **[Addison's disease. hypoadrenalism:]** Need gluco/mineralocorticoid replacement, increase Na+ intake in hot weather. IV steroids in times of stress - **[Cushing's. Hyperadrenalism]:** May need to remove pituitary or adrenal tumor removal, and/or drugs to reduce steroid production - **[HYPOPITUITARISM:]** Interprofessional Collaborative Care - - - - - **[HYPERPITUITARISM:]** Surgical management. - Transsphenoidal hypophysectomy- remove tumor Medications - Octreotide suppresses GH secretion/shrink tumor - GH receptor antagonist- can normalize GH level in 3 months - TSH, thyroid stimulating hormone. Thyroid hormones, thyroxine, T3, T4. We talked about the thyroid stimulating hormone stimulating the release of T3 and T4. If thyroid not functioning right, we might have a high THS, trying to stimulate more thyroid hormones bc it doesn't know thyroid is failing. That sort of thing. What is the relationship between TSH and your other thyroid hormones. When is it going to be high, when is it going to be low, etc. When the level of thyroid hormones (T3 & T4) drops too low, the pituitary gland produces Thyroid Stimulating Hormone (TSH) which **stimulates the thyroid gland to produce more hormones**. Under the influence of TSH, the thyroid will manufacture and secrete T3 and T4 thereby raising their blood levels. Thyroid Disorders- Pituitary & Thyroid relationship? - - - - - Hypothyroidism - - - - - - - Myxedema Coma\ (Hypothyroid Crisis) - - - Hyperthyroidism\ Many etiologies including adenomas, - - - - - Management - - - - Learned about Graves disease. Being in there with your thyroid disorder and treating it with radioactive iodine. So make sure youre looking into all that - Radioactive iodine, treatment for hyperthyroidism (graves disease) - Graves' disease (most common)- autoimmune thyroid stimulating autoantibodies (low TSH, High T3/T4): - S/s- - Hallmark is heat intolerance (sweating in otherwise comfortable temps) nervousness, insomnia, weight loss. - All body systems affected-Goiter, exophthalmos, a-fib/HF. pretibial myxedema (skin thickening and non-pitting edema in anterior of lower legs) - Diabetes insipidus. Talked about the endocrine disorders and lab values. - **Class Note: C**heck blood sugar and differentiate DM from DI. Symptoms of dehydration. **Diabetes Insipidus** \--Posterior pituitary insuff = lack of ADH aka central DI (or nephrogenic, kidney don't respond to ADH) \--May occur as a genetic mutation, head trauma, infections, toxins, etc \--Water loss problem resulting in excretion of large volumes of dilute urine \--Systemic s/s Urine SG:low Bl SG:High Serum Na+ levels: High - - - - - - Also want to think about other lab values as far as calcium levels. Talked about thyroid and parathyroid disorders. What's going to happen to happen to my calcium levels for both of those. Hyper vs hypo. (**Normal calcium levels: 8.6-10.3)** Hyperparathyroidism - Calcium (high) and phosphate balance (low), Decreased bone density, kidney stones - S/s RT the above - Diuretic and hydration therapy - Monitor cardiac function - If surgical removal is indicated, pt is at risk for hypo calcemic crisis. If all 4 are removed, a piece of one can be implanted in forearm to help stabilize Ca+ and P- Hypoparathyroidism - - - - - - Also started talking about endocrine. So were going to think about diabetes and all of the diagnostic criteria for diabetes! Know for test. - Measure BG to differentiate DM (which also has polyuria/dipsia & dehydration) from DI Diagnosing DM - Gold Standard: Fasting plasma Glucose levels \>126 on 2 separate occasions or random BG \>200 more than once - Oral Glucose Tolerance Test (OGGT)- given 75gm glucose load (drink usually) and measure BG after 2h, If postprandial BG is \>140 prediabetes is Dx. If BG is \>200 then DM is Dx - HgbA1c-gycosolated hemoglobin measures BG average over last 3 months. 5.7%-6.4% is prediabetes. Greater than that is DM Clinical Manifestations - - - - - - Complications of diabetes. Type 1 vs type 2. DKA and HHS. [DKA- more commonly type 1]. [HHS- more commonly type 2]. Which one has acidosis? How are we treating both of them? Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can\'t produce enough insulin. Treatment of DKA - - - - - Hyperglycemic Hyperosmolar Syndrome - - - - - - Treatment of HHS - - - - Being able to analyze an ABG. ABG interpretation, easy! \| Nursing school survival, Nursing school studying, Nursing school - How do we treat hypoglycemia? (rule of 15s, oral glucose we can give.) If patient is difficult to arouse, lower level of consciousness, how are we going to treat them? We have glucagon, we have dextrose IV. Look into how are we going to treat conscious vs unconscious patients. Managing Hypoglycemia - Rule of 15's" - 1 Carbohydrate = 15 gm (Carbohydrate) & re check in 15 min (if conscious) - Each 5 g of carb, raises blood glucose 15 mg/dL.  Diagram Description automatically generated If the person is **unconscious**, having seizures, or too disoriented to swallow 1. Locate a glucagon emergency kit or glucagon nasal powder, if it\'s available. \... 2. Administer the glucagon emergency kit or glucagon nasal powder... DEXTROSE IV OR GLUCAGON (50% dextrose iv) Q: Since the person is unconscious/unresponsive with severe **hypoglycemia**, glucagon should be administered as the **first**-**line treatment**. - There are specific creiteria for metabolic syndrome. Know exactly what those are. So you can pick it out of crowd here. - Metabolic Syndrome: Box 25-2 - HTN, dyslipidemia (high bads and low goods), hyperinsulinemia, central or "apple shaped" obesity, elevated fasting glucose (100 or higher), and predisposition to DM (familial or gestational) Book: ELEVATED WAISTE CIRCUMFERENCE. Men: equal or greater than 40 in 102 cm. Women: equal or greater than 35 in 88 cm. Elevated triglycrides: equal or greater than 150 Reduced HDL cholesterol. Men: lower than 40 mg, women lower than 50 mg Elevated blood pressure: equal or greater than 130/85 mm Hg Elevated fasting glucose: equal or greater than 100 mg/dL (presence of 3 or more) - Appendicitis. Where is the appendix? The name of the location of that organ and the symptoms. The appendix is located in the **lower right quadrant** of the abdomen (right iliac region) **McBurney's Point\ (Appendicitis)** Clinical Manifestations - - - - - - - We talked about mucous and goblet cells. The production of mucous comes from goblet cells. Have some in respiratory tract, GI tract. Look into those concepts. - Stomach-parietal cells have proton pumps which, along with histamine and others, help produce HCl acid. Goblet cells secrete mucous to protect from HCl. Pepsinogen or pepsin to digest protein. Intrinsic factor sent to ilieum to help absorb B12 - Small intestine: villi are vascular have goblet cells: secrete mucous, absorb nutrients and digestive enzymes. Absorption is occurring, and bile acids are being sent back to liver for recycling. - Ducts from liver and pancreas enter duodenum - Be able to compare and contrast what's going on with ulcerative colitis vs Crohn's. How deep do those lesions go? One is more superficial, one goes all the way into the by later. Recall those 2. Which predisposes a client to cancer? There is a chart there, compare and contrast. Need to know for test. **Crohn's disease** - - - - - - - - **Ulcerative colitis** - - - - - - - Liver dysfunction. Think about function of liver. What causes each symptom? Coagulation problems bc of liver dysfunction. Caput medusa. Swollen and engorged abdominal veins. Those might be a result of portal hypertension and fluid shifts. We also think about hepatic Encephalopathy. Build up of toxins. Now we get that serious confusion leading into coma and death and seizures. What are my symptoms of hepatic encephalopathy? Looking at stupor, looking at he **flapping tremor.** Decreased level of conscious. - Hepatic encephalopathy is **a nervous system disorder brought on by severe liver disease**. When the liver doesn\'t work properly, toxins build up in the blood. These toxins can travel to the brain and affect brain function. People with hepatic encephalopathy may seem confused. - **Prevent Hepatic encephalopathy (Confusion, stupor, asterixis)** - **Lactulose for ammonia, poss neomycin** - **Alters ammonia, the by product of protein metabolism, so it does not harm the body (ammonia is VERY neurotoxic \> hepatic encephalopathy!).** Asterixis is **a disorder in which a person loses motor control of some parts of the body**. It is commonly called [flapping hand tremor] because the muscles in the fingers and the wrists are typically affected. ‌A person with asterixis loses muscle control and experiences irregular jerking movements in the hands Stupor: unconscious. Common abnormality in hepatic encephalopathy. - Portal hypertension S/S. Ascites. What might you see with ascites? Shifting dullness with percussing, palpating. Recall all those things. - **S/s PV HTN: Ascites (on percussion nurse will hear shifting abdominal dullness), esophageal varices, splenomegaly, Caput Medusa, Hemorrhoids** - Clients who have liver disease are going to be predispose to coagulopathy. It's a bleeding disorder. How do we reverse bleeding disorders? We wouldn't give them anything like an anticoagulant. We would give them vitamin K. Because they aren't making vitamin K because their liver is failing to treat bleeding. So go back to functions, what are they missing, what are the symptoms we are going to see because of what they are missing because of the failure. And how we're going to treat that. Diagnostic tests in liver disorder - - - Difference between acute pancreatitis vs chronic pancreatitis. What are symmptoms of acute pancreatitis? With crhonidc we might see those sort of things, but gradual scarring over time. Or multiple episode of acute pancreatitis would cause chronic pancreatitis. Look at those speicfici symptoms. Showed you guys some pictures of acute pancratitis. What are thos symptoms going to look like on a patient? Why are they going to have high blood sugar? What are the symptmos of acute pancreatitis? What are symmptmos of acute gallstones? Also talkeda bout gallstones and kidneystones. What are tehose symptoms vs acugte pancreatitis symptoms. What is one vs the other. - Acute Pancreatitis - **Turner sign** (reddish-brown discoloration along flanks) **Cullen Sign** (bluish discoloration around the umbilicus) - - - - - - Assessment - Ranson Criteria (Box 32-2) Determines need for hospitalization based on severity and risk of complications - [increased pain in the abdomen and in the epigastric region radiating to the back when lying supine, fever, hypotension] - Treatment: supportive case - Patients should not receive any oral fluids or food until abdominal pain and tenderness have subsided - Pain and fluid management Chronic Pancreatitis - - - - - - - Kidney stones. May have pain radiating down to the groin. So those specific symptoms, where pain refers to, and when they feel pain. When lie supine, sit up, touch, etc. important assessment criteria for GI symptoms. Urolithiasis & Nephrolithiasis- KIDNEY STONES! - **Assessment- Pain! Flank pain radiates downward to genitalia and inner thigh. Dysuria (UTI Possible), hematuria, Renal colic. n/v.** - Pain-relief measures, fluid therapy, let stone pass if small enough (strain urine), or surgical removal/lithotripsy, dietary changes based on stone type Acute Pancreatitis - - Neuro. The different lobes of the brain. Lobes and Responsibilities - - - - - - - - -  - Multiple sclerosis. Multiple Sclerosis - - - - - - - - - - - - - - - Gulliain-Barre Syndrome Guillain-Barré Syndrome - - - - - S/s peak around 2-4 wks\ Medical management - - - - Whats going on with parkinsons disease? Parkinson's Disease - - - - - Classic triad - Bradykinesia (also episodes of akinesia) - Resting tremor ("pill-rolling") - Muscle rigidity (cogwheel, ratchet movement) - Additional symptoms - Postural instability, shuffling gait, emotionally labile, mask-like facial feature, fatigue as the day progresses. Etc. - TRAP -**T**remor at rest, **R**igidity, **A**kinesia (or bradykinesia), **P**ostural/gait instability - Encourage independence with ADL's exercises and deep brain stimulation. Exercise in the morning when they have the most energy. Initiate movement with bradykinesia by rocking back and forth in chair, Buy clothes that do not require dexterity (Velcro, etc. No buttons) to increase ability to dress themselves. - Sinemet (levodopa-carbidopa) Dopamine agonists - What is the diagnostic criteria for stasis epilepticus? When we talked about seizures. - Note from class: Status epilepticus is a seizure continuing or a series of 3 tonic-clonic seizures. Therefore, client who is experiencing series of 3 tonic-clonic seizures expected to have status epilepticus. - When do we do tensilon testing? What is the reversal? - A Tensilon test is a diagnostic test used to evaluate myasthenia gravis, which is a neuromuscular condition characterized by muscle weakness [Dx: Tensilon Test] - - - - (Depending on the results, you\'ll be given atropine to stabilize you.) - Client is having seizure. What is primary interventions? Dos and don'ts? **Plan of Care for a Patient Experiencing a\ Seizure** [Seizure Precautions] - - - - - [Acute seizure Management ] - - - - - - - **Seizure meds** - - - - Do not hold the person down or try to stop his or her movements. Do not put anything in the person\'s mouth. This can injure teeth or the jaw.  - What is the Babinski reflex? - To perform the Babinski test, your doctor will use their finger or a tool like a stick or a hammer to stimulate the bottom of your foot. They'll run it firmly from the outer edge of the foot at the heel to the bottom of the big toe. - In older children and adults without neurological problems, the foot will remain still, or the toes may curl downward during the Babinski test. If you do have a Babinski sign, your big toe will bend back, and your other four toes will spread out like a fan.  - Know some of the signs and symptoms of osteoporoisis. (Vs osteomallacia and osteoarthritis. But I would focus on osteoporosisl) think about what patient appearance might e if they osteoporiosis. **Osteoporosis** - - - - - - - - - - - How does osteoarthritis differ from rhemuotoid arthritis. Think of one as an autoimmune and syystmeic and one is just bone and problem with calcium and age and degeneration. - Osteoarthritis, the most common form of arthritis, involves the wearing away of the cartilage that caps the bones in your joints. Rheumatoid arthritis is a disease in which the immune system attacks the joints, beginning with the lining of joints. - LOOK IN BOOK - Going back to gout. What is going on with the patient with gout? What's building up in their body? What dietary changes are they going to make to prevent their disease process from worsening? - Uric acid (byproduct of protein metabolism) accumulates and crystals may be deposited in subcutaneous tissue ("tophi") and synovial fluid. Hyperuricemia triggers inflammation - **Avoid organ meats, red wine, aged cheese/steaks, shellfish, etc** - We talked about clinical systemic illness. Talked about SIRS, CARS. Talked about septic, septic shock, MODS. **In what order do those progress?** - - A few questions are cumulative. Again, going back to Coagulation pathway. Intrinsic vs extrinsic. What test do we do vs intrinsic vs extrinsic. What medications are given in the intrinsic vs extrinsic pathway. What the reversals are for those drugs? All important. Clotting time of intrinsic pathway [Activated partial thromboplastin time (aPTT)] (**Heparin** anticoagulant) Clotting time of extrinsic pathway - [Prothrombin time (PT) examines extrinsic pathway] (**Warfarin** anticoagulant) - International normalized ratio (INR) Anticoagulants prolong clotting time, so PT, INR, and aPTT should be higher than normal Normal INR = 1, so anticoagulant usage should have INR greater than 1 (usually 2 to 3) [Heparin] - -Careful monitoring with aPTT - -STOP heparin first! May need ***Protamine sulfate* used to neutralize if bleeding occurs** - -controlled aPTT aprox 30-40 sec. Aim heparin level at 2-3x the control value. - [Warfarin] - -Interferes with vitamin K-dependent clotting factors - -**Frequent PT (normal is 10-14 sec but we want 1.5-2 x normal)) and INR (normal I 1, we want it at 2-3)** monitoring. High indicates prolonged clotting time, which is want we want - -**Counteracted by giving vitamin K. Avoid bleeding and keep lab appts** - Cumulative question on client having *severe* chest pain. How do we treat chest pain? You know angina. Occurs at rest (or activity) and severely limits activity May present with ST changes but no changes in troponin levels MONA! - Morpine - O2 - **Nitro** - ASA-Chew 4 Baby ASA (81mg/each) **Nitro**: 0.4 mg x3 Q 15 min. **Potent Vasodilators** - Select all that apply question on basically client who has hepatic encephalopathy and portal hypertension. What body system disorder do they have with those two things? Look into that. Know its liver failure. - - - - - - (GI powerpoint 41) Other notes from class: \*Respiratory monitoring. Any test question w/that Gullian Barre Syndrome, think respiratory. \*Slide 3 cerebrovascular disorders. Test questions on these. "These symptoms, what lobe/side brain damaged?" \*Status epilepticus. Client who is experiencing series of 3 tonic clonic seizures expected to have status epilepticus.