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Patient MW Picture1, Hypertension Connections: This patient has many…
Patient MW
Hypertension
Pathophysiology
Blood pressure becomes increased with an increase of cardiac output, peripheral vascular resistance, or both. Cardiac output is affected by heart rate and stroke volume. Peripheral resistance relates to the nervous system and hormones. Anything that increases heart rate or circulating volume will increase blood pressure.
Increased sodium intake retains fluid and increases the pressure inside blood vessels
The renin-angiotensin-aldosterone system causes vasoconstriction which increases blood pressure
Aldosterone in high amounts can retain sodium and water to increase blood pressure
Increased sympathetic nervous system activity causes vasoconstriction and increases resistance and blood pressure
Normal blood pressure has a systolic reading less than 120 mm Hg and diastolic reading less than 80 mm Hg. Stage 1 hypertension is diagnosed when the systolic reading is 130-139 or the diastolic reading is 80-89.
Risk Factors
Cigarette smoking
Obesity (BMI greater than or equal to 30)
Physical inactivity
Excessive alcohol use
Diet
Stress
Dyslipidemia
Diabetes mellitus
Microalbuminuria or glomerular filtration rate less than 60 mL/min
Age older than 55 for men and 65 for women
Family history of cardiovascular disease
Signs and Symptoms
Only usually seen after long-term hypertension that results in target organ damage
Symptoms of chronic uncontrolled hypertension are headaches, chest pain, vision changes, shortness of breath, renal dysfunction, dizziness, fatigue, nosebleeds
Secondary hypertension symptoms are related to the disease process causing the high blood pressure
Treatments
Medications
Diuretics
Act on kidneys to help body eliminate sodium and water. Reduce blood volume and blood pressure
Calcium channel blockers (amlodipine, diltiazem, nifedipine)
Relax/dilate muscles of blood vessels. Slow heart rate
Angiotensin-converting enzyme inhibitors
Relax/dilate blood vessels by blocking formation of angiotensin II
Angiotensin II receptor blockers
Relax/dilate blood vessels by blocking action of angiotensin II
Beta blockers
Reduce afterload on the heart and dilate the blood vessels, causing decreased HR and force
Vasodilators
Relax muscle tissue in blood vessel walls and lower blood pressure
Combined alpha and beta blockers
Reduce nerve impulses that promote vasoconstriction and slow HR and reduce afterload
Central agonists
Decrease blood vessel ability to contract and cause vasoconstriction
Lifestyle changes
Weight
Excess weight raises blood pressure. Weight loss has a positive impact in BP control by reducing blood volume and balancing pressure-regulating hormones
Diet
High salt intake causes hypertension by retaining water and vasoconstriction. Reducing salt intake can reduce BP. Including calcium, magnesium, and potassium into diet can regulate blood pressure
DASH diet is recommended for people with hypertension and includes high fruits, vegetables, and low-fat dairy products
Stress management
The stress response releases hormones that raise blood pressure. Breathing exercises, relaxation technique, and fitness activities can help the patient be calm and reduce blood pressure
Alcohol consumption
Alcohol in heavy amounts increases blood pressure and constricts arteries. Men should have no more than 2 drinks per day and women should have no more than 1 per day
Exercise
Regular physical activity makes the heart muscle stronger, reduces weight, and reduces blood pressure. A stronger heart can pump blood with less effort
Lab Values
Renal
Proteinuria, elevated BUN and creatinine
Endocrine
Increased sodium, increased potassium, increased TSH
Metabolic
Fasting glucose greater than 100 mg/dL, increased LDL and triglycerides, decreased HDL
Other
Left ventricular hypertrophy, decreased hematocrit
Atrial Fibrillation
Pathyphysiology
Disruption in the cardiac conduction pathway or disorder of electrical impulse
Results in deviations from normal HR and/or rhythm, causing decrease in cardiac output
Increased risk of heart-related complications and increased risk of stroke
No P waves. Multiple pacemaker cells generating independent electrical impulses and causing chaos within the atria. Irregularly irregular.
Narrow QRS complexes with irregular R-R intervals
Can range from 300 to 600 beats per minute
Risk Factors
Risk increases with age
Cardiomyopathy, pericarditis, hyperthyroidism, hypertension, valvular disease, obesity, diabetes, chronic kidney disease, patients undergoing cardiac procedures, coronary artery disease
Signs and Symptoms
Palpitations- fast fluttering or beating in the chest or skipping beats
Hypotension, diaphoresis, shortness of breath, syncope, lightheadedness, weakness and fatigue, dizziness, anxiety
Complications
Loss of cardiac output which can cause syncope, palpitations, and shortness of breath
Clots from blood pooling in the atria. Puts the patient at risk for strokes
Treatments
Treat the underlying cause: acute MI, several mitral valve diseases, thyrotoxicosis, COPD, pericarditis, cardiomyopathy, hypertension, coronary artery disease
Rate control through medications
Rhythm control through medications, cardiac ablation, or cardioversion
Cardioversion
May urgently be required if patient is symptomatic
Medications
Antiarrhythmics
Slows cardiac action potential and heart rate
Amiodarone, dronedarone, dofetilide
Anticoagulants
Inhibits clot formation
Warfarin, dabigatran, rivaroxaban, apixaban, edoxaban, heparin
Beta blocker
Negative chronotropic effects to slow heart rate and decrease cardiac workload and oxygen demand
Sotalol used in AF with RVR for rate and rhythm control
Calcium channel blocker
Slows conduction through the AV node
Diltiazem
Cardiac glycoside
Slows conduction through the AV node; improves cardiac contractility
Digoxin
Lab Values
ECG changes
No P waves
Irregularly irregular rhythm
Narrow QRS complexes
Irregular R-R intervals
Rate ranging from 300-600 beats per minute
Uncontrolled
HR greater than 100 bpm
Controlled
HR maintained less than 100 bpm
Type II Diabetes Mellitus
Pathophysiology
Defects at the cell membrane cause the cell to resist insulin in transport of glucose into the cell. This requires increased insulin levels to drive glucose into the cells
Over time the pancreas fails to keep up with the increased demand for insulin and beta cell failure progresses. Most patients eventually need exogenous insulin delivery to keep normal blood glucose
Risk Factors
Modifiable
BMI greater than 26 and an even greater risk if BMI greater than 30
Physical inactivity
High density lipoprotein less than or equal to 35 mg/dL and/or triglyceride level greater than or equal to 250 mg/dL
Metabolic syndrome
Obesity
Increased serum triglycerides greater than or equal to 150 mg/dL
Decreased high-density lipoprotein less than or equal to 40 mg/dL in men, less than 50 mg/dL in women
Hypertension greater than or equal yo 130/85 mm Hg
Fasting blood glucose greater than 100 mg/dL
Non-modifiable
First-degree relative with diabetes
Members of high risk ethnic population (African American, Latino, Native American, Asian American, Pacific Islander)
Women who delivered a baby weighing greater than or equal to 9 lb or who were diagnosed with gestational diabetes
Hypertension ( >140/90 or on therapy for hypertension)
Women with polycystic ovary syndrome
HgbA1c greater than or equal to 5.7% on previous testing
History of cardiovascular disease
Signs and Symptoms
Polyuria, polydipsia, polyphagia
Fatigue
Poor wound healing
Cardiovascular disease
Visual disturbances
Renal insufficiency
Recurring infection
Treatments
Education
Education should encourage patients to take responsibility for diabetes management. It should include how to maintain a healthy lifestyle and implement behavioral goals. Blood glucose monitoring and treatment plans are included
Monitoring glycemic control
Self-monitoring of blood glucose
Continuous glucose monitoring
Monitoring of HbgA1c
Goals
Fasting
70-130 mg/dL
2-hour postprandial
Less than 180 mg/dL
HgbA1c
Around 7%
Nutrition
Goal is to improve metabolic outcomes by modifying nutrient intake. It should include food intake, carbohydrates, medications, metabolic control, measurements of height, weight, and body composition, and physical activity
Carbohydrate counting. Insulin should be adjusted to match carbohydrate intake
Carbohydrates distributed throughout the day in small meals and snacks. Keep consistent
Exercise
At least 150 minutes per week of moderate-intensity activity and strength training 3 times per week
Monitoring for complications
Vascular health and protection are key to avoiding devastating end-organ damage by diabetes
Management of hypertension, hyperlipidemia and hypercoagulability
Smoking cessation
Routine monitoring of the skin and feet to avoid wounds and infection, which can lead to amputation
Medications
Usually used in combination because of different mechanisms of action
Biguanides (metformin)
Decrease glucose production in the liver; increase insulin sensitivity in skeletal muscle
Meglitinides
Stimulate beta cells to produce more insulin
Alpha-glucosidase inhibitors
Slow breakdown and absorption of sugars and starches
DPP-4 inhibitors
Prevent breakdown of naturally occurring GLP-1, which stimulates insulin release from pancreas
Sulfonylureas
Stimulate beta cells to produce more insulin
SGLT-2 inhibitors
Lower renal threshold for glucose excretion with blood glucose lowering and weight loss
Thiazolidinediones
Decrease glucose production in liver; increase insulin sensitivity in skeletal muscle
Insulin therapy
In patients with loss of beta-cell function and progressing disease. Also used if HgbA1c greater than 10%
Lab Values
2 hour postprandial
Greater than or equal to 200 mg/dL
Hemoglobin A1c
Greater than or equal to 6.5%
Fasting blood glucose
Greater than or equal to 126 mg/dL
Random blood glucose
Greater than or equal to 200 mg/dL
Peripheral Autonomic Neuropathy
Pathophysiology
Incompletely understood. Prolonged hyperglycemia from diabetes mellitus damages nerve cells, affecting several areas of the body
Diabetic peripheral neuropathy: when nerves to the feet and hands are damaged
Autonomic neuropathy: damage to nerves of the autonomic nervous system
Risk Factors
Approximately one-third of people with diabetes over the age of 40 have some impaired sensation to their feet
Diabetes, especially when poorly controlled, is the biggest risk for neuropathies
Other disease processes, medications, nerve trauma, autoimmune disorders, degenerative disorders, alcoholism
Signs and Symptoms
Numbness, tingling, or pain
Loss of protective sensation can lead to injury that may not be felt. Infection and amputation are more likely
Diabetic gastroparesis. Delayed or erratic emptying of stomach contents into intestine
Bloating, early satiety, nausea, vomiting
Erectile dysfunction, orthostatic hypotension, urinary problems
Treatments
Aim is to slow progression of the disease (diabetes)
Keeping blood sugar within target range. See Type II Diabetes Mellitus Treatment section.
Maintain blood pressure, healthy weight, and regular physical activity
Relieve pain
See Medications
Alternative medicine
Capsaican cream to reduce pain sensations
Alpha-lipoic acid antioxidant may relieve pain
Transcutaneous electrical nerve stimulation therapy can deliver tiny electrical impulses to specific nerve pathways to prevent pain signals from reaching the brain
Acupuncture
Manage complications and restore function
Urinary tract problems
Can be affected by some medications. Strict urination schedule. Self-catheterization may be needed to remove urine from a nerve-damaged bladder
Orthostatic hypotension
Avoid alcohol, drink plenty of water, change positions slowly. Medications to treat
Digestive problems
Eat smaller, more frequent meals to help relieve gastroparesis, diarrhea, constipation, and nausea
Sexual dysfunction
Medications may improve sexual function in some men. Women may find relief with vaginal lubricants
Medications
Anti-seizure drugs
Can be used to ease nerve pain
Pregabalin, gabapentin
Antidepressants
Can ease nerve pain
Tricyclic antidepressants
Amitriptyline, desipramine, imipramine
Serotonin and norepinephrine reuptake inhibitors
Duloxetine, venlafaxine
Pain-relieving medication
Acetaminophen, ibuprofen, skin patch with lidocaine
Lab Values
Comprehensive metabolic panel
High blood or urine glucose suggestive of diabetes
Elevated BUN and creatinine may indicate poor kidney function which can cause neuropathy and influence treatment
Complete blood count
Vitamin B12 deficiency
Thyroid function
Elevated or depressed levels of thyroid hormones are associated with neuropathy
Tests for inflammation and autoimmunity
Tests for infections: HIV, Lyme antibodies, Hepatitis C
Oral glucose tolerance test
For diabetes and prediabetes
Renal Calculi
Pathophysiology
Calcifications in the urinary system. Nephrolithiasis refers to calculus in the kidney.
Occur when microscopic crystals in the urinary tract aggregate together, causing a stone to occur. Most stones are calcium. Others are cystine, uric acid, and xanthine
Risk Factors
Male gender
Caucasians are affected more than African Americans
Summer months
Humidity, sweating, decreased water consumption
Dehydration
Family history
Dietary habits such as increased sodium intake
Industrialized countries have higher risk due to increased dietary protein intake
Previous history of stones
Signs and Symptoms
Severe pain, distention and obstruction of urine flow
Pain is colicky and associated with nausea and vomiting
Location of stone influences location of pain
Upper ureteral stones causing referred pain to the flank
Lower ureteral stones causing lower abdominal, genital pain and irritative voiding symptoms
Gross hematuria and microhematuria present
Treatments
First-line treatment is trial of passage. A patient has the opportunity to pass the stone on their own for smaller stones, minimal pain, and no hydronephrosis or infection
Pain relieving medications, muscle relaxant medications
Surgical treatment required if patient does not pass stone after 4-6 weeks or develops renal colic, unresponsive to meds, nausea/vomiting, signs of UTI
Depends on stone size, location, and urgency of treatment
Ureteroscopy
Used for mid/distal ureteral stones where a scope is inserted through the urethra, bladder, and ureter to remove the stone
Percutaneous nephrolithotomy
For stones greater than 2 cm and staghorn calculi, stones in the renal pelvis and branching into the calyces. Direct access gained to kidney where a nephroscope removes the stone
Extracorporeal shock-wave lithotripsy
For renal and ureteral stones less than 2 cm. Noninvasive procedure that uses shock waves to break stones into smaller pieces and allowing the patient to pass the fragments
Medications
Narcotics and/or nonsteroidal anti-inflammatory medicine, along with antiemetics
Used for pain and nausea/vomiting with trial of passage
Alpha-adrenergic blockers
Tamsulosin, doxazosin, terazosin
Relax the musculature of the lower ureter and aid in stone passage
Lab Values
Urine pH
Acidic stones are formed in acidic urine
Urine culture
A positive culture indicates the need for aggressive management with antibiotics, stone removal, and possible hospitalization
Complete blood count and serum chemistries
Elevated WBC count may indicate antibiotics are required
Monitoring BUN and creatinine to assess renal function. BUN may be elevated if dehydrated. Creatinine may be elevated in acute obstruction of the kidney with resulting renal damage
Urine output/color
Minimal urine output should be between 30 and 50 mL/hr. Decreased urine output may indicate dehydration or obstructed kidney
Hematuria present. Can range from iced-tea color to fruit punch
Aggressive stone removal is indicated for thick urine, "ketchup" consistency, or blood clots
Obesity
Pathophysiology
Obesity is a complex disease where genetic, environmental, biochemical, and behavioral factors are related. Energy expenditure is often in the form of basal metabolism. The hormone leptin, communicates satiety to the brain and regulates energy expenditure balance. Energy expenditure comes from an increase in physical activity and metabolic requirements, along with thermogenesis. Weight gain occurs when the intake of caloric nutrients exceeds energy expenditure.
Risk Factors
Genetics: people with relatives who are obese are more likely to develop obesity. Specific genetic mutations play a role and usually affect appetite (leptin)
Environmental: increased availability and access to high-calorie, high-fat foods increase caloric consumption. Decreased energy expenditure from automation due to the availability and preparation of food requiring much less activity
Behavioral: physical inactivity promotes obesity as well as binge eating and compulsive eating
Biochemical: medications can sometimes cause obesity and increase appetite
Hypoglycemic agents, antihypertensive medications, hormones, antihistamines, anticonvulsants, antipsychotics, antidepressants
Secondary causes: Cushing's disease, insulinoma, hypothyroidism, polycystic ovarian syndrome, hypogonadism, pregnancy, growth hormone deficiency
Signs and Symptoms
Body mass index (BMI) = weight (kg)/height(meters2)
Overweight: 23.0-29.9
Obesity (class 1): 30.0-34.9
Obesity (class 2): 35.0-39.9
Extreme obesity (class 3): greater than 40.0
Obesity linked to numerous chronic health conditions and may be associated with signs and symptoms of these comorbidities
Diabetes mellitus
Heart disease, metabolic syndrome
Central obesity, high triglycerides, low HDL, high total cholesterol, hypertension, elevated fasting blood glucose
Airway obstruction
Chronic kidney disease
Decreased GFR
Nonalcoholic fatty liver disease
Cancer
Increases the risk of cancer and the likelihood of dying from cancer
Gastroesophageal reflux disease, cholelithiasis
Infertility issues
Psychiatric disorders
Osteoarthritis
Increased in non-weight bearing and weight-bearing joints
Decrease in psychosocial aspects of health such as well-being and quality of life
Increased weight circumference > 102 cm in men and 88 cm in women
Treatments
Diet therapy
Individualized
Calorie reduction of 500 to 1,000 kcal/day can cause stable weight loss. Very low calorie diets only used in limited circumstances
Physical activity
Long-term goals of 30 minutes of moderate-intensity exercise on most/all days of the week
Increased physical activity increases energy expenditure and basal metabolic rate by increasing lean body mass
Weight-loss therapy
Weight-related goals and treatment for BMI greater than 30. Also include those with a BMI greater than 25 or with high-risk waist circumference and greater than or equal to two other risk factors
Behavioral therapy
Combined with diet and physical activity is recommended
Self-monitoring with food logs, stimulus control, social support, cognitive restructuring
Weight loss programs and psychological evaluation
Surgical management
Bariatric Surgery
Types
Restrictive Procedures
Cause weight loss by reducing gastric capacity
Malabsorptive Procedures
Induce weight loss through decreased nutrient absorption
Combination Procedures
Induce weight loss primarily through restriction but also create a component of malabsorption
Indications for surgery
BMI greater than or equal to 40. Also patients with BMI 35 to 39.9 with comorbidities or a significant reduction in quality of life
Medications
Phentermine/topiramate extended release
Combination medication that suppresses appetite and enhances satiety
Bupropion-naltrexone
Combination medication that is used in adjunct to diet and exercise to lose weight
Lorcaserin
Affects chemicals in the brain that help regulate appetite and increase satiety after eating so less food is eaten
Liraglutide
Adjunct to reduced-calorie diet and increased physical activity for chronic weight management
Orlistat
Inhibits pancreatic lipase, reducing dietary fat absorption
Phendimetrazine, diethylpropion, benzphetamine, phentermine
Short-term treatment up to 12 weeks for obesity. Decrease appetite, increase satiety, and potential weight loss
Lab Values
Aimed at identifying secondary causes and comorbid risk factors
Screening for diabetes mellitus, dyslipidemia, thyroid dysfunction, fatty liver disease
Fasting blood glucose or hemglobin A1c
Liver function tests
Fasting lipoprotein panel
Thyroid-stimulating hormone
Elevated TSH may point to primary hypothyroidism
Decreased triiodothyronine and thyroxine may indicate secondary hypothyroidism
24-hr urine collection
In patients with physical characteristics of Cushing's disease for excessive cortisol secretion leading to weight gain
Assessment and History of Patient MW
Admitting Diagnosis: right renal calculus
Chief complaint: flank pain
Relevant History
Medical
Morbid obesity, BMI 39.73
Hyperlipidemia, hypertension
Type II Diabetes Mellitus
Peripheral autonomic neuropathy
History of previous renal calculi
Surgical
Guided nephrostomy catheter placement and kidney stone removal (2020, 2021)
Family
Family history of diabetes and hypertension
Former cigarette smoker, some current alcohol use
Right renal calculus in renal pelvis scan on CT (2 cm.), stent placed
Assessment findings
Right surgical flank pain that is sharp and continuous, relieved by rest, distraction, and medications. Rated a 9/10, then a 4/10 after medication administration
Tea-colored output indicating concentrated urine and hematuria
Shaking tremors of the upper extremities characteristic of diabetic neuropathy
Labs
Complete blood count revealed decreased red blood cells from hematuria
Basic metabolic panel revealed elevated blood glucose, elevated BUN, and elevated creatinine
Hypertension Connections:
This patient has many of the risk factors of hypertension. Obesity contributes to hyperlipidemia which causes atherosclerosis in the blood vessels. She is an older adult and has family history risk as well. She has previously used cigarettes and is physically inactive. Many of the patients conditions contribute to the development of hypertension and increase the risk for serious complications. She has elevated BUN and creatinine as well as blood glucose. Her hypertension may be caused by many contributing factors and may also be causing other health concerns.
Atrial Fibrillation Connections:
This patient has experienced atrial fibrillation before from her risk factors of age, obesity, hypertension, and diabetes. The workload of the heart is increased and conduction may be disrupted by these diseases. The patient is on antiarrhythmic medication to control this problem
Type II Diabetes Mellitus Connections:
Diabetes is primarily caused by obesity, physical inactivity, and hyperlipidemia. All of which this patient has. She also has a relative with diabetes, has hypertension, and elevated blood glucose. The patient takes insulin at home due to the insulin resistance associated with the disease. Diabetes can, in turn, cause further complication and worsen cardiovascular conditions. This patient also has neuropathy from microvascular damage.
Renal Calculi Connections:
Renal calculi in this patient are a risk due to previous renal calculi. She most likely experiences these due to white race, dietary habits, and dehydration. Hypertension is associated with increased sodium which raises blood pressure. A diet high in sodium probably has contributed to her hypertension as well as renal calculus formation without adequate water intake. The patient has hematuria that is tea-colored and right flank pain associated with this condition. She is on medications to relieve pain and has underdone catheter placement for stone passage. BUN and creatinine are also elevated in this patient which may indicate dehydration
Morbid Obesity Connections:
This patient has a BMI that is borderline extreme and dangerous. Some of the reasons this might be caused are genetics and a high calorie, high fat diet without physical activity. These risks may also contribute to hypertension and diabetes. The patient also is on antihypertensive medications and anticonvulsants that may also contribute to weight gain. Morbid obesity with cardiovascular disease, diabetes mellitus, and other chronic diseases can be detrimental to health. An increase in weight puts extra work on the heart to supply the body with the oxygen and nutrients it needs to function properly.
Peripheral Autonomic Neuropathy Connections:
This condition experienced by this patient can be attributed to her type II diabetes. On assessment, the patient experienced painful muscle spasms and tremors of her upper extremities related to this condition. It is also evidenced by high blood glucose suggestive of diabetes and elevated BUN and creatinine. She is on gabapentin for this disease.
