(NUR302) Exam 1 Exemplars

Cardiac hypertrophy

Cardiac hypertrophy

• Heart gets big

• Hypertrophic cardiomyopathy

• A disease affecting cardiac muscle resulting from excessive workload and functional demand

• Disorganization of myocardial cells leading to impaired cardiac muscle contractions

Pathophysiology of cardiac hypertrophy

• Primary cardiac hypertrophy:

  • Genetically inherited

• Secondary cardiac hypertrophy:

  • Underlying condition causing increased ventricular workload

• Left ventricular hypertrophy

  • the wall of the left ventricle, responsible for pumping blood out into the body, becomes thickened and stiff as a result of increased myocardial cell size

  • The muscle becomes less effective at contracting

  • The stiffness of the ventricle may prevent adequate filling and therefore may lower cardiac output

  • rigidity of the ventricle combined with smaller chamber size eventually leads to “pump failure” and cardiac decompensation.

Clinical manifestations of cardiac hypertrophy

• Asymptomatic

• Severe limit in function

• Heart murmur

• Decreased perfusion causing ischemia or angina

• Decreased cardiac output

• Pump failure

  • shortness of breath

  • Chest pain

  • Syncope (MARKER FOR SUDDEN DEATH)

  • Irregular heart rate and rhythm

Diagnostic testing/criteria of cardiac hypertrophy

• Genetic testing

• HTN testing

• ventricular arrhythmia monitoring

• Heart murmur monitoring

• 12 lead EKG (identifies electrical defects at rest)

• Ambulatory Holter EKG (identifies arrhythmias at rest)

• Exercise stress test

• Systolic pressure gradient of 30mmHg (moderate = 50; severe = 75)

Treatment of cardiac hypertrophy

• First choice

  • Angiotensin II receptor blockers (ARBs)

  • Angiotensin-converting enzyme (ACEs)

  • Calcium channel blockers

• Beta blockers

• Activity restriction

• Surgery

Acromegaly

• A condition of hyperplasia prompted by excessive growth hormone stimulation

• Commonly manifests as abnormal growth of the hands and feet

Pathophysiology of acromegaly

• Secretion of excessive growth hormone from the pituitary gland and secondary increase in (insulin-like) growth factor 1 (IGF-1) causes exaggerated skeletal and organ growth after epiphesial/growth plate closure (after puberty)

• The hypothalamus produces and releases growth hormone releasing hormone (which triggers growth hormone release) and somatostatin (which reduces the secretion of growth hormone by the pituitary)

  • Growth hormone secretion stimulates IGF-1 production in the liver, which usually triggers somatostatin in the hypothalamus to decrease growth hormone production (from the pituitary gland)

  • The negative feedback system fails and growth hormone secretion is unregulated

• Or adenoma

Clinical manifestations of acromegaly

• Soft tissue swelling

• Enlarged hands and feet

• Altered facial features

  • Prominent brow, jaw, and nasal bones

  • Enlarged tongue and lips

  • Increased spacing between teeth

• Pain and numbness in teeth

• Deepening voice

• Snoring

• Skin changes

  • Coarse hair growth

  • Oily appearance

  • Sweating

  • Body odor

• Altered reproductive functioning

• Menstrual cycle changes

• Impotence

• Breast discharge

• Cardiac hypertrophy

Clinical manifestations of acromegaly caused by adenoma

• Pressure on brain tissues and nerves

• Headaches

• Vision changes

Diagnostic criteria for acromegaly

• Elevated IGF-1

• Measurement of growth hormone

• Glucose tolerance test

• MRI to rule out adenoma

• History and physical

Treatment of acromegaly

• Designed to decrease the overproduction of growth hormone and IGF-1

• Pharmacologic

  • Somatostatin analogs to inhibit growth hormone secretion

  • Dopamine agonists to decrease pituitary secretion

  • Growth hormone agonists to block growth hormone receptors

• Nonpharmacologic

  • Surgical removal of adenoma

  • Radiation (can be used solely)

Cervical metaplasia and dysplasia

• Cells of the cervix responding to the hormonal environment

• Promoting adaptive and maladaptive responses

Metaplasia

• changing of onecell type to another as a response to environmental stressors

Dysplasia

• Abnormal growth and disordered differentiation in dividing cells

Pathophysiology of cervical metaplasia and dysplasia

• The cervical lining is comprised of columnar epithelium and squamous epithelium; the squamocolumnar junction/ transformation zone is where the two cell types merge and is where most common place for abnormal cells

• Metaplasia occurs through the squamous epithelium changing to columnar and/or the columnar epithelium changing to squamous

  • Can be triggered by high/low estrogen levels

• Dysplasia occurs through the physical change in cell structure (i.e the nucleus and DNA inside it)

  • Can be caused by infection (ex. HPV)

  • Can be cancerous cells

Risk factors of cervical metaplasia and dysplasia

• Early onset of sexual activity

• Multiple sexual partners (>3)

• Exposure to HPV

• Smoking

screening/diagnostic testing for cervical metaplasia and dysplasia

• Physical

• Cervical sampling (specimen collection)

• Cervical assessment

• Diagnostic excisional procedure

• HPV screening

• Papsmears

• Colposcopy

  • Biopsy of cervical tissue for microscopic examination

Treatment for cervical metaplasia and dysplasia

• HPV vaccine (primary prevention)

• Ablation

  • Removal of superficial cells

  • Cryosurgery

  • CO2 laser alation

  • Cold coagulation

  • Electrocoagulation diathermy ablation

• Hysterectomy

Pancreatitis

• Inflammation of the pancreas resulting in the destruction of the pancreas by pancreatic enzymes

• Digestive enzymes that usually only activate in the intestines attack the pancreas when inflamed through auto-ingestion

• Acute or chronic (more commonly chronic and seen in men)

Functions of the pancreas

• Endocrine gland

  • Produces insulin and glucagon

• Exocrine gland

  • Produces and secretes digestive enzymes for metabolism

• Pancreatic enzymes (amylase and lipase) mix with bile from the gallbladder to digest food

Pathophysiology of pancreatitis

• In a functioning negative feedback system, the secretion of pancreatic enzymes to the intestines stops when digestion is complete

• malfunction/injury to the pancreas and the negative feedback system causes the activation of the enzymes in the pancreas, forcing auto-ingestion and destruction in the pancrease

• Increased vascular permeability within the pancreas causes edma as inflammatory mediators are attracted (acute edematous pancreatitis)

Acute pancreatitis

• Sudden inflammation of the pancreas that resoles within a few days of treatment

• Occurs with injuries to digestive enzyme producing cells,  the pancreatic duct, or the digestive enzyme feedback mechanism

Causes of acute pancreatitis

• Pancreatic duct blockage by gallstones (hardened bile)

• Alcoholism

  • Triggers autoaccumulation of digestive enzymes

  • Premature enzyme activation and release

  • Increased permeability of the ductules

  • Increased protein content of secretions and protein plugs

• Inflammatory response

Clinical manifestations of acute pancreatitis

• Fever

• Pain in the upper abdominal, epigastric, and back areas

• Tachycardia

• HTN

• GI:

  • Nausea

  • Vomiting

  • Anorexia

  • Diarrhea

  • Abdominal tenderness

  • Guarding

  • Bruised ubilicus (cullen sign)

  • Ecchymotic sides (greys turner sign)

Treatment of acute pancreatitis

• Aggressive IV hydration within the first 24 hrs

• Nutritional support

• Analgesics

• Surgical removal of blockages

• Monitoring mental status, blood glucose, electrolytes, infection, respiration status, and pain

• Prevention of shock, renal failure, or systemic multiorgan failure

Chronic pancreatitis

• An ongoing inflammatory process of the pancreas with irreversible cellular and tissue changes

• Lasting longer that 6 months after acute episode (?)

Causes of chronic pancreatitis

• Chronic alcohol abuse

• autoimmune/hereditary disease

• Gallstones

• Cystic fibrosis

• High triglycerides

• Certain medications

Pathphysiology of chronic pancreatitis

• Alcohol abuse

  • Causes duct obstruction due to enzyme and protein accumulation

  • Obstruction causes ischemia of the cell and loss of function

  • Oxidative stress promoting greater cell injury and organ damage

Clinical manifestations of chronic pancreatitis

• Constant pain radiating from the upper abdomen to the back

  • Debilitating pain

• Malabsorption of food

  • Diarrhea

  • Fatty stool

  • Weight loss

• Diabetes

Treatment for chronic pancreatitis

• Pain management

• Nutritional support

• Pancreatic enzyme pills

• Insulin

• Low fat diet

• Surgery

  • Restore drainage

  • Remove blockage

Diagnostic criteria for pancreatitis

• Hx

• Physical

• CBC

• ESR

• C-reactive protein >10mg/dL

• Elevated serum amylase within 12 hours of onset; normal to low due to loss of function in chronic cases

• Elevated lipase within the first 24 hours

Diagnostic tests for pancreatitis

• Pancreatic function test

  • Tests for digestive enzyme levels

• Glucose tolerance test

  • Measures damage to insulin making cells

• Ultrasound

• CT scan

• ERCP

  • Gold standard pancreatitis test

  • Looks at obstructions in the pancreatic ducts using contrast dye

• Biopsy

Rheumatoid arthritis

• A systemic autoimmune disease characterized by chronic inflammation and hyperplasia of synovial membranes

• Leads to swelling and thickening of synovial membranes, joint erosion, and pain

Causes of rheumatoid arthritis

• Genetic susceptibility

• An autoimmune triggering event

• Development of aoutoimmunity against synovial cells

• Antibodies see others as foreign and trigger exaggerated inflammatory response

• Progressive damage through:

  • Pannus formation

  • Cartilage erosion

  • Fibrosis

  • Joint fixation and deformity

Pannus

• Granulation tissue that forms over the inflamed synovium and cartilage as a result of accelerated angiogenesis

• Produces enzymes that break down cartilage and erode bone

• Deprives cartilage of nutrients

Pathophysiology of rheumatoid arthritis

• Inflammatory response from lymphocytes and plasma cells form antibodies against specific antigens in the synovial membrane and cartilage that “see” other antibodies within the body as foreign

  • Rheumatoid factor (RF) signifies that antibodies (IgM, IgG, or IgA) are working against other antibodies mostly (IgG).

  • Exaggerated immune response is triggered from the antigen-antibody complexes formed

• inflammatory response is marked by excess production and release of inflammatory mediators (neutrophils and macrophages)

Clinical manifestations of rheumatoid arthritis

• Symmetric s/s

• Erythema

• Pain

• Swelling

• Lowgrade fever

• Anorexia

• Warmth

• Decreased mobility

• Pink deviation

• Malalignment

• Weight loss

• Weakness

Diagnostic criteria for rheumatoid arthritis

• No definitive test

• Hx and physical

• Elevated serum ESR

• Rheumatoid factor significant for antibodies against IgG

• Antinuclear antibody

Treatment of rheumatoid arthritis

• Pharmacologic

  • Anti-inflammatories

  • Immunosupressants

  • Medications to induce remission

  • Steroids

• Nonpharmacologic

  • Rest

  • Light activity

  • Physical therapy

  • Splints

  • hot/cold therapy

  • Remove stress

  • Surgery