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PATHOPHYSIOLOGY FINAL STUDY
GUIDE
ALTERED CELLULAR AND TISSUE BIOLOGY
Cellular adaptation = reversible, structural, or functional response
- Atrophy – shrinking of the cell; ex: skeletal muscle - Hypertrophy - increased cell size; ex: cardiac cells - Hyperplasia – increased number of cells; ex: lining of the uterus - Metaplasia – replacement of mature cell w/another type - Dysplasia (atypical hyperplasia) – abnormal change in size/shape of cells; ex: cervix Reperfusion injury - Results from the generation of highly reactive oxygen intermediates including hydroxyl radical (OH-) Superoxide radical and hydrogen peroxide. - These radicals can all cause further membrane damage and mitochondrial calcium overload. Necrosis = sum of cellular changes after local cell death inflammation/organelle breakdown - Coagulated o Primarily in the Heart, Kidneys, Adrenal Glands o Results from Hypoxia from severe ischemia/chemical injury; Appear firm/opaque - Liquefactive o Neural o Ischemic brain injury/bacterial infection; rich in hydrolytic enzymes and lipds - Caseous o Tb infection o Mix of both coagulated and liquefactive; soft granular tissue - Fatty o Occurs in breast tissue, pancreas, and other abdominal structures o Caused by Lipase enzymes - Gangrene o Results from sever hypoxic injury/blockage of major arterial arteries Acid Base imbalances Acidic < 7.35 7.45> alkaline 45 <CO2< 35 22 >HCO3> 26 Compensation – abnormal values - Acidosis = Increase H+ concentration o Metabolic: Ex: Kussmaul respirations, Hyperkalemia, DKA o Respiratory; Ex: Hypoventilation, Hyperkalemia - Alkalosis = Decreased H+ concentration o Metabolic; Ex: Hypokalemia, excessive antacid use o Respiratory ; Ex: Hypokalemia, Hyperventilation Inflammatory process
- Damaged tissues release histamines, increasing blood flow to the affected area
- Histamines cause capillaries to leak releasing phagocytes and clotting factors into the wound
- Phagocytes engulf bacteria, dead cells, and cellular debris
- Platelets move out of the capillary to seal the wounded area 4 primary signs: Redness ( rubor ) , heat ( calor ), swelling ( edema or tumor ), & pain ( dolor ). Sex linked disorders – usually expressed by males because females have additional X-chromosome to mask the abnormal gene; X-linked
- Turner syndrome
- Females with only one X chromosome
- Characteristics
- Absence of ovaries (sterile)
- Short stature (~ 4'7")
- Webbing of the neck
- Edema
- Underdeveloped breasts; wide nipples
- High number of aborted fetuses
- X is usually inherited from mother
- Klinefelter syndrome
- Individuals with at least two Xs and one Y chromosome
- Characteristics
- Male appearance
- Develop female-like breasts
- Small testes
- Sparse body hair
- Long limb CANCER Tumor Staging - Staging gives a good indication as to a patient’s prognosis & the viability of possible treatment options. o Stage 1 - Cancer that is confined to the organ of origin o Stage 2 - Cancer that is locally invasive o Stage 3 - Cancer that has spread to regional structures o Stage 4 - Cancer that has spread to distant sites - A common scheme used to standardize staging is the WHOs TNM system (0-2) o T = tumor (0= none, 1=<2cm, 2= 2-5 cm) o N= nodes (0=none, 1= mobile, 2= fixed) o M= Metastases (0=no meta, 1= demonstrated, 2= suspected) Hallmarks of Cancer o Sustained proliferative signaling- uncontrolled cellular proliferation. ▪ Cancerous cells express mutated oncogenes, which are independent of the normal regulatory mechanisms (they engage in uncontrolled cell growth) o Evading growth suppressors - tumor-suppressor genes normally regulate the cell cycle, inhibit proliferation resulting from growth signals, stop cell division when cells are damaged, and prevent mutations. Tumor suppressor genes are inactivated in cancer growth. ▪ A classic tumor suppressor gene is tumor protein p53 (TP53). TP53 controls initiation of apoptosis, suppresses cell division until DNA repair is complete. o Genomic instability - increased tendency of alterations (mutability) in the genome during the life cycle of cells. ▪ Mutations in BRCA1 and BRCA 2 are clinically important.
- Mutations in either greatly increase risk for a variety of tumors, especially breast
Cushing Triad Late Sign (Increased SBP, Low HR, Irregular Breathing) Reflexes – Babinski (fanning toes, not normal in adults) Unconsciousness— late sign Seizures HA— early sign Emesis Deteriorated motor function (hemiplegia) Subdural Hematomas - bleeding between the dura mater and the brain
- arise in 10% to 20% of persons with traumatic brain injury. - Acute subdural hematomas develop rapidly, commonly within hours, and usually are located at the top of the skull (the cerebral convexities) ****Venous** Epidural Hematoma = bleeding between dura mater an the skull. Artery is the source of bleeding in 85% of cases. Intracerebral Hematoma = bleeding within the brain. May be single or multiple and is associated w/contusions. Secondary Brain Injury**
- Hypoxia and/or insufficient CPP
- Insufficient oxygen for Na+-K+-ATPase
- Swelling of (uninjured) brain cells
- Decreased CPP as ICP increases **Types of Spinal Cord Injury
- Cord concussion:** Results in a temporary disruption of cord-mediated functions; “stinger” injury - Cord contusion: Bruising of the neural tissue causing swelling and temporary loss of cord- mediated functions - Cord compression: Pressure on the cord causing ischemia to tissues; must be relieved (decompressed) to prevent permanent damage to the spinal cord - Laceration: Tearing of the neural tissues of the spinal cord; may be reversible if only slight damage is sustained by the neural tissues; may result in permanent loss of cord- mediated functions if spinal tracts are disrupted - Transection: Severing of the spinal cord, causing permanent loss of function - Hemorrhage: Bleeding into the neural tissue because of blood vessel damage; usually no major loss of function. - Damage or obstruction of spinal blood supply: Causes local ischemia Cause of Multiple Sclerosis (MS) - Autoimmune; affects myelin sheath (CNS); neuron inflammation/scarring; decreases nerve transmission; NOT rapid o Plaque formation on the brain - Most common in women 20-40 y/o - No cure; unknown cause - Clinical Manifestations depend on demyelination progression: emotional/cognitive - speech, sensation - (+) Romberg’s, vision, elimination - UTI Cerebral Palsy (children) - a group of non-progressive syndromes that affect the brain and cause motor dysfunction
- Causes: - Hypoxia - Hemorrhage - Infection
- Low birth weight and birth asphyxia are commonly identified risk factors for cerebral palsy. ENDOCRINE/HORMONAL ALTERATIONS Functions/Actions of AD, TH, PTH, Aldosterone o Hypothalamus (control center) ▪ TRH ▪ CRH o Anterior Pituitary Gland (Tropic hormones/Master glands) ▪ TSH (Metabolism) - Stimulates Thyroid T3/T ▪ ACTH - Stimulates Adrenal CortexCortisol (Stress hormone) ▪ GH (Bone/Tissue) - Increases cell anabolism of amino acids ▪ FSH/LH (Ovaries/Testes) ▪ Prolactin (Mammary Glands) ▪ MSH o Pineal Gland (melatonin release stimulated by light exposure) o Posterior Pituitary Gland ▪ ADH (Vasopressin) - Increased H2O absorption in the kidney tubules ▪ Oxytocin - Smooth muscle contraction (pregnancy) o Parathyroid Gland ▪ Parathyroid Hormone (PTH) acts directly on bone to release Ca+ by stimulating osteoclast activity; Acts on kidney to increase calcium reabsorption while decreasing phosphate reabsorption.
- Hyperparathyroid = hypercalcemia o Primary = increased bone resorption of Ca+ and increased GI absorption of Ca+
- Hypoparathyroid – commonly caused by damage during thyroid sx o Adrenal Glands ▪ Cortex ( SSS = Sugar, Salt, Sex)
- Glucocorticoids (increases blood sugar) o Cortisol - Regulated by ACTH, neg feedback, diurnal rhythm, stress
- Mineralocorticoids o Aldosterone - RAAS (Na+ retention, K+ loss)
- Sex Hormones ▪ Medulla
- Catecholamines o Epinephrine/Norepinephrine o Thyroid hormone actions (Negative Feedback Loop) ▪ HypothalamusTRH Pituitary GlandTSHThyroid GlandT3/T
- T3 (more potent) ; T4 (more abundant)
- Required for normal growth/neuro development in fetus/infant Type I/II DM (causes, symptoms, acute/chronic complications) - Type 1
o Manifestations: Low BP/Sugar/Sodium. Bronze skin. Hyperkalemia (muscle cramps) Hyperaldosteronism (Conn Syndrome)
- Excessive adrenal secretion of aldosterone, causing fluid and electrolyte imbalances
- Hypertension, hypokalemia, neuromuscular manifestations are hallmarks
- Promotes increased renal sodium and water reabsorption with hypervolemia and hypertension, and renal excretion of hydrogen and potassium SIADH/DI o Syndrome of Inappropriate Anti Diuretic Hormone (SIADH) ▪ High ADH ▪ Seen in: Lung cancer, damaged hypothalamus, lung/neuro infection Clinical Manifestations:
- Fluid overload (edema/ high HR/high BP/low urine output)
- Hyponatremia (Increased H20, Na remains the same)
- Anorexia (GI distress/no appetite); Menstrual changes o Diabetes Insipidus (DI) ▪ Low ADH ▪ Seen in: damaged pituitary/hypothalamus, stroke, tumor ▪ Neurogenic – requires ADH replacement ▪ Nephrogenic – caused by drugs/disorders; treat underlying condition Clinical Manifestations:
- Water Loss (polyuria, dehydration, low BP)
- Polydipsia
- Hypernatremia Signs and Symptoms DI SIADH Urine Output High Low
Urine Osmolality Low (¿ 100−200 mOsm/L) High ( ¿ 800 mOsm/L)
Urine Specific Gravity Low ( ¿ 1.010) High ( ¿ 1.020 ¿
Serum Sodium Hypernatremia^ (^ ¿ 145 mEq/L)^ Hyponatremia^ (^ ¿ 135 mEq/L)
Serum Osmolality Hyperosmolar^ (^ ¿ 300 mOsm/L)^ Hypoosmolar (^ ¿ 285 mOsm/L)
Primary Hyperparathyroidism - inappropriate excess secretion of PTH by one or more of the parathyroid glands.
- It is one of the most common endocrine disorders. Approximately 80-85% of cases are caused by parathyroid adenomas, another 10 to 15% result from parathyroid hyperplasia. - Calcium levels increase because of increased bone resorption and GI absorption of calcium HEMATOLOGIC **Clinical Manifestations of Anemias
- Macrocytic-Normochromic Anemias (normal RBC)** Pernicious Anemia - dietary deficiency of B12 or failure of the stomach lining to produce intrinsic factor which allow B12 to be absorbed Folate Deficiency Anemia - NOT enough Folate; develops slowly, so it is usually severe once treatment is sought.
Early symptoms are vague- infections, mood swings, GI, cardiac, kidney ailments. Anemic symptoms described above can be seen when Hgb drops below 7-8 g/dl Neurologic manifestations (ataxia, spasticity, depressive symptoms)
- Microcytic-Hypochromic Anemias (small pale RBC) Iron Deficiency Anemia - excessive menstrual bleeding (menorrhagia) - Early symptoms nonspecific- fatigue, weakness, shortness of breath, pale earlobes, palms, conjunctivae Hypoxemia - Reduced oxygen level in blood causes dilation of arterioles, capillaries, and venules, increasing flow through them - Increased peripheral blood flow and venous return contributes to increased heart rate and stroke volume in an effort to meet normal oxygen demand (these compensatory mechanisms may lead to heart failure) - Tissue hypoxia creates demands and effects on the pulmonary and hematologic systems. - Rate and depth of breathing increase in an effort to increase oxygen availability. - These compensatory mechanisms may cause shortness of breath, rapid and pounding heartbeat, dizziness, and fatigue (in mild cases may be present only when there is an increased demand for oxygen but in severe cases symptoms may be experienced even at rest) Infectious Mono - Benign, self-limiting, lymphoproliferative clinical syndrome characterized by acute infection of B cells - Most common cause is Epstein-Barr virus (EBV) Clinical manifestations- early flulike symptoms (headache, malaise, joint pain, fatigue) may appear during the first 3-5 days, although some people go without symptoms Classic group of symptoms include- fever, sore throat, cervical lymph node enlargement, fatigue Hodgkin’s/Non-Hodgkin’s Sickle Cell Anemia - Autosomal Recessive Disorder; Most common in African American - Vaso-occlusive crisis –blood flow is obstructed by sickled cells - Sequestration crisis- large amounts of blood acutely pooled in the liver & spleen (young child)
Electrolytes that affect CV System
- Sodium o Due to fluid retention in blood vessels from high levels of sodium (hypernatremia), the heart has to work harder to pump blood to the body - Potassium o Hyperkalemia tachycardia, then bradycardia, and death (Peaked T wave) o Hypokalemia **bradycardia and death (Prominent U wave)
- Magnesium** o Modifies nerve impulse transmission o Required to support the heart muscle’s normal contraction-relaxation actions o Decreased levels may cause irregular contraction of ventricles leading to arrhythmias - Calcium o Plays a central role in excitation-contraction of both cardiac and vascular smooth muscles ▪ Hypocalcemia QT prolongation ▪ Hypercalcemiashorted ST segment - Chloride o Follows transport of sodium o Helps to maintain electrical neutrality at the cellular level by moving into or out of the cells as needed Cardiac Cycle
RAAS
Hypertension - HTN is the most common primary diagnosis in the US
- Silent Killer: Early Stages usually have NO clinical manifestations other than **elevated blood pressure. **** o Results from a sustained increase in peripheral resistance (arteriolar vasoconstriction), an increase in circulating blood volume, or both o Early stages have no clinical manifestations other than elevated BP o Most manifestations are caused by complications that damage organs and tissues outside the vascular system o Heart dz, renal insufficiency, CNS dysfunction, impaired vision, impaired mobility, vascular occlusion, or edema can all be caused by sustained HTN Risks: o Fam Hx ▪ Genetic predisposition is thought to be polygenic and associated with epigenetic changes influenced by diet and lifestyle ▪ Inherited defects are associated with renal sodium excretion, insulin and insulin sensitivity, activity of the sympathetic nervous system and RAAS, and cell membrane sodium or calcium transport o Age o Cigarette Smoking o Obesity o Alcohol Consumption o Black/African heritage o Gender (M>F before 55 years, then F>M) o High dietary sodium intake o Low calcium, potassium, magnesium o Glucose intolerance Primary (Essential) HTN Mechanisms/Consequences of HTN: o Myocardium: Increased workload combines w/diminished blood flow through coronary arteries ▪ left ventricular hypertrophy (LVH), myocardial ischemia, heart failure o Coronary arteries: Accelerated atherosclerosis
- Fusiform – most common (spindle shape that is wide in the middle and tapers at both ends) and circumferential - Saccular - localized dilatation of a vessel wall in which a small area is distended, forming a sac- like swelling are basically spherical in shape. - False aneurysm - extravascular hematoma that communicates with the intravascular space ; common cause of this type of lesion is a leak between a vascular graft and a natural artery. Clinical manifestations depend on where the aneurysm is located: - Most commonly occur in the thoracic or abdominal aorta - Atherosclerosis is the most common cause of arterial aneurysms; HTN also a factor - Aortic aneurysms are often asymptomatic until they rupture, then cause severe pain and hypotension - Thoracic or Abdominal aorta aneurysms (most common location) cause dysphagia and dyspnea - If an aneurysm impairs flow to an extremity, symptoms related to ischemia could be present - Cerebral aneurysms are associated with signs and symptoms of increased ICP - Aneurysms in the heart present with dysrhythmias, heart failure, and embolism of clots to the brain and other vital organs Dyslipidemia – abnormal concentration of lipids, cholesterol, and triglycerides CAD - Usually caused by atherosclerosis; diminished myocardial blood supply until myocardial metabolism is impaired and causes ischemia - Persistent ischemia or the complete occlusion of a coronary artery acute coronary syndromes including infarction (irreversible myocardial damage) o Widowmaker Left Anterior Descending (LAD) artery blockage heart attack (usually the most damage from atherosclerosis) - Frequency similar in African Americans/Caucasians; African Americans higher death rate Risk Factors: o Advanced age o Male gender or women after menopause o Fam Hx o HTN ▪ Endothelial injury myocardial hypertrophy increased myocardial demand for coronary flow o Cigarette smoking ▪ Direct effect on endothelial cells & generation of oxygen free radicals ▪ Nicotine stimulates release of catecholamines (epi and norepi) which increase HR and peripheral vascular constriction ▪ This increases BP, which increases cardiac workload and oxygen demand o DM/insulin resistance ▪ Damage to endothelium, thickening of vessel wall, increased inflammation, increased thrombosis o Obesity ▪ Abdominal obesity has the strongest link w/increased CAD ris k, and is related to inflammation, insulin resistance, decreased HDL, increased BP o Sedentary Lifestyle o Atherogenic diet (high sat fat/cholesterol/low fruit) o Dyslipidemia - refers to abnormal concentrations of lipids, cholesterol, & triglycerides (lipoproteins) ▪ Low-density lipoproteins (LDL)- responsible for delivery of cholesterol to tissues
▪ High-density lipoproteins (HDL)- responsible for “reverse cholesterol transport” (return of excess cholesterol from tissues to the liver for processing and elimination in bile); participates in endothelial repair & decreased thrombosis Unstable Angina - result of reversible myocardial ischemia , increases in severity and frequency, and is an indication of impending infarction.; ECG most commonly shows ST segment depression and T wave inversion during pain that resolve when the pain is relieved. CHF - Heart is unable to generate an adequate cardiac output, causing inadequate perfusion of tissues or increased diastolic filling pressure of the left ventricle, or both, so that pulmonary capillary pressures are increased
- Ischemic heart disease and HTN are the most important predisposing risk factors
- Most causes of heart failure result from dysfunction of the left ventricle (heart failure with reduced ejection fraction or heart failure with preserved ejection fraction). Shunting of Blood of Congenital Heart Disease - Normal movement of blood through the right side of the heart and into the pulmonary system is separate from the blood flow through the left side of the heart into the systemic circulation (figure A) - Abnormal movement from one side of the heart to the other is a shunt
- Acyanotic defect - shunting of blood flow from the left heart into the right heart is called a left- to-right shunt; this increases blood flow into the pulmonary circulation; because blood continues to flow through the lungs before passing into the systemic circulation, there is no decrease in tissue oxygenation or cyanosis)
- Cyanotic defect (caused by shunting of blood from the right side of the heart directly into the left side of the heart; this decreases blood flow through the pulmonary system, causing less than normal oxygen delivery to the tissues and resulting in cyanosis) PULMONARY Pneumonia - Infection of the lower respiratory tract; caused by bacteria, virus, fungi, or parasites; leading cause of death >65 y/o; Often due to aspiration of oropharyngeal secretions, especially in sedated patients or those with artificial airways
- Many cases of pneumonia are preceded by a viral upper respiratory tract infection.
- Can be defined as community-acquired (CAP), healthcare-associated (HCAP, hospital- acquired (HAP), or ventilator-associated (VAP)
- The incidence and mortality of pneumonia are highest in the elderly; therefore, it should always be suspected with acute change in level of consciousness in older adults Risk factors: advanced age, compromised immunity, underlying lung disease, alcoholism, altered consciousness, impaired swallowing, smoking, endotracheal intubation, immobilization, residence in nursing home (often presented as HCAP)
Aspiration in Adults and Children Adult
- Passing of fluid or solid particles into the lungs (“went down the wrong tube”)
- Right lung, especially the right lower lobe, is more susceptible to aspiration than the left lung because the branching angle of the right mainstem bronchus is straighter than the branching angle of the left mainstem bronchus Children
- Especially in children 1-4 years of age
- Most objects can be expelled by the cough reflex, but some objects may lodge in the larynx, trachea, or bronchi **- FBO: Presentation is often dramatic and frightening, can cause cough, stridor, hoarseness or inability to speak, respiratory distress, agitation and panic
- The larger the item, the more occlusive and life-threatening
- Most objects can be expelled by cough reflex Asthma in Children
- Narrowing of the airways seen in asthma is usually reversible** but in some patients with chronic asthma the inflammation may lead to irreversible airflow obstruction.
- Important risk factors: early exposure to allergens (air pollution, dust mites, cockroach antigen, cat exposure, and tobacco exposure), respiratory tract infections, preterm birth, childhood obesity
- Acute asthma attack includes coughing, expiratory wheezing, shortness of breath; Breath sounds may because faint when air movement is poor; Barrel chest (hyperinflation) may be visible; May appear anxious or diaphoretic
- Viral respiratory tract infection commonly associated in children w/asthma COPD (bronchitis/emphysema) “ blue blowers” vs “pink puffers ”; **most common lung disease
- Chronic bronchitis** : hypersecretion of mucus and chronic productive cough for at least 3 months a year (usually winter months) for at least 2 consecutive years - Emphysema : abnormal permanent enlargement of gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis Clinical Manifestations Bronchitis Emphysema Productive cough Classic sign With infection Dyspnea Late in course Common Wheezing Intermittent Common History of smoking Common Common Barrel chest Occasionally Classic Prolonged expiration Always present Always present Cyanosis Common Uncommon Chronic hypoventilation Common Late in course Polycythemia Common Late in course Cor pulmonale Common Late in course
RENAL
Neurogenic bladder - General term for bladder dysfunction caused by neurologic disorders
- Types of dysfunction are related to the sites in the nervous system controlling sensory and motor bladder function ; o Spastic bladder- most common type, caused by associated with upper motor neuron lesion (stroke, brain tumor, trauma, to brain or spinal cord) ▪ Loss of conscious sensation and cerebral (voluntary) motor control o Flaccid bladder- associated with a lower motor neuron lesion (trauma to the lower spinal cord, or a complication of diabetes mellitus--diabetic nephropathy) ▪ Flaccid bladder fills and becomes greatly distended- retention with overflow (constant incontinence but bladder is full) Glomerulonephritis - inflammation of the glomerulus caused:
- Primary glomerular injury: immunologic responses, ischemia, free radicals, drugs, toxins, vascular disorders, and infection.
- Secondary injury: systemic diseases, including DM, HTN, Lupus, CHF, HIV
- Destruction, inflammation, and sclerosis of the glomeruli of both kidneys occurs. Clinical manifestations - Onset may be sudden or insidious and significant loss of nephron function can occur before symptoms develop ▪ Oliguria (urine output of 30 ml/hr or less) ▪ Hypertension and possibly renal failure ▪ More severe- Gross hematuria, Proteinuria Causes : o Immunological or autoimmune response – major cause of glomerular injury o Grp A beta-hemolytic streptococcal infection o Hx pharyngitis or tonsillitis 2 to 3 weeks before symptoms (strep infection) Kidney Stones - Masses of crystals, protein, or other substances that are common causes of urinary tract obstruction in adults
- Most kidney stones are unilateral
- Risk of formation is influenced by age, sex, race, fluid intake, diet, and occupation
- Formation is related to supersaturation of one or more salts in urine, precipitation of salts from a liquid to a solid state, growth through crystallization, the absence of stone inhibitors o Supersaturation is the presence of higher concentration of a salt within a fluid (in this case, urine) than the volume is able to dissolve to maintain equilibrium Clinical manifestations o Renal colic type pain
- Moderate to severe pain often originating in the flank and radiating to the groin usually indicates obstruction of the renal pelvis or proximal ureter
- Colic that radiates to the lateral flank or lower abdomen typically indicates obstruction in the mid-ureter, and bothersome lower urinary tract symptoms such as urgency, frequency, voiding, urge and incontinence. Pain can be severe and incapacitating ▪ May be accompanied by nausea and vomiting. ▪ Hematuria may be present ▪ Fever only if there was an infection also present. (UTI)
- Untreated or undertreated chlamydial infections are the primary cause of preventable infertility/ ectopic pregnancy - Other complications of STDs include pelvic inflammatory disease (PID), chronic pelvic pain, neonatal morbidity/ mortality, genital cancer - 15-24-year-old individual account for half of all new STD infections Effects of Estrogen
- Estrogen is needed for maturation of reproductive organs, development of secondary sex characteristics, growth and maintenance of pregnancy
- Nonreproductive effects are closure of long bones after pubertal growth spurt (in both males and females), maintenance of skin and bone, and systemic organ function Progesterone effects in pregnancy include
- Maintaining the thickened endometrium
- Relaxing smooth muscle in the myometrium, which prevents premature contractions and helps the uterus expand
- Thickening the myometrium, which prepares it for the work of labor
- Prepares breast for lactation
- Allows for tolerance against fetal antigens (so the mother’s immune system does not attach the fetus) Effects of Testosterone
- Affects nervous and skeletal tissues, bone marrow, skin and hair, and sex organs
- Anabolic effect on skeletal muscle tissue
- Directly stimulates bone marrow and indirectly stimulates renal erythropoietin production to achieve increased hgb and hct
- Required for spermatogenesis and for secretion of fluid by prostate gland, seminal vesicles, and Cowper glands DIGESTIVE GERD - Gastroesophageal Reflex Disease (GERD) - Reflux of acid and pepsin or bile salts from the stomach into the esophagus that causes esophagitis Risk factors: older age, obesity, hiatal hernia, drugs that relax the lower esophageal sphincter (anticholinergics, nitrates, calcium channel blockers, nicotine)
- Abnormalities in lower esophageal sphincter function, esophageal motility, and gastric motility or emptying can cause GERD Leads to reflux esophagitis and Barrett esophagus (a precancerous lesion ) Clinical manifestations:
- erosive esophagitis are heartburn (pyrosis)
- acid regurgitation
- dysphagia
- chronic cough
- asthma attacks
- upper abdominal pain 1 hr after eating
- The symptoms worsen if the individual lies down or if intra-abdominal pressure increases. Treatment:
- PPIs are the agents of choice for controlling symptoms and healing esophagitis
- Weight reduction, smoking cessation, and elevation of the head of the bed 6 inches also help alleviate symptoms.
Children Specific:
- Normal and nonpathological in healthy infants and may be asymptomatic or exhibited by regurgitation and vomiting
- Frequency is highest in premature infants (but also affects healthy infants) and usually will resolve without treatment by 12-14 months Clinical Manifestations: include excessive regurgitation or vomiting; food refusal/ anorexia; and abdominal or epigastric pain, or both Small Bowel Obstruction (SBO) - caused by postop adhesions, tumors, Crohn disease, hernias
- Leads to distention caused by impaired absorption and increased secretion with accumulation of fluid and gas inside the lumen proximal to the obstruction
- Distention decreases the intestine’s ability to absorb water and electrolytes and increases secretion of these substances into the lumen Clinical Manifestations:
- Colicky pain caused by intestinal distention followed by nausea and vomiting
- Pain intensifies for seconds or minutes as a peristaltic wave of muscle contraction meets the obstruction
- If ischemia occurs, the colicky pain is resolved and the pain is more constant and severe
- Fever, severe leukocytosis, abdominal distention, and rebound tenderness develop as ischemia progresses to necrosis, perforation, peritonitis
- Severe fluid and electrolyte disturbances can be caused by excessive vomiting and inability to reabsorb fluids
- Extracellular fluid volume and plasma volume decrease, causing dehydration, increased hct, hypotension, and tachycardia
- Metabolic alkalosis initially develops because of excessive loss of hydrogen ions that would normally be reabsorbed from gastric juice and vomiting
- Metabolic acidosis is more likely to occur because bicarbonate from pancreatic secretions and bile cannot be reabsorbed (with prolonged obstruction or obstruction of lower intestine) Gastritis - inflammatory disorder of the gastric mucosa Acute – caused by injury of the protective mucosal barrier
- Drugs, chemicals, H. pylori infection
- NSAIDS inhibit the action of COX-1, inhibiting normal secretion of mucus Clinical Manifestations: vague abdominal discomfort, epigastric tenderness, bleeding Diverticulitis - inflammation or infection of the diverticula (when a diverticula tears); usually in sigmoid S/S: may be vague or absent in uncomplicated disease
- Diarrhea, constipation, distention, or flatulence
- If diverticula become inflamed/abscess forms fever, leukocytosis, tenderness of LLQ may occur Duodenal vs Gastric Ulcers
- Duodenal ulcer- caused by acid and pepsin penetrating the mucosal barrier in the duodenum Clinical manifestations- chronic intermittent epigastric pain; pain begins 2-3 hours after eating, when the stomach is empty; pain can be relieved by ingestion of food or antacids
- Gastric ulcer- ulcers of the stomach Clinical manifestations- similar to those of duodenal ulcers, but the pain also occurs immediately after eating; Worsens with food UC vs Crohn’s Disease – both are chronic relapsing inflammatory bowel diseases
