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MCA1 Test Prep - MCA 1 exam 4 test prep

MCA 1 exam 4 test prep
Course

Medical Surgical 1 (MCA1)

23 Documents
Students shared 23 documents in this course
Academic year: 2019/2020
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Samuel Merritt University

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MCA1 Test Prep Inflammation is always present with infection, but infection is not always present with inflammation Vascular response – redness, swelling and heat Cellular response – WBC components Local Manifestations of Inflammation: Manifestation: Rubor (redness) Cause: Hyperemia from vasodilation Manifestation: Calor (Heat) Cause: Increased Metabolism at inflammatory site Manifestation: Dolor (pain) Cause: Change in pH. Nerve stimulation by chemicals (e. histamine, prostaglandins), pressure from fluid exudate Manifestation: Tumor (Swelling) Cause: Fluid shift to interstitial spaces, fluid exudate accumulation Manifestation: Loss of function (function lessa) Cause: Swelling and pain(nothing necessarily broken, but just pain and swelling) Immunity Note differences between B Lymphocytes and T Lymphocytes T Lymphocytes are for viruses, cancers, tumors and fungi, transplant rejections B Lymphocytes are Antibodies NK Cells – significant role in surveillance for malignant cells Soluble Factors secreted by WBCs and other cells IgM is the first type of antibody formed upon initial exposure IgG is the primary antibody found in the secondary (subsequent) exposure Human Leukocyte Antigen System (HLA) – Crucial to organ/tissue donation Types of organ rejection: Hyper acute (within 24 hours), acute (first 6 months) and chronic (months to years). Acute rejection is somewhat manageable with long-term use of immunosuppressants. Antibiotic resistance: HCPs contribute to the problem because:

 They prescribe antibiotics for viral infections  They prescribe antibiotics unnecessarily  Prescribing inadequate drug regimens  Using broad spectrum antibiotics when not needed

Patients contribute to the problem:  skipping doses  not taking medication for full duration of treatment  saving unused antibiotics for later use

Fluids and Electrolytes DKA = High serum osmolality. Glucose concentration in serum leads to cellular dehydration. Edema – Second Spacing (fluid in the interstitial tissues) Third Spacing – abnormal accumulation of fluid (ascites, abdominal cavity) When we talk about fluid volume, the nurse’s primary responsibility is to track the I/Os or administer fluids as ordered or restrict pts on fluid restriction. A good way of determining how much fluid a patient lost is to weigh them. Weight is a good measure of fluid deficit, balance or overload. BUN is a measure of dehydration while creatinine is a measure of kidney function. Normal Serum Electrolyte Values: Sodium (Neuro) - 135 – 145mEq/L (135 – 145 mmol/L) Confusion, seizures Potassium (Cardiac) - 3 – 5/L (3 -5 mmol/L) Arrhythmias Calcium (Muscle) - 8 – 10/dL weakness Phosphorus - 2 – 4/dL

Magnesium - 1 – 2/L (0 – 1 mmol/L)

See tables starting on page 279 for symptoms of imbalances in above electrolytes

NEVER EVER GIVE K+ IV PUSH – CAN CAUSE

CARDIAC ARYTHMIAS, usually through central

line but with a limited rate (may cause

peripheral irritation)

Memorize the Lab values for Na, K, Ca, P and Mg.

5 Rights of Delegation

  1. The right task
  2. Under the right circumstances
  3. To the right person
  4. With the right directions and communication
  5. Under the right supervision and evaluation Decision Tree of Delegation
  6. Assessment and Planning\
  7. Communication
  8. Surveillance and Supervision
  9. Evaluation and Feedback

Calcium 8 – 10 mg/dL Magnesium 1 – 2 mg/dL Phosphorous 2 – 4 mg/dL Potassium (K+) 3 – 5 mEq/L Sodium (Na+) 135 – 145 mEq

Diabetes: T1DM Treatment:

  1. Continuous glucose monitoring
  2. Insulin
  3. Diet and exercise – to control glucose levels and prevent complications The only option to treat T1DM is insulin.

Complications of T1DM

  1. Death

  2. Hypoglycemia

  3. DKA

  4. Microvascular and Macrovascular complications (same as T2DM)

  5. Psychological

  6. Integumentary DKA This is a profound deficiency of insulin and often the first sign that a pt has T1DM. Often precipitated by an infection or illness or not administering enough insulin. The pathology really is lack of insulin production from pancreas which leads to lipolysis and protein catabolism which leads to production of ketones (gluconeogenesis which is endogenous glucose production). Ketosis alters pH of blood leading to metabolic acidosis. Signs and Symptoms Profound dehydration (dry skin and mucous membranes) Kussmaul respirations (deep rapid respirations related to metabolic acidosis, trying to correct metabolic acidosis through expiration of CO2): No need for O2 at this time except sats are low. The problem is not insufficient O2. Kussmaul respirations will reverse once the hyperglycemia is treated. Remember, this is not a respiratory problem, it’s METABOLIC ACIDOSIS! N/V Tachycardia Orthostatic hypotension Acetone on breath (sweet fruity smell to breath) Ketones in urine – you shouldn’t normally have ketones in urine Serum glucose levels ≥250mg/dL Blood pH <7. Bicarbonate <16mEq/L

  7. Expect Low K+ (because he’s been urinating and K+ is excreted with urine. Just like when u administer Lasix, it’s most likely that the person will have low K+).

  8. Warning!!! Potassium must be >3 mEq/L to administer insulin. This warning applies to only IV administration of insulin and is not relevant to sub-q injections. The insulin causes glucose to be pushed into the cells from the blood and the insulin takes serum potassium with it. If the K+ levels are low when this happens, the heart will not have enough serum K+ left to use for beating and this can cause arrhythmias due to hypokalemia , sometimes fatal. Note that this issue with K+ and insulin is only when it is administered IV and has nothing to do with when it is administered sub-q because absorption of sub-q insulin by the body is slower

  9. WBC may be elevated. Remember infections normally precipitate DKA. Anticipated Treatment:

  10. IV insulin (Required for treatment)

  11. Warning!!! The only insulin that can be given IV is REGULAR INSULIN (Lispro)

  12. Initially IV push Insulin followed by IV infusion (usually happens in only the ED or ICU).

  13. Antiemetic – to control N/V

  14. IV Potassium replacement ( May need to replace potassium prior to giving IV insulin). Depending on the situation, IV K+ may be administered with insulin at the same time.

  15. NaHCO3 (Sodium bicarbonate) IV push if severe acidosis T2DM Primary pathology not fully understood Insulin Resistance : Even though you’re producing insulin, somehow your muscle cells are not able to use it. Liver continues to produce insulin, there’s muscle cell resistance to this insulin which causes hyperglycemia Defects in Insulin Secretion: At diagnosis, 50% of β-cells are destroyed and multiple factors contribute to this process.

It’s a progressive disease that develops over several years and there’s a genetic link because certain peoples have increased risk for diabetes genetically. Family history (mainly first degree relative is also a strong factor that shows it has a genetic link). Men tend to have more incidence of T2 than women. Obesity, sedentary lifestyle interact with genetic risk factors. Symptoms

  1. The 3Ps usually present in T2 but are less pronounced
  2. Fatigue
  3. Recurrent infection
  4. vision changes (blurry vision)
  5. vaginal yeast (candida)
  6. prolonged wound healing SYMPTOMS OF T2 ARE VAGUE, THEREFORE SCREENING IS KEY. Asymptomatic adults should be tested if: Testing should be considered in overweight or obese adults with BMI ≥25kg/m or ≥23kg/m in Asian Americans who have one or more of the listed risk factors including:
  7. A1C ≥5% (39mmol/L), IGT or IFG on previous test
  8. For all patients, testing should begin at age 45.
  9. If normal, testing should be repeated every 3 years, but yearly for those with prediabetes. Criteria for the diagnosis of Diabetes:
  10. FPG ≥126mg/dL (7/L) Fasting is no caloric intake for at least 8 hours
  11. 2-hour PG ≥200mg/dL (11 mmol/L) during an OGTT (Oral glucose tolerance test). W.H requires that the test be performed using a glucose load containing the equivalent of 75g anhydrous glucose dissolved in water.
  12. A1C ≥6% (48mmol/mol) using a NGSP (National Glycohemoglobin Standardization Program) certified method and standardized to the DCCT (Diabetes Control and Complications Trial) assay. This is a great measure of blood glucose over a 3-month period.

Pathology of HHS: Lack of ability to use insulin leads to hyperglycemia which leads to fluid volume deficit due to excess urination. Signs and Symptoms of HHS:

Profound dehydration (dry skin, mucous membranes, tachycardia, orthostatic hypotensionMore severe neurologic manifestations than DKA due to higher serum osmolarity (somnolence, coma, seizures, hemiparesis, aphasia)Electrolyte imbalancesNo ketonesSerum glucose level ≥600mg/dL

Nursing assessment and Actions are the same as for DKA but Warning!! Because HHS occurs more frequently in older adults (DKA is more in younger people), the nurse has to be cautious when rehydrating the patient to avoid fluid overlaod. Potassium must be >3 mEq/L to administer insulin IV regular insulin is a required treatment Must replace potassium FIRST IF ≤3/L 4. Micro and Macrovascular Complications (same as for T1)  Angiopathies, Nephropathies, Retinopathies, Neuropathies, Infections and Amputations

  1. Psychological
  2. Integumentary
  3. Death from the complications listed and not related to T1 death from no insulin. Macrovascular and Microvascular Complications for T1 and T2: Macro – Stroke and MI (KEY POINT HERE – TIGHT CONTROL OF HYPERTENSION AND CHOLESTEROL IS ESSENTIAL) Micro (RNN)– - Retinopathy (yearly eye exams)

- Nephropathy (yearly urine screening for protein (microalbumin) - Neuropathy – tiny vessels in distal extremities (yearly diabetic food exams)

2 types of Neuropathies: Peripheral Neuropathies : - Distal Extremities present as pain: shooting and burning sensations. - Adjuvant Pain Medication – Gabapentin (Neurontin)

CNS Neuropathies (related to autonomic disfunction): - Postural hypotension - Silent MIs – internal nerve damage causes this because of reduced feeling - Hypoglycemia unawareness - Gastric Paresis – nerve damage causes impaired peristalsis and this may lead to obstruction.

Prediabetes (Increased Risk for Diabetes): FPG - 100 to 125 mg /dL (5 to 6 mmol/L) OR 2-hour PG in the 75g OGTT – 140 to 199mg /dL (7 to 11 mmol/L) IGT OR A1C 5 to 6% 39 to 47 mmol/mol The ADA now says that for older adults, an A1C of 8 is okay because they may not have that many more years to live. Treatment First step in treatment of T2 is weight loss. This can be achieved with lifestyle programs that achieve a 500-750kcal/day energy deficit or provide approximately 1,200 – 1,500 kcal/day for women and 1500 – 1800 kcal/day for men adjusted for the individual’s baseline body weight. Although the benefits may be seen with as little as 5% weight loss, sustained weight loss of ≥7% of body weight is optimal.

jittery

  • Sweaty
  • Hungry
  • Headachy
  • Blurred

vision

  • Sleepy or

tired

  • Dizzy or

lighthead

ed

  • Confused

or

disoriente

d

  • Pale

ed

  • Irritable or

nervous

  • Argumentati

ve or

combative

  • Changed

behavior or

personality

  • Trouble

concentratin

g

  • Weak
  • Fast or

irregular

heart beat

or drink

  • Seizures or

convulsions

(jerky

movements)

  • Unconsciousn

ess

All patients with diabetes in the hospital will have a hypoglycemia protocol in the MAR to reverse the effects of insulin. VIP when hypoglycemia is suspected:

  1. Remain with the patient
  2. Treat sooner rather than later if hypoglycemia is suspected – you can give amp of D50 (dextrose 50%) 12 to 25gm usually in a 10ml or 20ml syringe IV. Glucagon is usually for those without IV access. Usually a home kit IM injection administered by a family member or caretaker.
  3. Conscious or Unconscious? PO vs. IV/IM
  4. Monitor and repeat treatment every 15 minutes until BG >70 or 80mg /dL
  5. Call for help early
  6. Consider cause and address it. – Too much insulin, insufficient carbs All nurses should find out what the hypoglycemia protocol for the hospital they are working in is.

Asymptomatic — When self-monitoring of blood glucose (SMBG) reveals a blood glucose of ≤70 mg/dL (3 mmol/L), it is reasonable for a person with drug-treated diabetes to consider defensive actions. The options include repeating the measurement in the near term, avoiding critical tasks such as driving, ingesting carbohydrates, and adjusting the treatment regimen [8]. In order to treat early symptoms of hypoglycemia, patients should be certain that fast-acting carbohydrate (such as glucose tablets, hard candy, or sweetened fruit juice) is available at all times. Fifteen to 20 grams is usually sufficient to raise the blood glucose into a safe range without inducing hyperglycemia. This can be followed by long-acting carbohydrate to prevent recurrent symptoms. In patients taking insulin or an insulin secretagogue in combination with an alpha-glucosidase inhibitor (acarbose, miglitol, voglibose), only pure glucose (dextrose) should be used to treat symptomatic hypoglycemia. Other forms of carbohydrates, such as table sugar (sucrose), will be less effective in raising blood sugar as alpha-glucosidase inhibitors slow digestion of other carbohydrates

Treatment options for severe hypoglycemia include the following:  A subcutaneous or intramuscular injection of 0 to 1 mg of glucagon will usually lead to recovery of consciousness within approximately 15 minutes, although it may be followed by marked nausea or even vomiting.  Patients brought to the hospital can be treated more quickly by giving 25 g of 50 percent glucose (dextrose) intravenously (IV). A subsequent glucose infusion (or food, if patient is able to eat) is often needed, depending upon the cause of the hypoglycemia.  Although a comatose diabetic patient may have marked hyperglycemia (with or without ketoacidosis) rather than hypoglycemia, these disorders can be distinguished by estimating blood glucose with a glucose stick. If this is not available, then glucose should be given empirically. This will correct hypoglycemia and will not be particularly deleterious if the blood glucose concentration is high.

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MCA1 Test Prep - MCA 1 exam 4 test prep

Course: Medical Surgical 1 (MCA1)

23 Documents
Students shared 23 documents in this course

University: Samuel Merritt University

Was this document helpful?
MCA1 Test Prep
Inflammation is always present with infection, but infection is not always present with inflammation
Vascular response – redness, swelling and heat
Cellular response – WBC components
Local Manifestations of Inflammation:
Manifestation: Rubor (redness)
Cause: Hyperemia from vasodilation
Manifestation: Calor (Heat)
Cause: Increased Metabolism at inflammatory site
Manifestation: Dolor (pain)
Cause: Change in pH. Nerve stimulation by chemicals (e.g. histamine, prostaglandins), pressure from
fluid exudate
Manifestation: Tumor (Swelling)
Cause: Fluid shift to interstitial spaces, fluid exudate accumulation
Manifestation: Loss of function (function lessa)
Cause: Swelling and pain(nothing necessarily broken, but just pain and swelling)
Immunity
Note differences between B Lymphocytes and T Lymphocytes
T Lymphocytes are for viruses, cancers, tumors and fungi, transplant rejections
B Lymphocytes are Antibodies
NK Cells – significant role in surveillance for malignant cells
Soluble Factors secreted by WBCs and other cells
IgM is the first type of antibody formed upon initial exposure
IgG is the primary antibody found in the secondary (subsequent) exposure
Human Leukocyte Antigen System (HLA) – Crucial to organ/tissue donation
Types of organ rejection: Hyper acute (within 24 hours), acute (first 6 months) and chronic (months to
years).
Acute rejection is somewhat manageable with long-term use of immunosuppressants.
Antibiotic resistance: HCPs contribute to the problem because:

Students also viewed

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