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Fin Em Dibi Mlus Pathophysiology - Type 1 ● Insulin deficiency ● Beta cells of pancreas no longer produce insulin ● Typically diagnosed before age 30

Pathophysiology - Type 2 ● Insulin resistant ● Defects at the cell membrane resist effective transporting of glucose into the cell. ● Typically diagnosed over 30, though it's seen more in children due to diet and sedentary lifestyle.

DKA Clinical Manifestations ● Clinical Manifestations ● Fruity breath, thirsty, dehydrated ● Kussmaul respirations (deep rapid breaths) ● Tachycardia, hypotension ● Acidosis

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Blood sugar >240 mg/dL Hyperkalemia/hypokalemia Hyponatremia – increased serum osmolality results in fluid shift from intracellular to extracellular Polyuria Nausea/vomiting Mental status changes: combative, drunk, coma

Self-monitoring of Glucose ● Self-monitoring via finger stick with glucose meter that provides a snapshot of blood glucose at a specific instance in time. ● DM1 patients should check their blood glucose at a minimum of before meals and at bedtime (4x total). ● Patients should increase their frequency when: ● Therapy is being initiated or actively adjusted ● There is an acute or ongoing illness ● There is hypoglycemia unawareness or an increase in hypoglycemic events ● Fasting and/or postprandial blood glucose levels are not consistent with HgbA1c Macrovascular vs microvascular complications ● Macrovascular Complications – Large Vessels ○ Cardiovascular disease ■ Coronary artery disease, myocardial infarction are the leading causes of diabetes-related deaths ● High BP and insulin resistance increase risk ■ Teach patients to diet and exercise ○ Cerebrovascular disease ■ Risk for strokes is 2-4 times higher ■ Risk for transient ischemic attack (TIA) ○ Peripheral vascular disease ■ Evidence for diminished blood flow to peripheral pulses ■ 36% of patients will have lower extremity PVD due to lower extremity blood pressure readings. ■ Peripheral neuropathy and PVD increase the risk of non-traumatic amputations of lower extremities (leading cause of amputations in the US) ■ Teach patients to not walk barefoot or wear tight shoes, and to check their feet daily for any cuts or ulcers. ■ Patients should have their toenails professionally trimmed. ● Microvascular Complications – Small Vessels & Capillaries ○ Eyes ■ Prolonged hyperglycemia results in retinal hypoxia ■ Diabetes is the new leading cause of blindness ■ Educate patients on the importance of annual eye exams. ○ Gums

Decreased circulation to the gums leads to periodontal disease and increased susceptibility of periodontal bacteria and dental caries ■ Most patients can experience early tooth loss as a result of decreased circulation ■ Educate patients on the importance of oral mucosa/dental exams every 6 months Kidneys ■ Hyperglycemia leads to affected kidney vasculature ■ Diabetes is the single leading cause of renal failure requiring dialysis in the US ■ Patients should have regular labs drawn for serum BUN, creatinine and microalbumin ■

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Hypoglycemia Treatment ● Primary management is to administer glucose. Oral glucose (15-20g) is preferred for the conscious patients. Rapidly absorbed carbohydrates may be used as well. ● Glucose should be measured within 15 mins of administration. If levels are still low, repeat treatment. Once levels return to normal the patient should consume a meal or snack to prevent the recurrence of the hospital setting if the patient is not able to swallow, D50 is administered IV. ● If there is no IV access and the patient is unconscious administer 1mg of IM glucagon. ○ Glucagon will raise BP and may cause nausea and vomiting so the patient should be turned to the side to avoid aspiration.

Neroc Ste Dres Cerebrovascular Accident (CVA) - Risk Factors ● Cerebral aneurysm – stretching of blood vessels of the brain ● DM ● Obesity ● Hypertension ● Hyperlipidemia ● Oral contraceptives ● Smoking ● Cocaine use Head Injury ● Head trauma ○ Pathophysiology ■ Caused by falls, motor accidents, bicycle injuries, drug and alcohol use, assault, and gunshot wounds ■ Types of TBI may involve the scalp, skull, meningeal layers, cerebral blood vessels, brain tissue, and neurons ■ Primary – injury occurs with the initial mechanical insult ■ Secondary – injury encompasses all processes that occur subsequent to the initial injury ■ Classification – open or closed/mild, moderate, or severe ■ Open are at risk for infection or bleeding ○ Clinical Manifestations ■ Changes in LOC – increase in drowsiness, confusion, difficult to arose ■ Pupils low to react or unequal ■ Seizures ■ Bleeding or watery drainage from nose or ears ■ Blurred vision ■ Loss of sensation to any extremity ■ Slurred speech ■ Vomiting ● Concussion ○ Pathophysiology ■ Transient and reversible ■ Results from trauma to the head

Instantaneous loss of awareness and unresponsiveness lasting from minutes to hours ■ Generally followed by amnesia and confusion Contusions and Lacerations ○ Pathophysiology ■ Describes visible bruising and tearing of cerebral tissue ■ Coup: bruising at point of impact ■ Contrecoup: bruising at site far removed from point of impact Diagnosis ○ Assessment of ABCs ○ Vital signs ○ Neuro exam, glasgow coma scale ○ CT, MRI, behavioral assessment Management ○ Care in hospital if injuries are sever, LOC for several minutes, prolonged or continued seizures ○ Respiratory status – maintain airways and sufficient oxygen saturation ○ NPO initially – potential for aspiration ○ Possible surgical interventions ○ Mannitol to treat cerebral edema – cerebral vasoconstriction ○ Barbiturates to decrease cellular metabolic demand ■ Barbiturate coma ○ Phenytoin (Dilantin) for seizures Nursing Care ○ Frequent assessment of VS and neuro checks ○ Provide analgesia and sedation ○ Careful observation and recording ○ Rehabilitation and prevention ■

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Increased Intracranial Pressure ● Clinical Manifestations ○ Headache ○ Nausea and vomiting ○ Decreased LOC ○ Pupillary asymmetry ○ VS (hypertension, bradycardia, respiratory depression) ○ Fundoscopic exam used to determine papilledema (optic nerve swelling) ○ Language comprehension issues, repetition ○ Restlessness, irritability ● Patient Positioning

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Keep HOB at 30-45

Unconscious Patient ● ABC is always priority with unconscious patients ● Check blood glucose to rule out hypoglycemia Brain Tumor ● Complications ○ ICP, bleeding, cerebral edema, seizures, and VTE (venous thromboembolism) Seizure Disorders ● Aura → sensory warning sign that a seizure is about to occur ● Status epilepticus ○ When seizures are continuous over a 5 min span or over 30 minutes intermittently ○ Administer Ativan and O2

Carasr Ste Coronary Artery Disease ● Oxygen use ○ To keep oxygen saturation greater than 93% ○ Supplemental oxygen optimizes oxygen delivery to the myocardium. Cardiac dysrhythmias especially tachycardia + anxiety increases myocardial oxygen consumption. Angina Pectoris ● Stable Angina ○ Episodes of intermittent chest pain present when the artery is narrowed 60% to 70%. ○ Typically associated with activity or exercise and is relieved by rest. ○ Not associated with damage to the heart muscle, but is a warning sign for potential heart muscle damage. ● Unstable Angina ○ Pain that is not associated with exercise and is not relieved by rest. ○ It may present with ECG changes but no elevation in cardiac markers. ○ Emergency requiring immediate treatment.

Myocardial Infarction ● Diagnostics ○ Cardiac biomarkers → Troponin - Gold Standard ■ Proteins expressed almost exclusively in the heart are specific markers of cardiac muscle damage. ■ Levels can elevate within 4 hours of injury and can say elevated as long as 10 days → this is why it is preferred. ● Medication Management ○ Analgesics (Morphine) ○ Oxygen ○ Nitroglycerin ○ Aspirin ○ Beta blockers

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Heparin infusions

Congestive Heart Failure ● Cardiac biomarkers → such as troponin I or T are used to rule out an acute ischemic event. ○ BNP and N-terminal pro-B-type natriuretic peptide (NT-proBNP) are increased because of overstretching of the ventricles ○ BNP: an increased BNP can be used to diagnose HF exacerbation ○ BNP lab value (NT-proB-type-natriuretic peptide) ■ A result greater than 100 pg/mL is abnormal. ■ The higher the number, the more likely heart failure is present and the more severe it is. ■ Levels above 400 pg/mL are considered high. ■ BNP levels increased in older adults. ■ BNP levels below 100 picograms per milliliter (pg/mL ) are considered normal. BNP

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Female and male

Less than 100pg/mL

0-74 yr

Less than 125 mg/dL

Greater than 75 yr

Less than 449pg/mL

Preload: amount of stretch in the heart at the end of diastole and is affected by the amount of pressure of blood returning to the heart ○ Aldosterone antagonists diuretics, such as spironolactone (Aldactone) and furosemide (Lasix), decrease preload in patients with fluid retention Afterload: refers to the resistance within vasculature. Increased afterload intensifies the workload on the heart, further impairing cardiac output. Afterload reduction is a main goal of medical management ○ Angiotensin-converting enzyme (ACE) inhibitors are usually the first line of medications used to control the RAAS (renin-angiotensin-aldosterone system) Contractility: is the force of the myocardial muscle contraction. ○ HF management via digoxin (Lanoxin), and oral positive inotropic medication used to increased cardiac contractility and reduce heart rate ○ Toxicity occur with this medication (nausea, vomiting, visual disturbances)

Basic EKG ●

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the P wave – It corresponds to the atrial depolarization produced by the propagation of the impulse from the SA node through the Atria the PR interval – starts at the beginning of the P wave until the beginning of the QRS complex the PR segment – the time immediately following the P wave ending to the beginning of the QRS complex the QRS complex – it corresponds with ventricular depolarization ○ ventricular contraction occurs after the QRS complex and in the ST segment the QRS interval – reflects the time required for the ventricular depolarization the T wave – it corresponds to ventricular repolarization the QT interval – it reflects the time required for ventricular depolarization AND repolarization the U wave – the Purkinje Fiber Repolarization ○ is rarely seen ○ looks like a small rounded U shape (AFTER T)

Hypertension ● Diagnosis ○ Two or more BP readings on >2 office visits ■ Normal - 120/80mmHg ■ Elevated - 120-129/80mmHg ■ Hypertension I - 130-139/80-89mmHg ■ Hypertension II - 140/90mmHg or higher ■ Hypertensive urgency - no target organ and BP greater than 120/80mmHg ■ Hypertensive emergency - evidence of TOD (target organ damage) and elevated 120/80mmHg ○ Laboratory tests are performed to identify secondary causes of hypertension → diabetes and high cholesterol tests ■ Renal → urinalysis with signs of proteinuria and elevated BUN + creatinine ■ Endocrine (serum sodium, potassium and calcium) → elevated sodium, potassium and TSH ■ Metabolic (fasting blood glucose, total cholesterol) → fasting glucose greater than 100 mg/dL, decreased LDL, triglycerides and HDL ■ Other (hematocrit, electrocardiogram and X-ray) → left ventricular hypertrophy and decreased hematocrit ● Stages ○ Essential or primary hypertension → has no identifiable cause. It appears to be a multifactorial, polygenic condition.

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Heredity is a predisposing factor Tends to be familial and is likely to be the consequence of interaction between environment and lifestyle factors ● Smoking or a poor diet

Secondary hypertension → elevation in blood pressure due to a specific cause. ■ Renal parenchymal is the most common cause → affecting renal medulla and renal cortex, where the “work” of the kidneys is done ■ Renovascular disease, Cushing’s syndrome, aldosteronism, hyperthyroidism

Peripheral Arterial Occlusive Disease ● Pathophysiology ○ Progressive/chronic condition where an occlusion forms form the blood flowing through the large peripheral arteries ○ can be caused by a combination of… ■ atherosclerosis, inflammation, stenosis, embolus, and thrombus ■ atherosclerosis – thickens the media and intima of the arteries and the formation of plaque causing an inadequate flow of blood ○ it deprives the lower extremities of oxygen and nutrients ■ can lead to ischemia and necrosis, or cell death ○ the tissue below the level of the arterial occlusion is where the damage mostly occurs ● Nursing management ○ loosen dressing ○ monitor the patient for impaired mobility, comfort levels, and use the 6 P’s ■ 6 P’s – used to assess the affected extremity’s decreased sensory perceptions ● pain, pressure, paralysis, paresthesia, pallor, pulseness ○ encourage the patient to exercise in order to build more collateral circulation ○ promote vasodilation by providing a warm environment for the PT ● Patient education ○ the medication’s effect might not be apparent for several weeks ○ monitor for any bleeding… ■ signs like abdominal pain, coffee ground emesis, black, tarry stool ○ avoid taking herbal supplements that contain clopidogrel due to the possibility of an increase in bleeding ○ instruct the patient to not cross their legs ○ they can elevate the legs but not above the heart level ○ refrain from wearing constrictive clothing ● Stages

Chronic Venous Insufficiency ● Pathophysiology ○ occurs after an incompetence in the valves of the lower extremities’ deep ravines ■ this allows pulling up blood and dilation of the veins ○ it precipitates the development of Swelling, Venous stasis ulcers, and advanced cases, Cellulitis ○ results from long periods of venous hypertension that results in the damage to the valve ■ causes a backup of blood, edema, and damage to the deep tissue ● Treatment ○ care of venous stasis ulcers require long-term management ○ a consultation with a dietitian and a wound care specialist would help to facilitate the healing process ○ promote venous return from the affected extremity and decrease the edema ○ provide care to the wounds and assess the client’s ability to care for the wound ● Nursing management ○ elevate the legs for at least 20 minutes (4-5 times a day) ○ elevate above the level of the heart while in bed ○ provide patient education ● Patient education ○ avoid crossing legs and wearing constrictive clothing or stockings ○ wear elastic compression stockings ■ applied after the legs have been elevated and the swelling has been minimized ○ adhere to a diet high in zinc, protein, iron, and vitamin A&C

Gasnet Syem Dde Gastritis ● Pathophysiology ○ Localized or patchy inflammation of the gastric mucosa resulting from repeated exposures to irritating agents → can be accompanied by hemorrhage into the mucosa ○ Aspirin and NSAIDs inhibit prostaglandin synthesis → disrupts the integrity of the mucosal surface ○ Most common cause of H. pylori ○ Infectious or inflammatory causes result in immune cell infiltration and cytokine production → damage mucosal cells ● Types of Gastritis ● Acute gastritis ○ Lasting several hours to few days ○ Mucosal inflammatory response may be accompanied by hemorrhage into the mucosa ○ Various degrees of mucosal necrosis, in severe cases, sloughing of the surface of mucosa may lead to acute GI bleed ● Chronic gastritis ○ Prolonged, persistent, or intermittent inflammation of the gastric mucosa ○ Characterized by patchy, diffuse inflammation of the mucosal lining of the stomach ○ Antibodies to parietal and intrinsic fact in chronic gastritis → impact protective factors ■ Contributes to low B12 levels → hemoglobin can't be synthesized → pernicious anemia ○ Chronic types ■ H. pylori → most common ■ Autoimmune gastritis ■ Atrophic gastritis → most common in older adults ● Clinical Manifestations ○ Epigastric pain → may be exacerbated by ingestion of spicy food ○ N/v → decreased appetite → weight loss ○ Stool color changes → black tarry, maroon ○ Atrophic gastritis may agave no symptoms ○ Hypovolemic shock → from excessive fluid loss ■ Pallor, tachycardia, hypotension ● Treatment ● Supportive care for relieving symptoms → NPO 6-12 hours for GI rest ○ Followed by slow reintroduction of clear liquids → working towards heavier liquids → normal diet ● Elimination of irritating foods → caffeine and spicy foods ● Healing is spontaneous and may occur in a few days

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Medications to relieve pain and discomfort ○ Proton pump inhibitors (PPIs) ○ H2-receptor antagonists ○ Antacids → aluminum or magnesium containing compounds ■ Decrease gastric acidity by neutralizing the acid ■ Shown to heal ulcers ○ Vitamin B12 → for chronic gastritis → prevention of anemia H. pylori cure depend on: ○ Type and duration of therapy ■ Triple antibiotic as first-line ■ Quadruple antibiotic for second-line ○ Patient compliance ○ Antibiotic resistance Surgical (rare) ○ Vagotomy → sever vagus nerve → reduce acid secretion ○ Partial or total gastrectomy → removal of stomach ○ Pyloroplasty → enlarging pylorus opening

Diet ● Avoid spicy foods and other foods noted to exacerbate symptoms ● Smaller frequent meals → minimize GI upset ● Avoid aspirin and NSAIDs ● Smoking cessation Nursing Process ● Assess → VS for possible bleed, presenting s/s, labs for H. pylori, I&Os ● Interventions ○ IV fluids → n/v can lead to severe fluid loss ○ H2-receptor antagonists → blocks gastric secretions ○ Antacids → buffers pH ○ PPIs → suppress gastric acid secretions ● Teach ○ Immediately report hematemesis (vomiting blood) → indicates GI bleed ○ Take meds as prescribed → complete regimen and no OTC ○ Avoid medication and other irritants that are associated with gastric episodes ■ OTC, aspirin, NSAIDs, caffeine, citrus juices, spices ○ Follow prescribed dietary teachings → NPO GI rest

Peptic Ulcer Disease ● Pathophysiology ○ Break in lining of the upper GI tract mucosa, with considerable depth and involvement of the submucosa ○ H. pylori releases toxins that promote mucosal inflammation and ulceration, stimulates release of cytokines and other mediators of inflammation → contribute to mucosal damage.

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NSAIDs inhibit prostaglandin synthesis → increases gastric acid and pepsin secretion → decreases bicarbonate → reduces gastric mucosal blood flow → decreases mucus production ■ Gastric acid diffuses into mucosa and injure small vessels → edema, hemorrhage and ulceration of stomach’s lining

Types ○ Duodenal ulcers ■ Approximately 80% of ulcers ■ Affects proximal part of the small intestine ■ Burning epigastric pain aggravated by fasting and improved with food or antacids ■ Characterized by remissions and exacerbations ● Healed scar tissue is imperfect → repeat episodes of ulceration ○ Gastric ulcers ■ Occur in the lesser curvature of the stomach, near the pylorus ■ Pain is triggered or worsened by eating; usually occurs shortly after meals with little/no relief from antacids. Risk Factors ○ Excessive smoking and alcohol use ○ Acid hypersecretory disorders ○ Crohn’s disease → will worsen the disease process Clinical Manifestations Gastric

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Duodenal

Food makes pain worse

Food makes pains better

Dull and aching pain

Gnawing pain; may wake up in the middle of night with pain

Weight loss

Normal weight

Severe: vomit with blood “coffee ground” or bright red

Severe: tarry, dark stool

Diagnosis ○ Upper GI endoscopy ■ Confirms the ulcer and permits cytology studies and biopsy to rule out H. pylori or cancer ○ Labs ■ CBC → rule out perforation and bleeding ■ Urea breath test → ingest urea tablet ● If H. pylori is ...