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image, Nursing Diagnosis: Risk for unstable blood glucose related to…
Atrial fibrillation
Pathophysiology
A type of atrial dysrhythmia caused by pacemaker cells firing not from the sinoatrial node but somewhere else within the atria
Has no P waves, multiple pacemaker cells generating independent electrical impulses and causes issues in the atria.
characterized as irregularly irregular
QRS complexes are usually narrow with irregular R-R intervals
HR or ventricular response determined by AV nodes ability to accept and transmit the impulses to the ventricle, when maintained less than 100bpm considered controlled and if greater than 100 considered uncontrolled and called AF with RVR
Risk factors
Risk increases with age
Possible causes: Pericarditis, cardiomyopathy, hyperthyroidism, HTN, valvular disease, obesity, diabetes (which pt has), chronic kidney disease, patients undergoing cardiac procedures & CAD
Pt. hx of diabetes, HTN, and CAD all put him at risk
Signs & Symptoms
paroxysmal or spontaneously self-limiting
persistent or continuing beyond 7 days
long standing or lasting more than 12 months
permanent or persistent AF that is resistant to rhythm control therapies
Treatments
Based on whether it is new onset or established diagnosis
Anticoagulation therapies to prevent clot formation
Heart rate and rhythm control with medication
Cardioversion- shocks meant to restore normal heartbeat
Medications
Anti-arrhythmic- Dofelitide- slows heart rate
Anticoagulant- Warfarin- inhibits clot formation
CCB- Diltiazem- slows conduction through the AV node
Cardiac glycoside- Digoxin- slows conduction through AV node
Labs
Electrolytes
EKG
Cholangiocarcinoma
Pathophysiology
rare type of liver cancer that develops in the bile ducts
often associated with primary sclerosing cholangitis (rare autoimmune disease often aligned with ulcerative colitis)
geographically associated with areas where there is a large amount of liver fluke present like Southeast Asia
Can occur anywhere along the bile duct and extends directly into the liver- usually as an unaccompanied lesion
difficult to distinguish invasion of cholangiocarcinoma from metastatic adenocarcinoma except from neoplastic changes in nearby ducts
Risk factors
Liver flukes (parasites that infect humans and cause liver and bile duct disease)
Primary sclerosing cholangitis (inflammation and scarring that can occur in those who also have UC or Crohns disease)
Mycotoxins including types of mold
Obesity
Alcohol abuse
Hepatitis B and C infections
Signs & Symptoms
Insidious presentation
abdominal pain
loss of appetite
weight loss
gradual onset of jaundice
Treatments
Biliary drainage- tube placed in duct (what the patient had to help restore some of the flow of bile- to reduce S&S of the cancer)
Surgical resection- removing part of the bile duct and possible parts of surrounding liver
Radiation
Chemotherapy
Immunotherapy
Medications
Chemotherapy drugs including: gemcitabine, cisplatin, flourouracil, oxaliplatin
Pain medications for associated pain: narcotics depending on severity and other analgesics like acetaminophen (which the patient takes)
Lab Values
Liver function tests (AST, ALT) help determine functionality of the liver
Patient has decreased Albumin (3.0) and decreased protein levels (5.7) which can also be indicative of poor liver function
Coronary Artery Disease
Pathophysiology
Traditionally characterized by blocked blood flow in the coronary arteries with the main cause as Atherosclerosis (plaque within the vessels)
begins with injury to the endothelium, which causes an inflammatory response
Low density lipoprotein enters the tunica intima and becomes trapped and is modified through the process of oxidation
LDL attracts macrophages which absorb the LDL to become foam cells which accumulate and form fatty streaks
Components in the blood adhere to the vessel forming plaque which accumulate and cause narrowing of the artery
Risk factors
Modifiable: smoking, high total cholesterol, high LDL, hypertension, diabetes, obesity, sedentary lifestyle, stress, excessive alcohol use
Non-modifiable: Gender, race, age older than 45 for men, genetics
Pt. hx of diabetes and no exercise regimen as stated in interview could helped put at risk (uncontrolled blood glucose and HTN combined with this can put pt at risk for adverse cardiac events such as a MI which the pt had)
Signs & Symptoms
Mostly silent CM until about 40% of artery is blocked; ischemia develops when there is an imbalance between supply and demand of oxygen rich blood to heart tissue
Stable angina- refers to chest pain or discomfort that occurs with physical activity
Unstable angina- chest pain that can occur at rest
Angina- can radiate to the left arm, back, or jaw. Women report more atypical angina and may report fatigue, weakness, nausea, and dyspnea.
Treatments
Aimed at stopping aggregation of blood components to injured epithelium, controlling factors that led to the damage, and relieving symptoms
Blood pressure monitored closely during medication regimens
PTCA- catheter with small balloon is inserted to open the lumen of the artery
CABG- blockages in the arteries are bypassed using other arteries from the chest or arm or veins from the leg
Medications
Patients with stable angina often prescribed: Nitroglycerin and aspirin (along with anti-hypertensives, anti-diabetics, and cholesterol lowering agents
Nitroglycerin: dilates arteries to improve blood flow and oxygen supply to the myocardial cells; can also be given to improve afterload
Aspirin- inhibits platelet aggregation to prevent clot development
Lab values
Markers of heart disease: CK myocardial bands (normal- 0-3ng/ml), Troponin (less than 0.4ng/ml), myoglobin (0-85ng/ml), BPN (less than 100pg/ml)
Diabetes Mellitus Type 2
Pathophysiology
Insulin resistance- below optimal response of insulin sensitive tissues to insulin
Abnormalities that contribute to the insulin resistance- abnormality of the insulin molecule, high amounts of insulin antagonists, down regulation of insulin receptor, alteration of GLUT proteins
the resistance that develops requires increased levels of insulin in order to get glucose into the cells
Over time, pancreas cannot keep up with this increased demand; beta cell failure then appears and progresses
Risk Factors
family history of diabetes
Age
Obesity (BMI greater than 26 kg/m, increased risk with >30kg/m)
Hypertension (greater than 140/90 or on HTN meds
Poor diet
Physical inactivity
Pt. reports no exercise regimen during interview
Metabolic syndrome
Signs & Symptoms
3 p's: polydipsia, polyphagia, polyuria
Fatigue
Poor wound healing
Cardiovascular disease
Visual disturbances
Renal insufficiency
Recurring infection
Treatments
Diet- include more complex carbs (not simple sugars), low fat, adequate protein and fiber
Exercise
Monitoring glycemic control
Pharmacological management with oral anti-diabetics and insulin
Medications
Biguanides (metformin often med of choice)- decreased glucose production & increase insulin sensitivity in SM
Sulfonylureas- stimulate beta cells to produce more insulin
Meglitinides- stimulate beta cells to produce more insulin
Thiazolidinediones- decrease glucose production in liver & increase insulin sensitivity in SM
Alpha-glucosidase inhibitors- slow the breakdown and absorption of sugars and starches
DPP-4 inhibitors- prevent the breakdown of naturally ocurring GLP-1
SGLT-2 inhibitors- lower the renal threshold for glucose excretion with blood glucose lowering and weight loss
Insulin types and mixes: long, short, rapid (humalog, regular, NPH, lantus etc)
Lab Values
Glycemic goals
Fasting blood glucose: 70-130, HgbA1C less than 7%
Postprandial- less than 180mg/dl
Hypertension
Pathophysiology
Combinations of mechanisms; can be complex
Increased sodium intake- causes fluid retention, increasing stroke volume and blood pressure
RAAS- excess angiotensin II results in vasoconstriction and increased blood pressure
Aldosterone- excess release results in sodium and water retention, which results in increased stroke volume & BP; enhanced potassium excretion also occurs, resulting in low plasma K; low plasma K increases vasoconstriction through closure of K channels
Sympathetic nervous system- increased activity is primary HTN precursor; can cause vasoconstriction which causes increased PVR, BP, and can increase heart rate
Risk factors
Smoking
Obesity (greater than 30 BMI)
Physical inactivity
Diet
Stress
Dyslipidemia
Excessive alcohol use
Signs & Symptoms
Manifestations are usually on present after long term target organ damage (TOD)
headaches, chest pain, vision changes, shortness of breath, renal dysfunction, dizziness, fatigue or nosebleeds
Treatments
Lifestyle management: weight loss, diet (DASH), lowered alcohol consumption, 90 to 150mins per week of exercise, stress management
Antihypertensive medications
Medications
Diuretics- helps eliminate sodium and water-reducing blood volume
CCB- help relax/dilate muscles of blood vessels
ACE inhibitors- help relax/dilate blood vessels by blocking the formation of angiotensin II
Beta blockers- reduce the afterload on the heart
Lab values
Renal: elevated BUN & Creatinine
Endocrine- increased sodium & potassium
Metabolic- fasting glucose greater than 100g/dl
Other- decreased hematocrit
Heart Attack (MI)
Pathophysiology
destruction of heart muscle from lack of oxygenated blood supply
extent of damage depends on location of blockage
Most common cause for heart obstruction is atherosclerosis (buildup of plaque in artery)
rupture of plaque results in formation of a thrombus and obstruction of blood flow which results in ischemia and death of heart muscle
damaged heart muscle results in decreased CO and systemic symptoms like chest pain
Risk factors
modifiable: High low density lipoprotein, cigarette smoking, type 2 diabetes, obesity, inactivity, and hypertension
non-modifiable: male gender, family history of heart disease
Pt. has family hx of heart disease, HTN, low physical activity, and type diabetes which could all be contributing factors
Signs & Symptoms
Women: atypical signs (neck, shoulder blade, jaw pain, abdominal pain)
Geriatric population- may not have classic angina, but mimicking angina symptoms- may experience dyspnea, syncope, weakness or confusion.
Some pts especially those with diabetes never have typical symptoms and present with symptoms like SOB or fatigue
Classic symptom is chest pain
Treatments
Immediate management- maximizing oxygenation, administering medications to control pain, dilate the coronaries, prevent clots, and decrease myocardial workload
Reperfusion therapy- revascularization by PCI or fibrinolytic therapy
Surgical management- CABG (bypasses blockages causing damage)
Medications
Aspirin & heparin- to prevent new clot formation
Nitroglycerin SL- dilates the coronary arteries, increasing blood flow and decreasing pain
Morphine- narcotic given for pain relief if nitroglycerin is not effective
beta blockers- decrease sympathetic response to an MI, decreasing cardiac workload and oxygen consumption
Fibrinolytics- work to dissolve clots
Lab Values
Troponin (proteins expressed almost exclusively in the heart- specific marker of cardiac muscle damage)
Creatine kinase (general marker of cellular injury)
CK-MB- (CK isoenzyme marker specific to cardiac tissue)
Nursing Diagnosis:
Risk for unstable blood glucose related to patient condition of type 2 diabetes as evidenced by inadequate blood glucose monitoring.
Acute pain related to recent biliary surgery as evidence by patient report of pain of 7 on 0-10 scale.
Goals:
Patient will maintain a blood glucose of less than 180 mg/dl, fasting levels of less than 140mg/dl. Patient will better educated on topic and acknowledge when glucose is out of range.
Patient will report pain relief as shown by a movement from 9 on a 0-10 scale to a number that is more realistic even with current cancer diagnosis (ex: 4). Patient will follow prescribed medication regimen.
Interventions/Rationales: Monitor glucose levels with fingerstick and lab values. Give insulin at correct dosage according to sliding scale and at correct times. Educate patient of process and reason for doing it. Closely monitoring and controlling glucose levels helps determine correct amount of insulin needed and helps prevent the worsening of other conditions and promotes better wound healing.
Determine pain history and relief measures used, administer pain meds as prescribed and use non-pharmacological comfort measures like repositioning and diversional activities as needed. Information about baseline pain or recent pain allows for better evaluation of the effectiveness of treatment. Non-pharmacological measures can help enhance other pain relief measures and provide more relaxation.
Evaluation: Evaluate to see if insulin dosages are improving glucose levels and monitor for any adverse effects including hyperglycemia or hypoglycemia. Evaluate if medications are providing relief and see what patient pain is on scale of 0-10 after administration of meds and non-pharmacological measures.
Labs:
• Sodium- 136
• Potassium- 4.1
• Chloride- 105
• CO2- 24
• BUN- 27 (increased- could be indicative of altered kidney function, dehydration, med effects)
• Glucose- 300- (very high- required need for insulin before other meds)
• Calcium- 8.2 (decreased-can indicate parathyroid issue or could be a drug effect)
• Phosphorus- 3.1
• Magnesium- 1.8
• Albumin- 3.0 (decreased- can be indicative of altered liver function due to Cholangiocarcinoma)
• Protein- 5.7 (decreased- can be related to altered liver function or nutrient malabsorption due to cancer)
• RBC- 2.92 (decreased- can be due to the cancer and its treatment)
• Hgb-9.3 (decreased- can be due to the cancer and its treatment)
• Hct-27.0 (decreased- can be due to the cancer and its treatment
• Platelet- 117 (decreased- can be due to cancer/treatment
Assessment:
• A&O x4
• PEERLA equal round reactive
• Lips symmetrical, throat intact
• Ears intact
• Mucous membranes intact, missing 2 teeth
• Reports high pain level 9 out of 10
• Incision clean and intact
• Weak LLE, RLE
• Moderate RUE, LUE
• Moderate hand grip
• Chest sounds equal, S1 and S2 heard
• Diminished clear breath sounds
• Bruising on skin from injection sites
• No recent BM
• Urine output of 100ml, yellow/clear color
• Pulses moderate
• Capillary refill <3sec
Surgical hx:
• Cardiac catheterization (diagnose heart conditions or blocked arteries)
• Coronary angioplasty (widen blocked or narrowed arteries- due to hx of MI or CAD)
• Dual pacemaker (for hx of atrial fibrillation)
• Hepaticojejunostomy (to drain bile even with cancer)
• Loop implant/removal (heart recording device or abnormal beats or rhythms)
• Tonsillectomy
• Total hip arthroplasty
