NUR 631 Topic 16 Final Exam Study Guide
NUR 631 Topic 16 Final Exam
NUR 631 Topic 16 Final
NUR 631 Topic 16
NUR 631
NUR 631 Topic 16 Final Exam
... [Show More] Study Guide
Cellular biology and Alterations
Genetics
Fluid and Electrolytes and Acid-base
Pulmonology
Cardiovascular
Endocrinology
Neurology
Gastroenterology
Nephrology
Urology
Musculoskeletal
Integumentary
Oncology
Hematology
Infection
Reproductive
Cellular biology and Alterations
• Compensatory hyperplasia after partial resections
o An adaptive mechanism that enables certain organs to regenerate
Example: Removal of part of the liver leads to hyperplasia of the remaining liver cells (hepatocytes) to compensate for the loss. Even with 70% of the liver removed, it will regenerate within about 2 weeks
o Occurs in epidermal and intestinal epithelia, hepatocytes, bone marrow cells, and fibroblasts. Some hyperplasia is noted in bone, cartilage, and smooth muscle cells.
Example: Callus or thickening of the skin as a result of hyperplasia of epidermal cells
• Tumor progress from benign to malignant
o Benign tumors are usually encapsulated and well differentiated
Retain some normal tissue structure
Do not invade the capsules surrounding them or spread to regional lymph nodes or distant locations
Generally named according to the tissues from which they arise and include the suffix –oma.
o Progression of benign tumors to cancer and referred to as malignant
More rapid growth rates and specific microscopic alterations such as anaplasia, or the loss of differentiation and absence of normal tissue organization
May have different degrees of encapsulation; some lack a capsule, and if capsule is apparent, its integrity has been compromised so that tumor cells can grow to invade nearby blood vessels, lymphatics, and surrounding structures
Able to metastasize
Genetics
• Recurrence of autosomal diseases
o Autosomal dominant – Affected offspring are produced by the union of a normal parent with an effected heterozygous parent
Affected parent can pass either a disease gene or a normal gene to his or her children
Each event has a probability of 0.5; on average half of the children will be heterozygous and will express the disease, and the other half will be normal.
o Autosomal recessive – Individual must be homozygous for a recessive allele to express the disease (carriers are phenotypically normal)
Characterized by delayed age on onset, incomplete penetrance, and variable expressivity
Most common is cystic fibrosis (CF)
• Klinefelter’s syndrome
o Causes
Chromosomal disorder XXY – genotype
Genetically male – due to Y
Male XY, female XX
Random, not inherited – nondisjunction in the X chromosomes in the mother
o Signs and Symptoms
Both male and female sexual characteristics
Decreased testosterone more female hormones causing
Less body and facial hair
Gynecomastia (risk breast CA)
Weak muscles and bones (osteoporosis), shy (tall, lanky, shy), elevated stature
Can result in decreased IQ
Higher risk of AI disorders
Small testes
High pitched voice
Majority - Infertility
o Present in individuals with at least two X chromosomes and a Y chromosome in each cell (47, XXY karyotype). Can also have variants such as XXYY, XXXY, and XXXXY
o Individuals have a male appearance (due to the Y chromosome)
o 1 in 1000 births
o Two thirds are caused by nondisjunction of the X chromosomes in the mother
o Testing
Clinical Exam
Chromosomal testing
Hormones
Immunology (The study of immune systems in all organisms)
• Rickets disease
o Caused by a deficiency of vitamin D or calcium, insensitivity to vitamin D, wasting of vitamin D by the kidney, or inability to absorb vitamin D and calcium in the gut
o Most common form is x–linked hypophosphatemic rickets in industrialized nations.
o Manifests in children as softening of bones, abnormal growth of bones, and enlargement of cartilage at the ends of long bones
o Growing bone fails to become mineralized (ossified)
o Can lead to short stature, bowing of the limbs with broad, irregular growth plates, often listless and irritable with hypotonia and muscle weakness may be unable to walk without support; abnormal parietal flattening and frontal bossing occur in the skull
o Normalization of calcium, phosphorus, and vitamin D levels before surgical intervention, deformity often improves when bone metabolism improves
o Hypocalcemia
• Epstein-Barr Virus (HHV 4)
o Human herpesvirus 4
o One of the most common human viruses
o Spread most commonly through bodily fluids, particularly saliva
o Can cause infectious mononucleosis (mono)
o Symptoms can include fatigue, fever, inflamed throat, swollen lymph nodes in the neck, enlarged spleen, swollen liver, and rash
o Associated with almost all cases (>90%) of Burkitt lymphoma
• Human Herpes Virus (HHV) 8
o Also known as Kaposi’s sarcoma-associated herpesvirus (KSHV)
o Causes rare cancer of connective tissue
o Bluish red nodules appear on the skin especially on the lower extremities
o Occurs in a particularly virulent form in individuals with AIDS
• Complement Cascade
o Activated by 3 pathways
Classical pathway – Activated by proteins of the adaptive immune system (antibodies) found to their specific targets (antigens)
Lectin pathway – Activated by mannose-containing bacterial carbohydrates
Alternative pathway – Activated by gram-negative bacterial and fungal cell wall polysaccharides
o The products have four functions:
Anaphylatoxic activity resulting in mast cell degranulation
Leukocyte chemotaxis
Opsonization
Cell lysis
• Passive-acquired immunity
o Does not involve the host’s immune response at all
o Occurs when preformed antibodies or T lymphocytes are transferred from a donor to a recipient
o Naturally: Maternal antibodies that cross the placenta to the fetus
o Artificially: Immunotherapy for a specific disease such as rabies
Only temporary since the donor’s antibodies or T cells are eventually destroyed
• IgM and IgG and IgA and IgE
o IgM
Largest of the immunoglobulins
First antibody produced during the initial, or primary, response to antigen
It synthesize early in neonatal life and may be increased as response to infection in utero
o IgG
Most abundant class of immunoglobulins (80-85%)
Account for most of the protective activity against infections
Selective transport across the placenta, maternal IgG is also the major class of antibody found in the blood of the fetus and newborn.
o IgA
Two classes – IgA1 and IgA2
IgA1 found predominantly in the blood
IgA2 predominantly found in normal body secretions
Anchored together through a J chain and “secretory piece”
Secretory piece may functions to protect these immunoglobulins against degradation by enzymes also found in the secretions
o IgE
Least concentrated in the circulation
Very specialized functions as a mediator of many common allergic responses
Defense against parasitic infections
When produced against relatively innocuous environmental antigens, it is also the primary cause of common allergies such as bee stings, hay fever, dust allergies.
Complement T helper cells and immune responses
IgE bind to receptors on the surface of mast cells causing release of histamine H1
o (1) Bronchial constriction (2) Edema (3) Vasodilation (4) H2 (5) Increase gastric secretions (6) Decreases the release of histamine from mast cells and basophils
o IgG, IgM, and IgA bind to the surface of parasites, activate complement, generate chemotactic factors for neutrophils and macrophages, and serve as opsonins for those phagocytic cells; unique to parasitic infections, the eosinophil is a primary cell in the granuloma
• IgE-mediated hypersensitivity
o Type 1 reactions – most common allergies such as pollen
o IgE can contribute to a few autoimmune and alloimmune diseases and many common allergies are not mediated by IgE.
o Short life span in the blood - binds rapidly to very high-affinity Fc receptors and on the plasma membranes of mast cells
o Repeated exposure to the antigen is normally required to elicit enough IgE for “sensitivity”
o Histamine is the most potent mediator that affects several key target cells
Contracts bronchial smooth muscles causing bronchial constrictions; increases vascular permeability causing edema; and vasodilation increasing blood flow into the affected area
Interaction of histamine with H2 receptors results in increased gastric acid secretion and a decrease of histamine released from mast cells and basophils – action of histamine through H2 receptors suggests an important negative-feedback mechanism that stops degranulation
• SLE (Lupus)
o Chronic, multisystem, inflammatory disease and is one of the most common, complex, and serious of the autoimmune disorders
o Characterized by the production of a large variety of autoantibodies against nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, and many other self-components
Most characteristic autoantibodies produced are against nucleic acids, histones, ribonucleoproteins, and other nuclear material
o Occurs more often in women, age 20-40
o Clinical Manifestations: arthralgias or arthritis, vasculitis, rash, renal disease, hematologic abnormalities (anemia)
Develops slowly and has frequent remissions and exacerbations
o 11 common clinical findings (dx based on serial or simultaneous presence of 4)
Facial rash confined to cheeks (malar rash)
Discoid rash (raised patches, scaling)
Photosensitivity
Oral or nasopharyngeal ulcers
Nonerosive arthritis of at least two peripheral joints
Serositis (pleurisy, pericarditis)
Renal disorder (proteinuria)
Neurologic disorder (seizure, psychosis)
Hematologic disorders (hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia)
Immunologic disorders
Presence of antinuclear antibody (ANA)
o No cure, treat symptoms, and minimize autoimmune response – NSAIDS, Steroids, immunosuppressive drugs, intravenous immune globulin (IVIg)
Protect from sun exposure. Ultraviolet light can worsen symptoms
Fluid and Electrolytes and Acid-base
• Treatment of Hyperkalemia
o Signs and symptoms of hyperkalemia
Tingling, cramps/diarrhea
Weakness, flaccid paralysis
Arrhythmias, cardiac arrest
o Calcium gluconate for neuromuscular irritability
o Glucose – stimulates insulin secretion
o Glucose + insulin – facilitates cellular entry of potassium
o Buffered solutions – correct metabolic acidosis and lowers serum potassium level
o Oral/rectal – exchanges sodium for potassium in the intestine
o Dialysis when renal failure has occurred.
• Calcium and phosphate balance
o Calcium is a necessary ion for many fundamental metabolic processes
Normal serum levels: 9-10.5
Major cation associated with the structure of bones and teeth
Enzymatic cofactor for blood clotting and is required for hormone secretion and function of cell receptors
Helps with contraction of muscles, transmission of nerve impulses, plasma membrane stability and permeability
o Phosphate is found primarily in bone, and smaller amounts in ICF and ECF spaces
Normal serum levels: 2.5-4.5
Acts as IC and EC anion buffer in the regulation of acid-base balance
o Balance of both are rigidly controlled – if the concentration of one ion increases or decreases, the other will increase or decrease
o Regulated by 3 hormones
Parathyroid hormone (PTH)
Vitamin D
Calcitonin
• Metabolic acidosis with partial respiratory compensation
o pH <7.35; CO2>45, HCO3<22
o Hyperventilation – the respiratory system compensates for a metabolic acidosis as the reduced pH stimulates hyperventilation, lowering the Paco2 and the amount of bicarb circulating in the blood.
o HA and lethargy are early symptoms, deep, rapid respirations (Kussmaul) are indicative of respiratory compensation.
Pulmonology
• Respiratory Distress Syndrome in a newborn (hyaline membrane disease or HMD)
o Major cause of neonatal morbidity and mortality
o Almost exclusively present in premature infants
o Caused by surfactant deficiency which decreases the alveolar surface area available for gas exchange
o Without surfactant, alveoli collapse at the end of each exhalation
• Silicosis pulmonary function test results
o Silicosis – inflammation of the lung resulting from the inhalation of free silica (silicon dioxide) and silica-containing compounds, which occurs in mining and related industries
o Decreased forced vital capacity (FVC), decreased forced expiratory volume in 1 s (FEV1) and decreased lung volume (LV)/total lung capacity (TLC)
• Pleural effusions
o Presence of fluid in the pleural space
o Source is usually blood vessels or lymphatic vessels lying beneath either pleura
o Occasionally an abscess or other lesion may drain into the pleural space
• Cystic Fibrosis
o A genetic disorder of the exocrine glands caused by a mutation in the CF transmembrane regulator gene, resulting in impairment in chloride transfer across all membranes and subsequent chloride and water accumulation in organs and in thickened secretions that block ducts and form cysts
o Autosomal recessive inherited disorder
Abnormal secretions that cause obstructive problems within the respiratory, digestive, and reproductive tracts
o CF gene is located on chromosome 7
o One of the most common lethal genetic disease in whites
o Classes 1 through 3 are severe disease and classes 4 through 6 with milder pulmonary disease
Cardiovascular
• Pulmonic valve complications
o Leaky pulmonary valve due to pulmonary hypertension or congenital heart defect (defect from Tetralogy of Fallot)
o Pulmonic valve stenosis
o Regurgitation
o Infective endocarditis
• Arteritis
o Inflammation of arteries
o Temporal arteritis, headache, giant cell arteritis
• Right heart failure
o Inability of the right ventricle to provide adequate blood flow into the pulmonary circulation at a normal central venous pressure
o Most often the result of left heart failure when the increase in left ventricular filling pressure that is reflected back into the pulmonary circulation is severe enough.
• Tetralogy of Fallot
o Four defects
A large ventricular septal defect (VSD) that is high in the septum
Overriding aorta that straddles the ventricular septal defect (VSD)
Pulmonary stenosis (PS)
Right ventricle (RV)
o Most common cyanotic congenital heart defect
o Two phases of embryologic growth:
During the division of the truncus arteriosus by the spiral septum in the third or fourth week of gestation
During the division of the ventricles between the fourth and eighth weeks of gestation
• Shock in newborns
o Etiology with examples
Hypovolemia: blood loss, inadequate placental transfusion, dehydration
Asphyxia: respiratory failure
Cardiogenic causes: cardiomyopathy, hypocalcemia, hypoglycemia, dysrhythmia, congenital malformation
Sepsis: early onset group B beta-hemolytic streptococcal infection
Drugs
Hypocarbia
o Clinical evaluation
Systemic arterial hypotension
Narrow pulse pressure
Tachycardia (In early asphyxia, bradycardia is present)
Tachypnea
Retractions
Grunting aspirations
Apnea
Prolonged capillary filling time
Oliguria
Hypothermia
Metabolic academia
o Treatment
Dependent upon etiology of shock
Rapid recognition of shock and identification of underlying causes are essential to prevent irreversible changes
• Raynaud’s disease
o Primary vasospastic disorder of unknown origin
o Endothelial dysfunction with an imbalance in endothelium-derived vasodilators and vasoconstrictors
o Genetic predisposition may play a role in its development
• Patent Ductus Arteriosus
o Vessel located between the junction of the main and left pulmonary arteries and the lesser curvature of the descending aorta, usually just distal to the left subclavian artery
o Pulmonary artery to aortic shunt doesn’t close
o Continuous machinery type murmur left upper sternal border throughout systole/diastole
o Bounding pulses; maybe asymptomatic if small
Endocrinology
• Obesity and Type 2 DM
o Causes
Familial predisposition
Lifestyle
Metabolic Syndrome/Insulin Resistance (incr. risk with obesity)
o Abnormal insulin secretion/action
Beta cell dysfunction
Insulin resistance
o Increased free fatty acids and fat deposition – incr. inflammation (release of cytokines) and intracellular lipid deposits
o Incr. glucagon secretion
o Alteration in the production of adipokines by adipose tissue - Leptin resistance
o 2 most important factors are positive family hx and obesity
o See figure 22-15 page 740
• Know Autoimmune disorders
o Graves Disease
AI Hyperthyroid
Causes
Incr. F > 20, FHX, Tobacco
Signs and Symptoms
Sxs of hyperthyroid exophthalmia, thyroid bruit, periorbital/ pretibial myxedema, diplopia
Goiter
Thyrotoxicosis tachycardia, HTN, delirium, N/V,D -- risk for ?
Testing
TSH, T3/4, Antibodies
• Hormones that cause hyperglycemia
o Glucagon
o Growth hormone
o Catecholamine
o Glucocorticoid
o High circulating or tissue levels of cytokine
o Epinephrine
• Antidiuretic Hormone (ADH)
o Directly regulates water balance
o Secreted when plasma osmolality increases or circulating blood volume decreases and blood pressure drops
o Action is to increase permeability of renal tubular cells to water, increasing water reabsorption and promoting the restoration of plasma volume and blood pressure
o Regulated by feedback mechanism
o Synthesized in hypothalamic neurons but stored and secreted by posterior pituitary
o Major homeostatic function is the control of plasma osmolality as regulated by ADH
o Effects may be inhibited by hypercalcemia, prostaglandin E, hypokalemia
o Increase in ADH – Stress, trauma, pain, exercise, nausea, nicotine, exposure to heat, drugs (morphine)
o Decrease in ADH – decrease in plasma osmolality; increase in intravascular volume; hypertension; increase in estrogen, progesterone, angiotensin II levels, alcohol ingestion
o Causes disease of posterior pituitary – abnormal secretion of ADH, SIADH, DI
• Diabetes Insipidus and associated labs
o Insufficiency of antidiuretic hormone (ADH)
Polyuria (frequent urination)
Polydipsia (frequent drinking)
o 3 types of DI
Neurogenic DI
Encountered most often and caused by insufficient amounts of ADH
When an organ lesion of the hypothalamus, pituitary stalk, or posterior pituitary interferes with ADH synthesis, transport, or release
Primary or secondary brain tumors, aneurysms, thrombosis, infections, and immunologic disorders
Nephrogenic DI
Associated with an insensitivity of the renal collecting tubules to ADH
Can be genetic or acquired; is often idiopathic
Acquired related to pyelonephritis, amyloidosis, destructive uropathies, polycystic disease, and intrinsic renal disease; all lead to irreversible DI
Drugs that may induce a reversible form are lithium carbonate, colchicine, amphotericin B, loop diuretics, general anesthetics, and demeclocyline.
Dipsogenic DI
Excessive fluid intake lowers plasma osmolality to the point it falls below the threshold for ADH secretion
May be associated with psychiatric disorders
Also found in individuals with a low osmotic threshold for inducing thirst
o Dx: Distinguish from other polyuric states
o Urine Spec grav, Urine osmo, Na, Serum Osm, Serum ADH, water restriction
o Tx: Desmopressin aka DDVAP
o All forms are characterized by the inability of the kidney to decrease permeability to water. Causes excretion of large volumes of dilute urine and an increase in plasma osmolality.
o Dehydration develops rapidly without ongoing fluid replacement.
o Serum hypernatremia and hyperosmolality occur.
o Clinical Manifestations: polyuria, nocturia, continuous thirst, polydipsia
• Hyperparathyroidism
o Characterized by greater than normal secretion of parathyroid hormone (PTH) and hypercalcemia
Classified as primary, secondary, or tertiary
o Primary
Sporadic disease characterized by inappropriate excess secretion of PTH by one or more of the parathyroid glands
One of the most common endocrine disorders
80-85% are caused by parathyroid adenomas, 10-15% are caused from parathyroid hyperplasia, and approximately 1% are caused by parathyroid carcinoma
o Secondary
Caused by an increased in PTH secondary to a chronic disease state such as chronic kidney disease or intestinal malabsorption, which causes a decrease in serum ionized calcium levels (hypocalcemia) or chronic vitamin D deficiency
o Tertiary
Excessive secretion of PTH and hypercalcemia that occurs after long-standing secondary hyperparathyroidism
Unknown etiology and develops in individuals with chronic secondary hyperparathyroidism and after renal transplantation
• Type 1 Diabetes
o Juvenile and IDDM
o Beta-cell destruction usually leading to absolute insulin deficiency, immune mediated diabetes is most common form
Cellular-mediated autoimmune destruction of pancreatic beta cells
Individual prone to ketoacidosis
Little or no insulin secretion, insulin dependent
Usually not obese
o Autoimmune (type 1A) and nonimmune (type 1B)
Type 1A – Multifactorial
Type 1B – Secondary to other disorders such as pancreatitis
o Genetics
First-degree relative such as a parent or sibling with type 1 diabetes (10-13%)
o Environmental
Viral infections such as H. pylori, cow’s milk, and a relative lack of vitamin D
o Clinical manifestations
Abnormal alpha and beta cell function
Gradual destruction of beta cells that eventually leads to insulin deficiency and hyperglycemia
Before hyperglycemia develops 80-90% of the function of the insulin-secreting beta cells in the islet of Langerhans must be lost.
Polydipsia, Polyuria
Polyphagia
Weight loss
Hyperglycemia
Neurology
• Fight or Flight syndrome
o Also called hyperarousal or the acute stress response
o Physiological reactions that occurs in response to a perceived harmful event, attack, or threat to survival
o Heart increases pump action during stress or fear
o Sympathetic nervous system
Activates and released norepinephrine
o Adrenal medulla produces a hormonal cascade that results in the secretion of catecholamines, especially norepinephrine and epinephrine. The hormones estrogen, testosterone, and cortisol, as well as the neurotransmitters dopamine and serotonin, also affect how organisms react to stress
• Arachnoid Villi
o Protrude through arachnoid space through dura mater and lie within the blood flow of the venous sinuses
o CSF is reabsorbed by means of a pressure gradient between villi and cerebral venous sinuses
o Function serves as one-way valves directing CSF outflow into the blood but preventing blood flow into the subarachnoid space
• Circle of Willis
o “Arterial circle”
o Has the ability to compensate for reduced blood flow from any one of the major contributors (collateral blood flow)
o Formed by the:
Posterior cerebral arteries
Posterior communicating arteries
Internal carotid arteries
Anterior cerebral arteries
Anterior communicating arteries
• Cranial nerves functions and abnormalities associated with them
1. Olfactory
• Sense of smell; purely sensory
• Tested by asking to sniff aromatic substances and identify them
2. Optic
• Vision; purely sensory
• Tested with visual eye chart, object moving into visual field, inside of eye is assessed with ophthalmoscope to observe blood vessels of eye interior
3. Oculomotor
• Eye movement and pupil constriction
• Pupils examined for size and pupillary reflex tested with penlight
4. Trochlear
• Eye movement
• Ability to follow moving objects
5. Trigeminal
• Facial muscles including chewing and facial sensations (motor and sensory)
• Sensations for pain, touch and temperature; corneal reflex tested with a wisp of cotton; clench teeth; open mouth against resistance, move jaw from side to side
6. Abducens
• Eyeball movement
• Lateral eyeball movement in conjunction with cranial nerve III
7. Facial
• Taste, tears, saliva, and facial expressions
• Anterior two thirds of tongue tested for ability to taste sweet, salty, sour, and bitter; symmetry of face checked; close eyes, smile, whistle; tears tested with ammonia
8. Acoustic (Vestibulocochlear)
• Auditory
• Air and bone condution by use of tuning fork
9. Glossopharyngeal
• Swallowing, saliva, taste
• Gag and swallow reflexes; speak and cough; posterior one third of tongue may be tested for taste
10. Vagus
• Sensory/motor to pharynx; control of parasympathetic nervous system (PNS); supply smooth muscle of abdominal organs and receives sensory impulses from viscera
• Same as for cranial nerve IX (IX and X) are tested in common); both serve muscles of the throat
11. Accessory
• Sensory and motor fibers for sternocleidomastoid and trapezius muscles and muscles of soft palate, pharynx, and larynx
• Check strength by rotating head and shrugging shoulders against resistance
12. Hypoglossal
• Muscles of tongue and sensory impulses from tongue to brain
• Stick out tongue and observe for any position abnormalities
• Multiple Sclerosis
o Chronic inflammatory disease involving degeneration of CNS (brain, spinal cord, optic nerve) myelin, scarring or formation of plaque, and loss of axons
Affects white and gray matter
4 different types
Remitting and Relapsing
Progressive – Relapsing
Secondary Progressive
Primary Progressive
o Causes
Autoimmune – possible post viral infection such as Epistein-Barr
Vitamin D deficiency, cigarette smoking
Trauma, pregnancy
o Signs and Symptoms
Visual changes, optic neuritis
Balance, memory, weakness, parasthesias – increased deep tendon reflexes
Charcots triad – dysarthria, intention tremor, and nystagmus
Lhermitte sign – momentary paresthesia (shocklike or tingling sensation) in the trunk or limbs during active or passive flexion of the neck
o Risk factors
Genetic polymorphism
Environmental factors – Vitamin D deficiency, smoking, Epstein Barr Virus (EBV)
o Testing
MRI – brain and spinal cord
Lumbar puncture with CSF analysis
• Myofascial pain syndrome
o Associated with injury to muscle, fascia, and tendons and includes myositis, fibrositis, myofibrositis, myalgia, and muscle strain
o Pain results from muscle spasm, tenderness, and stiffness
o Neuroaxonal degeneration with alterations in neuromuscular transmission may occur
o Compression of the trigger point causes referred pain, motor dysfunction, and autonomic responses
o Early stages of the disorder, the pain is localized then becomes more deep and generalized
Begin as a result of poor muscle tone, inactivity, muscle or tendon strain, or sudden vigorous exercise and can evolve into a chronic pain state
Gastroenterology
• Jaundice is seen in what complications
o Hepatitis
o Destruction of heme
• Hepatitis B virus
o Transmitted blood-blood contact or sexually
o Major cause of chornic hepatitis, cirrhosis, and hepatocellular carcinoma
o Chronic infection develops in 15-30% of those with acute infection
• Intussusception and intestinal obstruction
o Telescoping or invagination of one portion of the intestine into another
o Most common cause of acquired intestinal obstruction in infants between 5 and 10 months of age
o Clinical manifestations
Abdominal pain
Colicky
Vomiting
Bloody stools
Tender, sausage-shaped abdominal mass
• Periduodenal band (Ladd’s band)
o Obstructing band over the duodenum
o Significant finding in intestinal malrotation
o Clinical manifestations
In infants, intermittent or persistent bile-stained vomiting after feedings
Abdominal distention
Dehydration and electrolyte imbalance
Fever
Pain, scanty stools, diarrhea, bloody stools, and severe dehydrations
Nausea after meals
• Meconium ileus
o Intestinal obstruction caued by meconium formed in utero that is abnormally sticky and adheres firmly to the mucosa of the small intestine, resisting passage beyond the terminal ileum
o Cause is usually a lack of digestive enzymes during fetal life
o Associated with cystic fibrosis (CF)
o Clinical manifestations
Abdominal distention
Does not pass meconium
Vomiting
Tachypnea, intercostal retraction, and grunting respirations in diagnosis of CF
• GI bleed presentation
o Hematemesis
o Melena
o Hematochezia
o Occult bleeding
• Celiac Sprue (Gluten-sensitive enteropathy)
o Autoimmune disease of the small intestinal villous epithelium when there is ingestion of the cereal protein gluten (gliadin) found in wheat, rye, barley, and oats in genetically susceptible individuals
o Complex disease and involves the interaction of genetic, immune, and environmental factors
o Clinical manifestations
Diarrhea
Vomiting
Abdominal pain
Anorexia
Failure to thrive
Malabsorption such as rickets, tetany, frank or occult bleeding, or anemia
Hypocalcemia and hypomagnesemia
o Treatment
Gluten free diet
• Hirschsprung’s disease
o Congenital aganglionic megacolon
o Functional obstruction of the colon caused by the absence of the enteric ganglia along a variable length of the colon with inadequate motility
o Caused by a malformation of the parasympathetic nervous system
• Congenital aganglionic megacolon
o Hirschsprung’s disease
o Functional obstruction of the colon caused by the absence of the enteric ganglia along a variable length of the colon with inadequate motility
o Caused by a malformation of the parasympathetic nervous system
• Complications after a partial gastrectomy
o Poor wound healing
o Abscess formation
o Suture failure
o Malabsorption syndrome
o Inadequate food intake
o Weight loss
o Abdominal pain
o Vomiting, diarrhea
• Meconium ileus associated with which other complications [Show Less]