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231 Cards in this Set
- Front
- Back
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Number 1 cause of death worldwide
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Ischaemic heart disease/CHD/CAD 12.8%
Stroke and other cerebrovascular disease 10.8% Lower respiratory infections 6.1% Chronic obstructive pulmonary disease 5.8% Diarrhoeal diseases 4.3% HIV/AIDS 3.1% Trachea, bronchus, lung cancers 2.4% Tuberculosis 2.4% Diabetes mellitus 2.2% Road traffic accidents 2.1% |
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Recent data on heart disease (prevalence, etc.)
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Number of adults with diagnosed heart disease: 26.8 million
Percent of adults with diagnosed heart disease in U.S. : 12% Common among men and women Deaths/yr: 616,067 Cause of death rank: 1 Hospitalization rank: 2 Big driver of US healthcare cost |
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S/S of CV disease
cardiac and vascular |
Chest, neck, or arm pain
Palpitations Dyspnea Syncope Cough Cyanosis Fatigue Nausea, sweating are all cardiac disease symptoms Peripheral edema Claudication are vascular disease symptoms |
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Diseases affecting the heart muscle
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Ischemic heart disease
-Arteriosclerosis, Atherosclerosis Angina pectoris Hypertensive CVD (in second lecture) Myocardial infarction Congestive heart failure Orthostatic Hypotension Congenital Heart Disease |
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Heart diseases affecting the CNS, heart valves, and blood vessels (respectively)
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Disease affecting the central nervous system
Arrhythmias Diseases affecting the heart valves Mitral stenosis, regurgitation, mitral valve prolapse Aortic stenosis, regurgugitation Diseases affecting the blood vessels Aneurysm Peripheral artery disease |
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Coronary heart disease
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Ischemic heart disease; Coronary artery disease; CHD; CAD; Heart Disease;
Definition: A narrowing of the small blood vessels that supply blood and oxygen to the heart, caused by the buildup of plaque in the arteries to your heart The build-up of plaque is also called hardening of the arteries- arteriosclerosis |
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Diagnosis of CHD (CAD)
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Angiography- inject contrast dye, then x-ray
Echocardiography- ultrasound Stress test MRI Blood markers |
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Anatomy of artery
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Adventitia
-Support for the artery Media -Adjust lumen size Intima -Endothelium permeable to LDL |
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Atherosclerosis
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Accumulation of lipids and other molecules on the intima, leading to:
Stenosis: abnormal narrowing of blood vessel Thrombosis :formation of a blood clot obstruction the blood vessel) Occlusion: blocking or closing of a blood vessel Necrosis: cell injury leading to premature cell death |
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Signs and symptoms of coronary heart disease
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Pathological process - atherosclerosis with damage to and narrowing of the coronary arteries
Coronary heart/artery disease (CHD/CAD) Key Symptoms: Chest tightness or pain (angina pectoris), neck, arm pain Dyspnea Fatigue with activity 1772 England William Heberden described angina pectoris: “they who are afflicted with it, are seized while they are walking (especially if it be uphill, and soon after eating) with a painful and most disagreeable sensation in the breast, which seems as if it would extinguish life if it were to increase or to continue; but the moment they stand still, all this uneasiness vanishes”. |
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Stable and unstable angina
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Stable:
Lasts between 5 and 15 minutes Exertional Predictable Usually associated with a set level of myocardial O2 demand Resolves with cessation of activity Pharmacologic intervention Unstable: Can occur at rest Longer episodes More severe intensity Indicator of progression of CHD |
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Sequelae (progression?) of Coronary Heart Disease
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Risk factors
-> Atherosclerosis Stenosis Thrombosis Occlusion -> Ischemia -> Angina (stable/unstable), Heart attack (MI), Over time: Heart Failure arrhythmias -> Cardiac arrest, Sudden death |
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Treatment of CHD
at different stages |
Modification of risk factors - can be done at any stage!
Pharmacological intervention - any stage Surgical intervention - once it has progressed to ischemia, to angina, MI, or to cardiac arrest |
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Non modifiable risk factors for CHD
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Age
Sex (more prevalent in males, except 75+ age group) Race (more in blacks, then whites, then native, then asian/islander) Family History |
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Modifiable risk factors for CHD
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High BP
Smoking Diabetes High LDL cholesterol Low HDL cholesterol Obesity Inactivity |
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Other risk factors for CHD
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Emotional stress
Oxidative stress Genetic factors Infections Moderate alcohol consumption (inverse) Inflammatory markers such as C-reactive protein Fibrinogen and other coagulation factors Erectile dysfunction |
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Risk factors: Cholesterol: LDL & HDL
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Cholesterol is transported around the body in two kinds of lipoproteins: low-density lipoprotein (LDL) & highdensity lipoprotein (HDL)
High LDL (> 160 mg/dL) can lead to clogging of the arteries, increasing the risk of heart attack and ischaemic stroke High HDL (> 40 for men or >50 for women) reduces the risk of CHD and stroke. Recommended cholesterol intake: less than 200 milligrams each day ((“Eat nothing that has a mother or a face”) |
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Hypertension (HTN)
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Blood pressure
Force exerted against the walls of the arteries and arterioles Prevalence: 31% American adults Many undiagnosed Normal: <120/<80 Prehtn: 120-139 OR 80-89 Stage 1 hypertension: 140-159 OR 90-99 Stage 2 hypertension: >= 160 OR >= 100 |
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HTN Risk Factors
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Non-modifiable
Family history of CVD Age (> 55 years) Gender Ethnicity Modifiable High sodium intake Obesity Diabetes mellitus Hypercholesterolemia Smoking Alcohol abuse Emotional stress Inactivity Hormonal status |
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Hypertension leading to heart disease
process |
High blood pressure increases the pressure in blood vessels. As the heart pumps against this pressure, it must work harder.
Atherosclerosis: High blood pressure also contributes to thickening of the blood vessel walls which may worsen atherosclerosis. This also increases the risk of heart attacks and stroke. Ischemia: High blood pressure can cause ischemic heart disease because the thicker heart muscle needs an increased supply of oxygen. Heart Failure: Over time, this causes the heart muscle to thicken. The heart must work harder to pump blood out to the body. Hypertensive heart disease is the leading cause of illness and death from high blood pressure. |
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Hypertensive heart disease
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Hypertensive heart disease is used to refer to enlarged heart as a result of persistently elevated BP
Left ventricular hypertrophy and diastolic dysfunction found in 10-30% of adults with high BP Similar symptoms to heart failure (see later) Clinical manifestations Often asymptomatic Symptoms: headache, vertigo, flushed face, spontaneous epistaxis, blurred vision Disease progression: SOB, chest pain, edema, drowsiness Diagnosis: BP in a variety of settings Treatment: based on total risk (not just BP measurement) Consequences: CVD, renal failure, retinopathy |
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Orthostatic Hypotension
definition causes symptoms |
Low BP when you stand up from sitting/lying down (see Fig. 12.15)
Defined as: Drop in systolic BP >20mm/Hg OR drop in both systolic and diastolic >10 mm/Hg+ Heart Rate increase of 15 beats Symptoms are common and usually last only a few seconds When it’s long-lasting or happens often, there may be more severe underlying cause! Causes: Prolonged immobility Starvation, malnutrition Autonomic nervous system deregulation Reduction in blood volume Venous pooling of blood Medication side effects Symptoms: Dizziness, lightheadedness Syncope Blurry vision Weakness Confusion Nausea |
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Surgical interventions for CVD
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Operations on the cardiovascular system 6,942,000
-Only 2nd to obstetric procedures, 2007 data (CDC) Balloon angioplasty of coronary artery 618,000 Insertion of coronary artery stent(s) 560,000 Coronary artery bypass graft 405,000 Cardiac catheterization 1,061,000 Insertion, replacement, removal, and revision of pacemaker leads or device 358,000 Hemodialysis 679,000 |
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Myocardial infarction (MI)
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A heart attack occurs if the flow of oxygen-rich blood to a section of heart muscle suddenly becomes blocked. If blood flow isn't restored quickly, the section of heart muscle begins to die (necrosis).
Necrosis in myocardium: Most caused by blood clot blocking a coronary artery, starving the heart of oxygen: heart cells die. Occlusion of coronary arteries Result of ischemia and anoxia Symptoms Angina Diaphoresis (profuse sweating) Palor Dyspnea Tachy- or bradycardia Prevalence: about 1.2 million/ year Diagnosis Electrocardiogram Serum enzymes and other markers of myocardial damage Imaging Treatment: re-establish blood flow Risk factor modification Pharmacologic Surgical interventions Cardiac rehabilitation |
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(Sudden) Cardiac arrest (SCA), Sudden cardiac death (SCD)
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(Sudden) Cardiac arrest = heart stops beating completely
May be caused by heart attack When unexpected cardiac arrest leads to death= sudden cardiac death Sudden cardiac arrest occurs when the electrical system to the heart malfunctions and suddenly becomes very irregular. In the first few minutes, the greatest concern is that blood flow to the brain will be reduced so drastically that a person will lose consciousness. Death follows unless emergency treatment is begun immediately. Over half the cases no prior symptoms Treatment Cardiopulmonary resuscitation (CPR) and defibrillation |
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Heart Failure (HF)
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Heart unable to sufficiently pump blood (‘insufficiency’)
Due to cardiac muscle dysfunction Systolic HF: heart muscle cannot pump (eject) the blood out of the heart very well Diastolic HF: heart muscles are stiff and do not fill up with blood easily Left or right sided heart failure Ejection fraction low (<40%) |
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Congestive Heart Failure
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In an attempt to compensate for insufficiency, the heart muscle "stretches," causing the left ventricle to enlarge (dilated cardiomyopathy)
As the heart's pumping action is lost, blood may back up in other areas of the body. Fluid builds up in the lungs, liver, gastrointestinal tract, and the arms and legs (hence congestive HF). Most common cause: CHD Other: smoking, obesity, diabetes, Hypertension, valvular diseases |
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Clinical manifestations of Heart Failure
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Common symptoms are:
Cough Fatigue, weakness, faintness Loss of appetite Need to urinate at night Pulse that feels fast or irregular, or a sensation of feeling the heart beat (palpitations) Shortness of breath when you are active or after you lie down Swollen (enlarged) liver or abdomen Swollen feet and ankles Waking up from sleep after a couple of hours due to shortness of breath Weight gain |
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NYHA heart failure classification
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Class I (mild)
No limitation in physical activity. Ordinary activity does not cause undue fatigue, palpitation, or dyspnea. Class II (mild) Slight limitation in physical activity. None at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea. Class III (moderate) Marked limitation in physical activity. None at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea. Class IV (severe) Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased. |
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Peripheral Artery Disease (PAD)
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Atherosclerosis of the large- and medium arteries supplying the extremities (usually LE)
Can be asymptomatic or symptomatic Intermittent claudication (IC) – seen in 20-60% with PAD Affects muscles distal to the obstruction: calf or foot Complete obstruction → necrosis and limb loss 90% of patients hospitalized with PAD also have CHD Diagnosis of PAD History Clinical exam Noninvasive vascular tests Imaging Risk factors Smoking and diabetes Hypertension High cholesterol Hemostatic factors -Fibrinogen -Homocysteine |
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Symptomatic PAD
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High cardiovascular mortality and morbidity
7% amputation rate, but symptom progression is 21% CVD mortality was three times higher for people with claudication Primarily by functional limitations Walking speed and distance Ability to perform activities of daily living (ADL) Functional independence Physical activity Muscle fiber denervation, with gastrocnemius muscle weakness |
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PAD treatment
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Improve functional ability
CVD risk factor reduction Surgical treatment Pharmacologic interventions Exercise rehabilitation -Most effective treatment - ACSM guidelines: intermittent weight bearing exercise, 20- 40min, 3-7 days/wk Increased Pain-free walking by 179% Max walking by 122% Frequency of physical activity Quality of life measures VO2 and CV risk factor profile |
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Myocardial disease - cardiomyopathy
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Cardiomyopathy - Impaired contraction and relaxation of the myocardium
Classified based on presentation and pathology: 1. Dilated 2. Hypertrophic 3. Restrictive Prevalence: ~50 million |
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Dilated cardiomyopathy
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Damaged myocardial muscle fibers
Cardiac enlargement Etiology Half idiopathic, half other Damaged myocardial muscle fibers More blood remains in L ventricle after systole - dialtion of L ventricle Risk factors Alcohol abuse Obesity Hypertension Smoking Symptoms: Similar to heart failure Fatigue and muscle weakness Chest pain Diagnosis: may not occur until advanced stages Treatment: Treat underlying cause/risk factor modification Pharmacologic interventions Surgical interventions/transplant |
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Arrhythmias
classification |
Definition: a disturbance of heart rate or rhythm caused by an abnormal rate of electrical impulse generation by the SA node or the abnormal conduction of impulses
Normal rate 60-100bpm Classification: By origin: Atrial or ventricular By pattern: fibrillation or flutter By speed/rate: Tachycardia or bradycardia |
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Factors associated with tachycardia and bradycardia
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Factors associated with:
Tachycardia (>100 bpm): • Cardioreactive Drugs • High fevers • Hyperthyroidism • Fear, pain, emotion • Anemia, hemmorrhage Bradycardia (<50 bpm) • Endurance training • Beta-blockers • Brain injuries or tumors • Suctioning/ vomiting in response to pacemaker • Disease of the sinus node |
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Causes & Symptoms of Arrhythmias
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Causes & Risk factors:
Congenital Hypertrophy of heart muscle fibers secondary to hypertension Previous MI Valvular heart disease Degeneration of conductive tissue (sick sinus syndrome) Chronic/ binge Alcohol (Holiday Heart syndrome) Age (after 50 doubles with each advancing decade) BMI (3% increase for each unit kg/m2) Symptoms: Tachycardia or bradycardia Palpitations (irregular heartbeats) Dyspnea (shortness of breath) Dizziness (check balance, fall risk!) Chest Pain Syncope (fainting) |
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Diagnosis and Treatment of Arrhythmias
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Diagnosis:
ECG Tape-recorded ambulatory ECG Holter monitoring Treatment (electrical or pharmacologic): Cardioversion Pharmacology Surgical: Radio-wave ablation Pacemaker Maze procedure PT implications: - Monitoring (HR, BP) - Be trained in defibrillation - Assessment of balance and fall risk - Screen for palpitations, syncope - Exercise may increase chance of arrhythmias |
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Aortic Aneurysm
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An abdominal aortic aneurysm is when the large blood vessel that supplies blood to the abdomen, pelvis, and legs becomes abnormally large or balloons outward.
Aneurysms develop slowly over many years and often have no symptoms. If an aneurysm expands rapidly, tears open (ruptured aneurysm), or blood leaks along the wall of the vessel (aortic dissection), symptoms may develop Suddenly -> go to ER Clinical manifestations Asymptomatic Depend on size and position Pain in the abdomen or back- severe, sudden, persistent, or constant. The pain may radiate to the groin, buttocks, or legs. Clammy skin Nausea and vomiting Rapid heart rate Shock Treatment: surgical repair, risk factor reduction |
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Diseases affecting the heart valves
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Stenosis
Regurgitation Prolapse Increased workload on the heart Force blood through stenosed valve (stenosis) Inadequate blood flow with seepage (prolapse and regurgitation) |
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Stenosis (disease affecting heart valves)
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Aortic valve
Progressive calcification -Heart disease or congenital -Inc Left ventricle pressure -Sudden death Mitral valve -May be sequelae of rheumatic HD -Increased left atrium pressure |
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Prolapse and Regurgitation (disease affecting heart valves)
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Prolapse – Leaflets don’t close properly: into left atrium during systole
Prevalence: up to 10% of population (usually benign) Cause – unknown Prolapse can lead to blood flowing back into the heart chamber it came from (regurgitation, insufficiency, incompetence) When the valve doesn't work properly, blood can't move through your heart or to the rest of your body as efficiently. Asymptomatic initially Symptoms: Chest pain -- unrelated to CAD\MI Cough Rapid breathing Sensation of feeling the heart beat (palpitations) SOB when lying flat (othopnea) Treatment: pharmacologic, surgical interventions, exercise training |
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An example of PT and cardiac patients (any cardiac condition): Cardiac conditioning & Wellness center
Patient population and evaluation |
Patient population:
12-14 patients a day Most common: stent/ angioplasty; Number of patients who do not quality for surgery Usually people are very de-conditioned Lots of smokers, diabetics, metabolic syndrome, lots of medications (beta blockers, calcium channel blockers, ACE inhibitors) Lots of depression (“I can’t do what I used to be able to”) Identify baseline fitness and functional limitations: Musculoskeletal E.g. ROM, muscle strength Neuro- e.g. balance, sensation Then, set goals together with patient: 6min walk distance, balance, range of motion, sit to stand etc. Sternal precautions Evaluate chest wall stability No pushing, pulling or lifting postoperatively > 10lbs for 6wks No driving for at least 4 wks |
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An example of PT and cardiac patients (any cardiac condition): Cardiac conditioning & Wellness center
training and monitoring |
Training:
Lots of education! (self-monitoring) 50-70% of MHR (220 - age), some variability Remember they may be on beta-blockers! Prevent complications due to immobility -skin breakdown, sore, venous thrombus etc. Monitoring: Know when to stop (e.g. RPE 11-14 recommended, but may vary by person, angina, 1-4, stop at 1 or 2, pain scale etc.) See contraindications (table 12.4) Telemetry to monitor cardiac functioning, if abnormalities possibly go ER What do PTs miss at orthopedics or other specializations, early signs? Continue with patient as long as they meet their goals Transition to gym program |
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Implications for the PT:
indications for discontinuing exercise (in CVD patient) |
Indications for discontinuing exercise (table 12.4, page 546)
Pallor, cyanosis, cold, moist skin Staggering gait, ataxia Confusion or unresponsiveness Resting HR> 130/min or <40/min More than 6 irregular heartbeats/ min Frequent premature ventricular contractions (PVCs) Uncontrolled diabetes Oxygen saturation < 90% Acute infection/ fever Persistent drainage Increased swelling, tenderness, redness around incision site Inability to converse during activity BP abnormalities (rise above 250mm/Hg systolic or 115 mm/Hg diastolic or drop larger than 10 mm/Hg with increase in exercise) Persons desire to stop Also: angina scale, RPE scale |
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Congenital Heart Disease
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Anatomic defect in the heart
Develops in utero and present at birth Affects 8/1000 babies born in the US Caused by Obstruction of blood flow to the lungs, or mixing of oxygenated and deoxygenated blood Left-to-right shunting from abnormal openings Etiology: genetic with chromosomal abnormalities, maternal conditions/behaviors examples: Transposition of the great vessels -Pulmonary artery from left ventricle and aorta from right ventricle Tetralogy of Fallot: 4 defects 1. Pulmonary stenosis 2. Large ventricular septal defect 3. Aortic communication with both ventricles 4. Right ventricular hypertrophy Atrial or ventricular septal defect -Abnormal opening b/w right and left ventricle (atria) Patent ductus arteriosus -Failure of the fetal ductus ateriosus to close -Continuous blood flow from the aorta to the pulmonary artery |
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Calculation of risk of heart disease
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10-year Framingham risk for ‘hard coronary events’ Myocardial infarction Sudden death
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Common meds for heart disease: Angiotensin-converting-enzyme inhibitor
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Angiotensin-converting-enzyme inhibitor-help relax blood vessels. ACE inhibitors prevent an enzyme in your body from producing angiotensin II, a substance in your body that affects your cardiovascular system by narrowing your blood vessels and releasing hormones that can raise your blood pressure.
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Common meds for heart disease: Beta Blockers
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Beta Blocker- medications that reduce your blood pressure. Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. When you take beta blockers, the heart beats more slowly and with less force, thereby reducing blood pressure. Beta blockers also help blood vessels open up to improve blood flow.
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Common meds for heart disease: calcium channel blockers
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Calcium channel blockers-prevent calcium from entering cells of the heart and blood vessel walls, resulting in lower blood pressure. Calcium channel blockers, also called calcium antagonists, relax and widen blood vessels by affecting the muscle cells in the arterial walls.
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Other terms used interchangeably for cancer:
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Other terms used interchangeably for cancer:
• Malignant neoplasm • Tumor • Malignancy • Carcinoma According to American Cancer Society, 5% of cancer due to genetics. 95% due to other (often modifiable) factors, such as diet, smoking. |
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Most common cancers among men in US
estimated deaths |
Most common cancers among men in US
Prostate - 25% lung and bronchus - 15% Colon and rectum - 10% urinary bladder - 7% non-hodgkin lymphoma, melanoma, kidney, oral cavity and pharnx, leukemia, pancreas estimated deaths: lung and bronchus - 31% prostate - 10% colon and rectum - 8% pancreas, liver and bile duct, leukemia, esophagus, urinary bladder, non-hodgkin lymphoma, kidney 2010 data slightly different |
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Most common cancers among women in US
estimated deaths |
Most common cancers among men in US
breast - 26% lung/bronchus - 14% colon and rectum - 10% uterine corpus, non-hodgkin lymphoma, thyroid, melanoma, ovary, kidney, leukemia estimated deaths lung/bronchus - 26% breast - 15% colon/rectum - 9% pancreas, ovary, non-H lymphoma, leukemia, uterine corpus, liver/bile, brain and other nervous system 2010 data slightly different |
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Differentiation
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– process in which normal cells undergo physical and structural changes as they develop in different tissues in the body. In malignant cells, differentiation is altered so that the malignant cells may not be recognizable in relation to the host cell. When a tumor has completely lost identity with the parent tissue, it is considered to be undifferentiated (anaplasia). When this happens it become impossible to identify the malignant’s cells origin. The less differentiated a tumor becomes, the faster the metastasis, or spread, and the worse the prognosis.
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Dysplasia -
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Dysplasia - a disorganization of normal adult cells; often caused by chronic irritation, and may reverse itself or progress to cancer.
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Metaplasia
Anaplasia |
Metaplasia – early dysplasia; reversible & benign but abnormal change where one adult cell changes from one type to another.
Anaplasia – most advanced form of metaplasia; characteristic of malignant cells only |
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Hyperplasia
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Hyperplasia - an increase in the number of cells in the tissue, causing an increase in tissue mass. Can be normal (eg, wound healing, breast changes during pregnancy or physiologic hyperplasia) or abnormal (neoplastic hyperplasia)
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Tumor –
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Tumor – neoplasms or abnormal growth of new tissue that serves no useful purpose; may harm host by competing for vital blood supply & nutrients.
Tumors are abnormal growths of new tissue that may harm the host organism by competing for blood and nutrients. Tumors can be primary or secondary – primary tumors arise from cells that are normally local to given structure; secondary tumor arises from cells that have metastasized from another part of the body. What is carcinoma in situ? |
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Classification of Tumors
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by cell type,
tissue of origin, degree of differentiation malignant/benign Cell type: named according to the tissue from which they arise (Refer to to Table 9-1 p 349 – Classification of neoplasms by cell type of origin) Read Classification to Neoplasm pp 349-350. carcinoma: epithelial cells (skin, mucous membranes, GI tract) sarcoma: connective tissue (bone, cartilage, fat, muscles) lymphoma: lymph tissue (lymph nodes, spleen) hematopoietic: (leukemia, multiple myeloma) Degree of differentiation: metaplasia, anaplasia 1.Normal transformation of tissue from one type to another, as in the ossification of cartilage to form bone. 2. Transformation of cells from a normal to an abnormal state. What is an undifferentiated cell? Benign - usually harmless and do not spread, but can cause problems |
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Staging and Grading of Tumors
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Read Staging and Grading, pp 350-351 Staging - “process of describing the extent of disease at the time of diagnosis in order to aid
treatment planning, predict prognosis, and compare different treatment options” • Reflects the growth and extent of the neoplasm; prognosis • Simplified staging system for cancer (p 350) – look up definitions • Stage 0 • Stage I • Stage II •S tage III • Stage IV Refer to Box 9-1 Ann Arbor Staging for Lymphomas p 350 TNM (tumor, node, metastesis) System developed by the American Joint Committee on Cancer • Used most often for solid tumors, has been adapted for other types of tumors •A natomic staging system describes anatomic extent of primary tumor, involvement of regional lymph nodes & distant metastases. Grading – 1 – 4 is another way to define a tumor; classifies degree of malignancy & differentiation of malignant cells |
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TNM
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TNM (tumor, node, metastesis) System developed by the American Joint Committee on Cancer • Used most often for solid tumors, has been adapted for other types of tumors
• Anatomic staging system describes anatomic extent of primary tumor, involvement of regional lymph nodes & distant metastases. Grading – 1 – 4 is another way to define a tumor; classifies degree of malignancy & differentiation of malignant cells |
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Cause of cancer varies, but can be classified as ___ or ___
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Cause of cancer varies, but can be classified as endogenous (genetic) or exogenous (environment).
Most cancers develop with multiple environmental, viral, and genetic agents working together to disrupt immune system and the failure of the aging immune system to recognize and respond to undifferentiated cells |
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Carcinogens
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Carcinogens –agents that can initiate malignant transformations of the cell
Viruses – e.g. Human Papilloma Virus leading to cervical cancer Chemical and physical agents (e.g. asphalt, asbestos) after close and prolonged contact Drugs – e.g. chemotherapeutic agents, corticosteroids. Hormones – e.g. estrogen stimulates the growth of the endometrial lining which can become anaplastic Excessive alcohol |
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Human Papilloma virus
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Human Papilloma virus is a sexually transmitted disease. There are 100 types of HPV and about 30 of these cause genital infections such as warts or cervical cancer.
Cervical cancer - Caused by HPV types16 & 18 (high-risk HPV strains) HPB virus enters the body through a cut, abrasion or tear in the outer layer of skin. It invades the cervical tissue cells and transfers genetic material. This leads to abnormal changes in the cells. |
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Read Etiology (pp 352-353) & Risk factors (Box 9-3 p 353) – aging & lifestyle (tobacco, diet & nutrition, alcohol, sexual & reproductive behavior, hormonal exposure, geography & environmental exposure, ethnicity, precancerous lesions, stress; pp 353-357
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Risk factors for cancer
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Risk factors can be exponential rather than additive
Age is one of the most significant risk factors for cancer. People > 65 years have 11 x greater risk of cancer than younger persons • Older people more susceptible to cancer as they have been exposed to carcinogens longer than younger people. Geography: related to exposure from different carcinogens (ie, farmers with sun exposure). Precancerous lesions: can undergo transformations into lesions and can include moles, burns, scars, and polyps ethnicity viruses Lifestyle • Tobacco is the most important cause of cancer. 1/3 of all cancers are thought to be related to smoking. •Diet and nutrition: Poor diet blunts immune system’s defense against genetic damage caused by exposure to environmental carcinogen •Certain foods can also positively (+) or negatively (-) affect cancer risk: • cured, pickled, smoked, or salted foods + • fat consumption/red meat + •fruits and vegetables (antioxidants) – • Sexual behaviors: increased incidence of cancer with earlier (younger) intercourse and number of sexual |
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Pathogenesis of Cancer
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Read Pathogenesis introduction pp 357-358
Cancer is fundamentally a disease of regulation of tissue growth. For a normal cell to transform into a cancer cell (malignant transformation), genes which regulate cell growth and differentiation must be altered. Genetic changes can occur at many levels, from gain or loss of entire chromosomes to a mutation affecting a single DNA nucleotide. Tumor suppressor genes - are genes which inhibit cell division, survival, or other properties of cancer cells. Generally, tumor suppressors are transcription factors that are activated by cellular stress or DNA damage. Tumor suppressor genes are often disabled by cancer-promoting genetic changes. Typically, changes in many genes are required to transform a normal cell into a cancer cell. Oncogenes - may be normal genes which are expressed at inappropriately high levels, or altered genes which have novel properties. |
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Oncogenes -
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Oncogenes - may be normal genes which are expressed at inappropriately high levels, or altered genes which have novel properties.
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Tumor suppressor genes -
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tumor suppressor genes are genes which inhibit cell division, survival, or other properties of cancer cells. Generally, tumor suppressors are transcription factors that are activated by cellular stress or DNA damage. Tumor suppressor genes are often disabled by cancer-promoting genetic changes.
Typically, changes in many genes are required to transform a normal cell into a cancer cell. |
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Metastasis of cancer
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Read Invasion & Metastases p 359
Metastases occur when cells break away from primary tumor, travel via blood or lymphatic system, trapped in capillaries of organs; infiltrate organ tissue and grow into new tumors Cancer can also spread through adjacent structures and penetrate body cavities Patterns of metastasis differ by type of cancer, but common sites include: the lymph nodes, liver, lung, bone, and brain Incidence: 30% of people with cancer will have clinically detectable metastases and another 30-40% of people with cancer will be clinically free, but have hidden metastases. (60-70%) Treatment can slow the spread of metastases. Figure 9-2 Major mechanisms of metastases. To metastasize, tumor cells must gain several unique biologic properties such as invasive growth (A), induction of vascular growth (B), vascular invasion (C), adherence to endothelial cells or thrombosis of peripheral sinusoids (D), continuation of invasive growth with extravasation (E), and formation of primary and secondary metastatic foci (F). Not all tumor cells develop all the abilities shown here; some cell clones may subspecialize and just create angiogenesis; others may invade and move on. (From Dorfman HD, Czerniak B: Bone tumors, St. Louis, 1998, Mosby.) |
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Be able to define the following terms:
Primary tumor Secondary tumor Angiogenesis Extravasation Metastasis |
Be able to define the following terms: work on this slide!
Primary tumor - Secondary tumor - Angiogenesis - development of new blood vessels Extravasation - "In the case of malignant cancer metastasis it refers to cancer cells exiting the capillaries and entering organs." Metastasis - spread of cancer beyond original site |
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Structure of Lymphatic System
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Structure
Superficial & deep lymph vessels & nodes Lymphoid organs and tissues include thymus, bone marrow, spleen, tonsils, Peyer’s patches etc. Lymphatic capillaries or pre-collectors (initial lymphatics) Collecting lymphatics Lymph nodes Lymph ducts Lymph circulates between cells, collects waste products left behind including dead blood cells, pathogens, and cancer cells |
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Three main functions of the lymphatic system
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Three main functions
Transport proteins and fluids, lost by capillary seepage, back to bloodstream Protects body against pathogens by phagocytosis & immune response. Serves as pathway for absorption of fats from small intestine into bloodstream The lymphatic system has three interrelated functions: Helps to maintain fluid balance in tissues by removal of excess fluids from body tissues, Assists in removal of cellular debris and waste products from extracelluar spaces Role in immunity Fights infection through production of immune cells (such as lymphocytes, monocytes, and plasma cells). Role in digestion - absorption of fatty acids and subsequent transport of fat, chyle (lymph that is milky from emulsified fats - An opaque, milky-white fluid consisting mainly of emulsified fats that passes through the lacteals of the small intestines into the lymphatic system), to the circulatory system |
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What is lymph?
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Blood plasma leaks from the capillaries of the circulatory system, becoming interstitial fluid, and filling the space between individual cells of tissue.
Together, blood plasma and interstitial fluid make up extracellular fluid (ECF). Plasma constitutes 20%, while interstitial fluid constitutes 80% of ECF. |
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Fluid Dynamics and Starling's Law
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Fluid flows from an area of high pressure to an area of low pressure until equilibrium reached
Hydrostatic pressure in arterial end of capillary forces plasma to filter out into interstitial compartment Most of the fluid is returned to capillaries through osmotic pressure – plasma proteins 90% of interstitial tissue fluid returns to capillary bed. Here it again becomes plasma and continues journey throughout body as part of venous circulation |
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Lymphatic Capillaries
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Lymphatic capillaries
any of the smallest lymphatic vessels that are blind at one end and collect lymph in organs and tissues The lymphatic capillaries form a mesh-like network of tiny tubes that are distributed throughout the tissue spaces. These capillaries branch and interconnect freely so that they extend into almost all tissues. |
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Lymph Nodes
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Lymph nodes
any of the rounded masses of lymphoid tissue that are surrounded by a capsule of connective tissue, are distributed along the lymphatic vessels, and contain numerous lymphocytes which filter the flow of lymph passing through the node -- called also lymph gland |
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Lymphatic capillaries converge to form
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bigger lymph vessels that ultimately return lymph fluid back to the circulatory system via the subclavian vein.
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Lymphatic Duct
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Lymphatic ducts
any of the lymphatic vessels that are part of the system collecting lymph from the lymphatic capillaries and pouring it into the subclavian veins by way of the right lymphatic duct and the left lymphatic duct duct (Thoracic duct) Thoracic duct (left lymphatic duct) the main trunk of the system of lymphatic vessels that lies along the front of the spinal column, extends from a dilatation behind the aorta and opposite the second lumbar vertebra up through the thorax where it turns to the left and opens into the left subclavian vein, and receives chyle from the intestine and lymph from the abdomen, the lower limbs, and the entire left side of the body |
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Fluid Exchange Between Capillaries and Tissues
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Capillaries are composed of a single layer of squamos epithelium surrounded by a thin basement membrane.
Most capillaries have pores (spaces) between the individual cells that make up the capillary wall (except those servicing the nervous system). Plasma fluid and small nutrient molecules leave the capillary and enter the interstitial fluid through these pores, in a process called bulk flow. Bulk flow facilitates the efficient transfer of nutrient out of the blood and into the tissues. However, blood cells and plasma proteins, which are too large to fit through the pores, do not filter out of the capillaries by bulk flow. Together, blood plasma and interstitial fluid make up the extracellular fluid (ECF). Plasma constitutes 20%, while interstitial fluid constitutes 80% of the ECF. Lymph originates as blood plasma that leaks from the capillaries of the circulatory system, becoming interstitial fluid, and filling the space between individual cells of tissue. Lymph is the 10 percent of the interstitial tissue fluid that is left behind. |
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Starling’s Law Simplified –
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fluid at arterial end of capillary will tend to flow into the tissue space because plasma (blood) hydrostatic pressure is higher at arterial end than tissue hydrostatic pressure (THP) of tissues.
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The composition of the interstitial fluid and the plasma is essentially the same except that
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plasma also contains plasma proteins not found in the interstitial fluid.
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Lymph originates as blood plasma that leaks from the capillaries of the circulatory system, becoming interstitial fluid, and filling the space between individual cells of tissue.
Lymph is the __ percent of the interstitial tissue fluid that is left behind. |
Lymph is the 10 percent of the interstitial tissue fluid that is left behind.
Normally the amount of lymph circulating in the body is ~2l/day (one to two quarts) and it makes up one to three percent of the body weight [6]. |
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Role of interstitial fluid and lymph
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Role of interstitial fluid is to deliver groceries to cells.
Role of lymph system is to take out trash that is left behind and to dispose of it. The net filtration of fluid out of capillaries into interstitial compartment is greater than net absorption of fluid back into capillaries 10% does not return to the capillary bed |
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Lymphatic Capillaries
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Lymph capillaries are blind-ended tubes with no opening to allow the lymph easy access.
The end of the capillary is only one-cell in thickness and these cells are arranged in a slightly overlapping pattern – like the shingles on a roof. Pressure from the fluid surrounding the lymphatic capillary forces these cells to separate for a moment. This allows fluid to enter, but not to leave, the lymphatic capillary. There are one-way valves within the lymphatic capillaries. These valves ensure the continued flow of the lymph away from the tissues. The presence of one-way valves in the lymph vessels ensures unidirectional flow of lymph fluid toward the subclavian vein. |
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Distribution of lymphatic capillaries
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The lymphatic capillaries form a mesh-like network of tiny tubes that are distributed throughout the tissue spaces. These capillaries branch and interconnect freely so that they extend into almost all tissues.
Lymphatic capillaries converge to form bigger lymph vessels that ultimately return lymph fluid back to the circulatory system via the subclavian vein. If excess fluid cannot be returned to the blood stream then interstitial fluid builds up, leading to swelling of the tissues with fluid, this is called edema. |
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Why are lymph nodes often sites of obstructions and lymph dysfunction?
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Lymph nodes offer 100 x the normal resistance of flow to lymph within the lymphatic vessels themselves – thus, often site of obstructions and lymph dysfunction
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Figure 13-7, p. 648
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Lymphatic Drainage
The dermal and subcutaneous lymph territories (lymphotomes are indicated by different shadings) of the lymphatic system are separated by watersheds marked by (= = = =). Arrows indicate the direction of the lymph flow. Normal drainage is away from the watershed, but collaterals cross the watershed (thick double arrows). When the main drainage paths from each of these regions are blocked, lymph (thick single arrows) has to be carried across the watersheds via collaterals and the plexuses. These initial lymphatics fill superficial collectors, which drain into deep ones and then into the lymphatic trunks (small arrows). Lymphatic drainage is organization into regional drainage collections called lymphotomes. These are the right and left drainage areas and normally lymph does not drain across the invisible lines that separate these areas. Border areas called “watershed” areas Characterized by sparse collateral flow to adjacent Lymphotomes, but connections do exist between Lymphotomes in the superficial and deep plexuses and via collateral lymphatics between deep collectors in adjacent Lymphotomes located just above the deep fascia. Structures within each area carry lymph to larger vessels and from there to its destination, which is to return to the circulatory system via venous system (subclavian veins). |
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Lymphatic drainage organization into two separate and very unequal right and left drainage areas
Normally lymph does not drain across the invisible lines that separate these areas. Right drainage returns to circulatory system via right subclavian vein Left drainage returns to circulatory system via left subclavian vein |
Figure 13-8 p. 649
Lymphatic ducts. The thoracic duct (black), leading from the cisterna chyli to discharge into the left subclavian vein, in the neck. (The blood vessels are shaded blue.) The right lymphatic duct is also shown (see figure on bottom). This carries far less lymph than the thoracic duct, draining mainly the right arm and head, the heart and lungs, and the anterior chest wall. These two main trunks sometimes are linked by large collateral lymphatics. |
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The Right Drainage Area removes lymph from the:
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Right side of the head and neck
Right arm Upper right quadrant of the body. Lymph from this area flows into the right lymphatic duct. This duct returns the lymph to the circulatory system by draining into the right subclavian vein. |
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The Left Drainage Area removes lymph from the:
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Left side of the head and neck
Left arm and the left upper quadrant Lower trunk Both legs The cisterna chyli temporarily stores lymph as it moves upward from the lower areas of the body. The thoracic duct carries lymph upward to the left lymphatic duct. The left lymphatic duct returns the lymph to the circulatory system by draining into the left subclavian vein. |
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Endocrine glands:
(list) |
pineal
pituitary: adenohypophysis neurohypopohysis (posterior pituitary) Adrenal Thymus Thyroid Parathyroid Pancreas Gonads: testes and ovaries (heart and adipose) |
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Endocrine hormones:
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pineal - melatonin
pituitary: adenohypophysis - HGH, LH, FSH, neurohypopohysis (posterior pituitary) - oxytosin, ADH (hypothalamus produces them) Adrenal - cortex = aldosterone, cortisol, testosterone (right?), medulla = epinephrine and norepinephrine Thymus - Thymosins Thyroid - T3, T4, thyroxine Parathyroid - parathormone Pancreas - insulin and glucagon Gonads: testes and ovaries - androgens (esp. testosterone), estrogen, progestins Kidney - erythropoietin, calcitrol (heart and adipose) - ANP and BNP, leptin, resistin |
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Read Endocrine system introduction p 453, hypothalamic control and hormonal effects pp 453-456.
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Yes Ma'am
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The ingestion of food and especially fats cause the release of a hormone, cholecystokinin, (CCK) which in turn signals
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the relaxation of the valve at the end of the common bile duct (the sphincter of oddi) which lets the bile enter the small intestine.
It also signals the contraction of the gallbladder which squirts the concentrated liquid bile into the small intestine where it helps with the emulsification or breakdown of fats in the meal. |
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The endocrine system has five general functions:
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1.Differentiation of central nervous system (CNS) and reproductive system of developing fetus 2.Stimulation of sequential growth/development during childhood and adolescence
3.Coordination of male/female reproductive systems 4.Maintenance of optimal internal environment throughout lifespan 5.Initiation of corrective and adaptive responses when emergency conditions occur |
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Refer to Table 11-1 Endocrine glands: secretion, target and action on p 455
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When you are reading a patient’s chart, it is important to know basic hormone functions or effects that may have an impact on physical therapy treatment. Over 30 different hormones have been identified, but the table on p 455 includes those most common to physical therapy clients.
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Read hormonal effects pp 453-456
The hypothalamus through multiple mechanisms, controls the release of hormones from many other organs, which include: |
Posterior pituitary secretes Oxytocin- stimulates the contraction of the uterus and affects milk production
Antidiuretic Hormone (ADH) - controls concentration of body fluids by altering the permeability of kidney membranes to conserve water Anterior pituitary secretes Prolactin - stimulates milk production Human growth hormone (HGH) – stimulates growth by increasing protein synthesis and fat mobilization and decreasing carbohydrate utilization; affects most body tissues Thyroid gland secretes Thyroid hormones – regulate basal metabolism (rate at which food and oxygen are converted into energy) in many tissues, increase metabolic rate and protein synthesis Parathyroid gland secretes Parathyroid hormone – regulates calcium and phosphate metabolism. POTH elevates serum calcium levels by stimulating resorption of calcium and phosphate from bone, resorption of calcium and excretion of phosphate from the kidneys, and with vitamin D, absorption of calcium and phosphate from the GI tract Adrenal cortex secretes Mineralocorticoids – (aldosterone) regulate blood pressure by regulating the resorption of sodium and the excretion of potassium Glucocorticoids (e.g. cortisol; called hydrocortisone when produced pharmaceutically) regulates metabolism of protein, CHO, lipids suppresses inflammatory Adrenal medulla produces Catecholamines (norepinephrine; epinephrine) flight or fight response Testes and ovaries, along with the adrenal cortex secrete hormones that aid in the development and maturation of secondary sexual characteristics, and sexual function. |
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Read endocrine pathology p 456
Hyperfunction or hypofunction can result from a tumor or acute or chronic inflammation originating in the hypothalamus, the pituitary, or in other Read Aging and the endocrine system pp 458-459 |
•The inflammation may be acute or subacute, but is usually chronic which results in glandular hypofunction.
endocrine glands. •Chronic endocrine abnormalities are common health problems requiring life-long hormonal replacement to survive (e.g., thyroid hormone or insulin) Aging is associated with higher incidence of disorders of the endocrine system, such as Type II Diabetes Mellitus. |
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Refer to Table 11-3 p 459 Signs and symptoms of endocrine dysfunction
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The signs and symptoms of endocrine dysfunction are variable and depend on the gland affected and if the dysfunction results in hyperfunction or hypofunction.
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Read pp 459-460 Musculoskeletal signs and symptoms of endocrine disease
The musculoskeletal system has clinical manifestations that are the most readily apparent to a PT and potentially the patient. Because growth and development are often controlled by hormones, dysfunction can alter the structure and function of connective tissue, leading to clinical manifestations. Be able to define/describe the following and the relationship of these musculoskeletal problems with possible endocrine disorders: Rheumatoid arthritis Muscle weakness, atrophy, myalgia, fatigue Carpal tunnel syndrome Tenosynovitis Periarthritis Pseudogout |
Rheumatoid arthritis
Muscle weakness, atrophy, myalgia, fatigue Carpal tunnel syndrome - Tenosynovitis Periarthritis Pseudogout Pseudogout occurs most often in the knees, can also affect wrists, hips, shoulders, elbows, ankles, toes, knuckles, and hands. Usually affects only one joint at a time, but may uncommonly affect multiple joints simultaneously. Symptoms similar to gout; however, caused by deposition of calcium pyrophosphate crystals; gout caused by deposition of uric acid crystals. Gout also has a more severe disease course and often a worse prognosis. |
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Acromegaly (hyperpituitarism)
Acromegaly occurs as a result of Possible Signs and Symptoms of Acromegaly |
excessive secretion of growth hormone after normal completion of body growth
Possible Signs and Symptoms of Acromegaly Symptoms caused by pituitary tumor: Headaches Visual problems Symptoms caused by GH oversecretion: Hypertension (high blood pressure) or other heart-related problems Diabetes Sleep apnea Excessive sweating Joint pains Enlargement of hands and feet Swelling of soft tissue Other signs and symptoms of acromegaly: Carpal tunnel syndrome, Skin tags, Menstrual cycle disturbances/impotence, Goiter (enlargement of the thyroid gland), Sinus congestion Skin changes, including thickening, oiliness, acne Coarsening of facial features, including forehead, nose, lips, tongue, jaw |
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Diatetes insipidus
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Diabetes insipidus is a condition in which the kidneys are unable to conserve water. Excessive urination and thirst, not related to diabetes mellitus.
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Syndrome of inappropriate antidiuretic hormone
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hypersecretion (SIADH)
characterized by excessive release of antidiuretic hormone (ADH or vasopressin) from the posterior pituitary gland. The result is hyponatremia and sometimes fluid overload. In SIADH the release of ADH is not inhibited by a reduction in plasma osmolality when the individual ingests water and the osmolality of the plasma drops. As the main solute of plasma is sodium, this hypo- osmolar state is usually detected as a low sodium level on laboratory testing. SIADH is therefore primarily a condition that results in the abnormal handling of water loading and not a problem with excessive solute loss. This is why it is usually treated with fluid (in particular water) restriction. Diuretics may also be given to decrease reabsorption of water, but care must be taken not to correct water imbalances too rapidly. This causes dilutional hyponatremia and all the consequences associated with that condition: headache, nausea, vomiting, and confusion may ensue. Severe hyponatremia may cause convulsions or coma. It is usually found in patients diagnosed with small-cell carcinoma of the lung, brain tumors, head trauma, strokes, meningitis, and encephalitis. |
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Hypersecretion of ADH
Hyposecretion of ADH |
SIADH
Diabetes Insipidus |
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Thyroid Gland – largest gland of the endocrine system
Hormone and effects |
•H-shaped organ located in the neck just below the larynx
•Produces thyroid hormone (TH) – the body’s major metabolic hormone •Increases rate of oxygen consumption & consequently rate at which carbs, proteins & fats are metabolized •TH hormone affects virtually every cell in the body with exception of: •Adult brain •Spleen •Testes/uterus •Thyroid gland •TH also influences GH & contributes to maintaining blood pressure •TH –two active iodine-containing hormones •Thyroxine (T4) •Triiodothyronine (T3) Also secretes calcitonin - helps bring calcium into bones and regulate blood levels |
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Cretinism -
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one form of hypothyroism in children – if untreated, leads to mental retardation, impaired growth, low body temp & abnormal bone formation. Does not show up at birth because infant has received thyroid hormones from mother’s blood during fetal development.
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Myxedema –
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hypothytoidism that develops in adults.
•Edema, low blood levels of thyroid hormones, weight gain, cold intolerance, fatigue, depression, muscle or joint pain, overall sluggishness. |
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Grave’s disease -
etiology s/s treatment |
One of the most prevalent disorders of hyperthyroidism Etiology – excessive sections (Hypersecretion) of T3, T4 or both. Signs & symptoms
•Elevated metabolic rate •Irregular heartbeats (arrhythmia, palpitations) •Abnormal weight loss despite increased appetite •Excessive perspiration •Muscle weakness •Anxiety •Insomnia •Exopthalamus – bilateral, anterior protruding of eyes, displacement of the eye is due to abnormal connective tissue deposition in the orbit & extraocular muscles Pain and/or irritation in the eyes Dry eyes Photophobia - Sensitivity to light Diplopia- double vision caused by the weakening of the eye muscles If the optic nerve is compressed - progressive blindness Difficulty in moving eyes - as the eye muscles weaken the patient may find it harder to move the eyes. Amblyopia - In some cases the eyes may turn inwards (‘cross-eyed) Treatment – depends on pathology May involve drug therapy to block production of thyroid hormones or surgical removal of thyroid. Another option – administer radioactive iodine to destroy thyroid secretory cells. |
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Hashimoto's disease -
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a form of chronic inflammation of the thyroid gland; also called chronic lymphocytic thyroiditis or autoimmune thyroiditis.
•The inflammation results in damage to the thyroid gland and reduced thyroid function or "hypothyroidism," meaning the gland doesn't make enough thyroid hormone for the needs of the body. • Hashimoto's disease is the most common cause of hypothyroidism in the United States. Hashimoto's disease is an autoimmune disorder, meaning the body's immune system attacks its own healthy cells and tissues. In Hashimoto's disease, the immune system makes antibodies that attack cells in the thyroid and interfere with their ability to produce thyroid hormone. Large numbers of white blood cells called lymphocytes accumulate in the thyroid. Lymphocytes make the antibodies that drive the autoimmune process. Many people with Hashimoto's disease have no symptoms at first. As the disease slowly progresses, the thyroid usually enlarges and may cause the front of the neck to look swollen. The enlarged gland, called a goiter, may create a feeling of fullness in the throat but is usually not painful. After years, or even decades, the damage to the thyroid causes it to shrink and the goiter to disappear. |
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Parathyroid Glands
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•At least 4 separate glands on posterior surface of thyroid gland •Secretes only 1 hormone (only 1 is known)
•Parathyroid hormone (PTH) •Helps regulate calcium balance by stimulating three target organs 1. Bones 2. Kidneys 3. Intestines •Stimulation of PTH – calcium & phosphates released from bones increasing concentration in blood. This makes calcium necessary for proper functioning of body tissues available in the bloodstream •At same time – PTH enhances absorption of calcium & phosphates from foods in intestines; causing increase in blood levels of calcium & phosphates •PTH also causes kidneys to conserve blood calcium & increase secretion of phosphates in urine. |
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Hypoparathyroidism –
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insufficient production of PTH caused by:
•Primary hyperthyroid dysfunction or elevated blood calcium levels •Usually due to injury or surgical removal of parathyroid glands in conjunction with thyroid surgery •Decreased calcium lowers electrical threshold causing neurons to depolarization more easily, increases number of nerve impulses resulting in muscle twitches and spasms (tetany) |
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Hyperparathyroidism –
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excessive production of PTH, commonly caused by benign tumor
•Leads to demineralization of bones (osteitis fibrosa cystica) – highly susceptible to fracture & deformity. •Calcium deposits in kidneys & kidney stones (nephrolithiasis) |
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Adrenal cortex – secretes three types of steroid hormones:
1. 2. 3. |
Mineralocorticoids – act mainly through kidneys to maintain electrolyte balance (sodium & potassium); primarily aldosterone
• Aldosterone causes kidneys to conserve sodium & excrete potassium • Promotes water conservation & reduces urine output Glucocorticoids – mainly Cortisol • Influences metabolism of carbohydrates, fats & proteins • Cortisol – helps regulate concentration of glucose in blood, protecting against low blood sugar levels • Also stimulates breakdown of fats in adipose tissue & releases fatty acids into blood, which causes many cells to use less glucose Sex hormones – androgens, estrogens & progestins • Helps maintain secondary sex characteristics, such as development of breasts & adult distribution of hair. Virilism – development of male characteristics Feminization – development of female characteristics |
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Cushing's syndrome occurs when the body's tissues are exposed to high levels of
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cortisol for too long.
Many people develop Cushing's syndrome because they take glucocorticoids- steroid hormones that are chemically similar to naturally produced cortisol—such as prednisone for asthma, rheumatoid arthritis, lupus, and other inflammatory diseases. Glucocorticoids are also used to suppress the immune system after transplantation to keep the body from rejecting the new organ or tissue. Other people develop Cushing's syndrome because their bodies produce too much cortisol. Normally, the production of cortisol follows a precise chain of events. First, the hypothalamus, a part of the brain about the size of a small sugar cube, sends corticotropin-releasing hormone (CRH) to the pituitary gland. CRH causes the pituitary to secrete adrenocorticotropin hormone (ACTH), which stimulates the adrenal glands. When the adrenals, which are located just above the kidneys, receive the ACTH, they respond by releasing cortisol into the bloodstream. |
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Cushing's Syndrome
Risk S/s |
relatively rare, most common ages 20-50
Increased risk: people who are obese and have type 2 diabetes, along with poorly controlled blood glucose and high blood pressure S/S: thinning hair, buffalo hump, moon face, increased body and facial hair, purple striae on skin, pendulous abdomen, supraclavicular fat pad, slow wound healing, thin extremities, easy bruising |
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Addison's Disease
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(also called adrenal insufficiency, AI, or hypocortisolism) is an endocrine disorder that occurs when the adrenal glands do not produce enough of the hormone cortisol and, in some cases, the hormone aldosterone.
Originally, the disease usually resulted from an infection of the adrenal gland; the most common infection was tuberculosis, which is still the predominant cause of Addison disease in developing countries. Currently, in developed countries, Addison disease most commonly results from nonspecific autoimmune destruction of the adrenal gland. Aldosterone is a mineralocorticoid, from adrenal glands. It helps maintain blood pressure and water and salt balance in the body by helping the kidney retain sodium and excrete potassium. When aldosterone production falls too low, the kidneys are not able to regulate salt and water balance, causing blood volume and blood pressure to drop. Addison's can occur in any age group and afflicts both males and females equally. The disease is characterized by weight loss, muscle weakness, fatigue, low blood pressure, dizziness and sometimes darkening of the skin in both exposed and nonexposed parts of the body. We know that President John F. Kennedy had Addison’s Disease, but now one doctor can pinpoint that the cause of his disease was autoimmune in nature. Addison’s disease causes fatigue, dizziness, muscle weakness, weight loss, difficulties standing up, nausea, sweating and changes in mood and personality.” A fraction of cases, about 20% of them, are caused by tuberculosis. When JFK ran for president, his opponents said he had Addison’s but his doctor denied that he had Addison’s because of tuberculosis. Technically, that was true. However, because he also had hypothyroidism, doctors have concluded that his Addison’s was caused by an autoimmune disorder, polyendocrine syndrome type 2, or APS 2. |
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Adrenal Glands – also known as suprarenal glands. Paired organs covering superior surface of the kidneys, divided into two parts:
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1. Adrenal medulla – inner part
2. Adrenal cortex – outer part, makes up bulk of the gland |
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Adrenal medulla – secretes two closely related hormones:
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1. 2. •
Epinephrine (adrenalin) – secreted in larger amounts Norepinephrine (noradrenalin) Both hormones activated when body responds to crisis situation • Considered sympathomimetic agents because effect produced mimics those produced by the SNS. • Epinephrine necessary for maintaining blood pressure & cardiac output, keeping airways open & raising blood glucose levels to respond to crisis. • All useful for frightened, traumatized, injured or sick types of crisis situations. Thus, the additional aid from hormones to augment what SNS does. Hormone response slower than SNS response, and lasts longer. • Norepinephrine reduces vasoconstricts diameter of peripheral blood vessels to raise blood pressure. • Because the hormones produced by the adrenal medulla only intensify activities set in motion by the SNS, deficiency in these hormones is not a problem. |
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Hyperinsulinism -
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A syndrome with excessively high insulin levels in the blood; it may cause hypoglycemia. Etiology varies including:
•hypersecretion of a beta cell tumor •autoantibodies against insulin (insulin resistance) •defective insulin receptor, or •overuse of exogenous insulin or hypoglycemic agents. |
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Glucagon
target organ and functions disorders |
Liver and blood - raises BG level by accelerating glycogenolysis and gluconeogenesis and releasing glucose into the bloodstream
Deficiency in glucagon - persistently low blood glucose levels (hypoglycemia) |
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Insulin
target organ and functions disorders |
Tissue cells - lowers blood glucose level by accelerating glucose transport into cells and the use of this glucose for energy production
hypo- diabetes mellitus hyper- hyperinsulinism |
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largest endocrine organ in the body
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adipose
Figure 11-8 Abdominal adipose tissue (fat) can accumulate as subcutaneous, intraabdominal, or intrahepatic (fatty lobules throughout the liver). The body has an almost unlimited capacity to store fat. Central obesity has been linked with serious health consequences (e.g., cardiovascular disease, insulin resistance, diabetes mellitus). Read pp 485-487 Adipose tissue, obesity, obesity and cancer, Type 2 diabetes mellitus, special implications for the therapist 11-15. |
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The pancreas (islets of Langerhans) secretes 2 hormones important for carbohydrate
metabolism – |
read pancreas - 487-488, table 11-10, fig 11-9
glucagon & insulin 1.Alpha cells – produce glucagon, a hormone from the fasting state •Stimulates the liver and muscles to break down stored glycogen to glucose (glycogenolysis) and release the glucose, so blood glucose levels rise. Overall effect, is a rise in blood glucose level. •Stimulates gluconeogenesis in the liver and kidneys •Makes glucose from protein store in the liver and kidneys. Cats rely on this process almost exclusively, lacking the enzymes to process carbohydrates. 2.Beta cells – when blood glucose levels are high, stimulated to produce & secrete insulin •Insulin causes glucose to enter body cells to be used for energy & acts to clear glucose from the blood by promoting its storage as glycogen. Insulin is required by almost all of the cells in the body, but major targets are liver cells, fat cells and muscle cells. The functions of insulin in these cells: •Stimulates liver and muscle cells to store glucose in glycogen •Enhances free fatty acid uptake and storage •Stimulates liver and muscle cells to make proteins from amino acids •Inhibits liver and kidney cells from making glucose from intermediate compounds of metabolic pathways (gluconeogenesis) •Thus, stores nutrients right after a meal by reducing the concentrations of glucose, fatty acids and amino acids in bloodstream. |
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The most common pancreatic disorder
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Read Pancreas – p 487-488
Diabetes Mellitus – definition and overview, prediabetes p 488-489 Diabetes Mellitus pp 488-497 chronic systemic metabollic disorder characterized by: hyperglycemia disruption of metabolism of carbs, fat, protein results from defects in: secretion of insulin (insufficient, Type I) Action of insulin (impaired, type II) |
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Diabetes incidence and prevalence and risk factors
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Read incidence and prevalence pp 489-490
Total: In US, approximately 24 million adults or about 8% of the population have diabetes. Prediabetes = 57 million – 1 out of 3 children and 1 out of 2 minority children on track to develop diabetes. (according to American Diabetes Association) Diagnosed: 17.9 million people Undiagnosed: 5.7 million people As many as 1/3 to 1/5 of US adults could have diabetes by 2050 unless current trends change (study just released by CDC) Read incidence and risk factors pp 489-491, Box 11-5 p 490 Risk factors for Type I DM Type I DM in first degree relative (sibling or parent) Risk Factors for Type II DM Family member with DM Overweight 45 or older Physically active less than 3x/wk Women with history of gestational diabetes Elevated blood pressure Low HDL cholesterol High triglyceride level Risk Factors – free online risk test at: http://www.diabetes.org/diabetes-basics/prevention/diabetes-risk-test/ 41 |
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Diabetes
Read pathogenesis p 490-492 Refer to Table 11-10 regulation of glucose metabolism p 488, figure 11-9 endocrine function of pancreas Normal function |
Blood glucose rises after meal; beta cells increase secretion of insulin
Liver takes up large amount glucose for storage Insulin transports glucose into cell for use as energy and storage as glycogen; thereby lowering blood glucose levels Insulin also stimulates protein synthesis and free fatty acid storage in fat deposits Dysfunction – Diabetes = insulin is insufficient (Type1) or its function impaired (Type2) Glucose is not taken up but remains in general circulation and accumulates in blood = high BG Further, because new glucose is not deposited in liver, liver synthesizes more glucose and releases it to general circulation, raising blood levels further Insulin deficiency compromises body’s access to nutrients for fuel or storage |
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Refer to Table 11-11 Differences between types of Diabetes Mellitus (DM) Review definition and overview pp 488-489 Type large categories of DM – Type 1 DM and Type 2 DM
Differences in etiology & pathogenesis (pp 490-492) Type I DM – |
Type I - previously referred to as insulin-dependent diabetes mellitus (IDDM) or
juvenile onset DM •Hyperglycemia - due to deficiency in insulin production and secretion •Identified by - autoimmune destruction of beta-cells in islet cells of pancreas •Require exogenous insulin for life. •Most common in infants and children, but can occur at any time •Genetic predisposition, and possible environmental factors, but they are poorly understood •10% of cases have no definable etiology Review incidence and prevalence, etiologic and risk factors pp 489-490 Refer to Box 11-5 Risk factors for type I and type II diabetes mellitus |
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Type I Diabetes Melitus
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Deficiency in insulin production and secretion
Autoimmune beta cell destruction Most common in infants and children (onset) Genetic predisposition -environmental factors? |
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Type II Diabetes Melitus
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Review Type 2 diabetes mellitus pp 490-491
Type 2 Diabetes Mellitus Previously referred to as late or adult onset diabetes Because occurred in people 60 or older. Starting in early 1990s, trend toward type 2 DM in children and adolescents with risk factors – excess body fat and sedentary. Endogenous production of insulin But ineffective insulin action at cellular level: Cellular resistance to insulin action Inadequate compensatory insulin secretory action May not need insulin treatment to survive but need other forms of therapy to prevent hyperglycemia. Etiology unclear, but it is NOT autoimmune destruction of beta-cells •Associated with obesity (at least 80% of persons with type 2 DM) •Sedentary lifestyle; habitual physical inactivity |
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Diabetes Mellitus
Results in three metabolic problems |
Results in three metabolic problems
1.Decreased utilization of glucose Refer to previous slide 2.Increased fat mobilization Occurs as body relies on fat for energy when glucose unavailable As fat is metabolized production of ketones metabolic acidosis (affect the acid-base balance) Body lipid level rises atherosclerosis 3.Impaired protein utilization Occurs because transport of amino acids into cells requires insulin Lack of amino acids in cells impairs protein synthesis Protein loss impairs inflammatory process and diminishes tissue’s ability to repair itself Read 491-492 |
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Main symptoms of diabetes:
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*= more common in type I
Central: polydipsia Polyphasia lethargy* stupor* Systemic: Weight Loss* Respiratory: Kussmaul breathing (hyperventilation)* Eyes: Blurred Vision Breath: Smell of acetone* Gastric: Nausea* Vomiting* Abdominal pain* Urinary: Polyruria Glycosuria |
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Diabetes Mellitus: clinical manifestations in Type I, Type II, and both I and II
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Type I:
polyphagia weight loss ketonuria Type II: Neuropathies, infections Dislypidemia obesity often asymptomatic Both: polyuria polydipsia blurred vision weakness, dizziness, fatigue |
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Refer to Table 11-13 Cardinal signs of diabetes at diagnosis
Read clinical manifestations pp 492 Pathophysiology of diabetic complications, cardinal signs and symptoms |
symptoms
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Clinical sequelae of Diabetes: Atherosclerosis
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Atherosclerosis
Read atherosclerosis pp 492-493 Chronic hyperglycemia of DM associated with long-term damage of tissues and organs, especially eyes, kidneys, nerves, heart, and blood vessels. Because of hyperglycemia and increased fat metabolism associated with type 1 DM, atherosclerosis begins earlier and more extensive compared with general population. Results in: cardiovascular and cerebrovascular changes Poor tissue perfusion Type 2 DM: 2-4 times the risk for CHD and CVA vs. people without DM Additive effect with smoking Most deaths in people with DM are from cardiovascular disease rather than strictly diabetes related |
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CVD sequelae with diabetes
Read cardiovascular complications pp 493 |
Read cardiovascular complications pp 493
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Clinical sequelae of DM: neuromuscular, integumentary
Slide notes |
Read retinopathy & nephropathy (pp 493-494), infection (p 494), sensory, motor and autonomic neuropathy (pp 496-497), and ulceration (p 497)
Retinopathy: leading cause of blindness Microvascular occlusion of retina ischemia and tissue death Tightly associated with duration and control of glucose Nephropathy: most common cause of end-stage renal disease Tissue changes in renal filtration structures Leads to need for permanent dialysis or transplantation Autonomic neuropathy Loss of sweat regulation, temperature control Sensory polyneuropathy Affects hands and feet Symptoms: tingling, burning, or numbness to complete loss Leads to foot deformities Motor neuropathy Bilateral, asymmetrical, proximal weakness Deformity (e.g. claw toes, severe flat foot) |
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Clinical sequelae of DM: neuromuscular, integumentary
Slide 1 |
Ulceration
-neuropathy increases risk -cause: repetitive stress on insensitive skin, esp. with bony deformities -dry and inelastic skin Infection - skin, urinary tract, vaginal tissue - blood vessel changes with resulting hypoxemia -impaired ability to detect wounds -increased glucose fosters pathogen growth |
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clinical outcomes of microangiopathy and autonomic neuropathy
(diagram of person) |
microangiopathy:
retinopathy nephropathy neuropathy autonomic neuropathy: heart rate disturbances postural fall in blood pressure GI dysfunction dysfunction of bladder impotence Both: diabetic foot From International Diabetes Federation |
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Musculoskeletal Sequelae of DM: upper extremity
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Pathologies unique to DM:
1. syndrome of limited joint mobility 2. Stiff hand syndrome: Type I Read Musculoskeletal problems upper extremity pp 494-495 Musculoskeletal complications often involve the hands, shoulder, spine, and feet leading to functional limitations and decreased quality of life. Persons with diabetes aged 60 years or older are 2–3 times more likely to report an inability to walk one-quarter of a mile, climb stairs, do housework, or use a mobility aid compared with persons without diabetes in the same age group. Other upper extremity pathologies commonly seen with DM Dupuytren’s contracture – flexion contracture and thickening of palmar fascia, usually involves 3rd - 4th digits in persons with DM instead of 4th - 5th in persons without DM Flexor tenosynovitis – accumulation of fibrous tissue in tendon sheath aching and contractures. Common in thumb, middle, and ring finger of women Carpal tunnel syndrome (secondary to neuropathy vs entrapment) Adhesive capsulitis, or periarthritis, with global versus regional tightness Figure 11-10 The prayer sign. The individual is unable to press the palms flat against each other, a diagnostic sign for the syndrome of limited joint mobility in diabetic persons. Other conditions also may result in loss of extension with a positive prayer sign. (From Kaye T: Watching for and managing musculoskeletal problems in diabetes, J Musculoskel Med 11:25-37, 1994.) Figure 11-11 Dupuytren’s contracture. Painless nodules develop in the distal palmar crease, often in line with the ring finger, that slowly mature into a longitudinal cord that is readily distinguishable from a tendon. The skin overlying the nodules is usually puckered. The contracture may be symptomatic (painful), but with or without pain it results in impaired hand function. (From Kaye T: Watching for and managing musculoskeletal problems in diabetes, J Musculoskel Med 11:25-37, 1994.) |
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Musculoskeletal Sequelae of DM: spine and Lower extremity
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Read spine p 495-496, osteoporosis p 496
Diffuse idiopathic skeletal hyperostosis: -osteophytes develop into bony spurs -Thoracic spine most commonly affected: si joint spared -unknown pathogenesis Osteoporosis: - most severe in type I -Inadequate bone matrix formation due to insufficient insulin - risk of fractures Joint contractures: knees and spine Figure 11-12 Diffuse idiopathic skeletal hyperostosis (DISH), or ankylosing hyperostosis, associated with type 2 diabetes mellitus (DM). DISH can occur with other conditions such as ankylosing spondylitis. Although the dense anterior bony bridging of the cervical vertebrae is pictured on this lateral roentgenogram, the thoracic spine most commonly is involved in diabetes. This type of DISH can be distinguished from ankylosing spondylitis by the preservation of sacroiliac joints, a site of typical involvement in ankylosing spondylitis. (From Kaye T: Watching for and managing musculoskeletal problems in diabetes, J Musculoskel Med 11:25-37, 1994.) |
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Screening and diagnosis of Diabetes
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Read screening and diagnosis pp 497-498
Screening – CDC recommends diabetes testing begin at age 25. Because 1⁄4 of all new cases occur in persons under age 20, CDC recommends screening begin at age 25. ADA (America Diabetes Association) recommends screening at age 45 and earlier for high risk groups including non-Caucasians, obese and those with family history of type 2 DM in a 1st degree relative Diagnosis - The following tests are used for diagnosis A fasting plasma glucose test measures your blood glucose after you have gone at least 8 hours without eating. This test is used to detect diabetes or pre-diabetes. Normal: <99 mg/dL pre-diabetes: 100-125 mg/dL Diabetes: > 126 mg/dL An oral glucose tolerance test measures your blood glucose after you have gone at least 8 hours without eating and 2 hours after you drink a glucose-containing beverage. This test can be used to diagnose diabetes or pre-diabetes. 2 hour plasma glucose result: Normal: <139 mg/dL Pre-diabetes: 140-199 Diabetes: >200 |
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Management of Diabetes
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Read treatment pp 499-500
Goal is regulation of blood glucose vs. cure Type 1 requires exogenous insulin (via injections or insulin pump) to maintain tight (near normal) glucose control and diet, exercise recommended, but not proven to provide increased glycemic control Type 2: - diet and hypoglycemic drugs - sometimes insulin - exercise a major contributor in control of hyperglycemia Read diabetes and exercise, general exercise considerations pp 504-509, refer to Box 11-6 key points to remember, p 505 Exercise is a recognized therapy for DM, esp. for glycemic control with type 2 DM Affects carbohydrate metabolism and insulin sensitivity Helps prevent CV disease and HTN Raise LDL Manage obesity |
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Glucose Control
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Read glucose monitoring p 498-499; exercise and insulin pump pp 508-509
Tight glucose control delays onset and progression of diabetic complications Every percentage point drop in A1c blood test results (e.g., from 8.0% to 7.0%) can reduce the risk of microvascular complications (eye, kidney, and nerve diseases) by 40%. Read complications of insulin therapy – hypoglycemia p 503; Table 11-16 clinical signs and symptoms of hypoglycemia p 503 Figure 11-14A, B The programmable insulin pump. Compact and worn like a pager, the programmable insulin pump delivers fixed amounts of insulin continuously, based on blood glucose levels determined by regular fingerstick glucose monitoring. The device includes the pump itself (including controls, processing module, and batteries), a disposable reservoir for insulin (inside the pump), and a disposable infusion set, including a cannula for subcutaneous insertion (under the skin) and a tubing system to interface the insulin reservoir to the cannula. (Courtesy Mini-Med, Sylmar, CA, 2000.) |
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Natural history of diabetes (timeline)
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Starts with genetic susceptibility along with environmental factors (nutrition, obesity, inactivity) - symptoms of insulin resistance, hyperinsulemia, decreased HDL lead to
Onset of diabetes symptoms of hyperglycemia and hypertension Lead to complications -nephropathy -neuropathy -retinopathy -atherosclerosis lead to Disability -blindness -renal failure -CHD -amputation lead to Death Read treatment of long-term complications pp 501-502, prognosis pp 502-503 IGT – impaired glucose tolerance For fact sheets on diabetes refer to International Diabetes Federation http://www.idf.org/diabetes-fact-sheets |
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Type I diabetes and exercise
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Read exercise and type 1 DM p 506
Can increase strength and facilitate weight management Not proven to provide increased glycemic control But Can result in hyperglycemia: with type 1 DM, too little insulin is available and the cells sense starvation, so glucagon and catecholamines are released further increase glucose mobilization into the bloodstream and increase blood glucose (hyperglycemia) |
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Type II diabetes and exercise
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Benefits:
increased carbohydrate metabolism improves insulin sensitivity and binding weight control Improves lipid profile decreases blood pressure Hypoglycemia not common, except with exogenous insulin Read exercise in type 2 DM pp 507-508 Read balancing insulin, food and exercise p 508 Read exercise precautions p 506 |
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Contraindications for exercise with DM (box 11-7)
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Poor control of blood glucose levels (>250 mg/mL)
unevaluated or poorly controlled associated conditions: neuropathy, nephropathy, hypertension, retinopathy Suspected or unstable heart disease Recent surgery Dehydration Extreme climate Hypoglycemia (BG<70) - shakiness, dizziness, headache, sweating, hunger Hyperglycemia (>300mg/dL) - dispnea, dry mouth, nausea |
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Type II diabetes and exercise: implications for PT
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Have snacks or glucose tablets on hand
Have glucose monitor (in clinic or w/ pt): check before and after activity Preferably exercise when insulin levels are low and not fasting don't exercise right before bed Inject insulin away from part of body involved in exercise Consider existing complications when choosing exercise module (neuropathy, hypertension) Foot care (monitor areas with swelling, skin changes, etc.), joint stabilization, maintaining muscular strength, minimizing risk of trauma |
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Pre-diabetes or insulin resistance
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Prevalence:
~54 million individuals Read insulin resistance syndrome pp 512-513, special implications for the therapist p 512-513 insulin resistance syndrome/metabolic syndrome Insulin resistance syndrome – condition with higher than normal blood glucose levels Not high enough to be classified as diabetes People with prediabetes have impaired fasting glucose (IFG) or impaired glucose tolerance (IGT). Some people have both IFG and IGT. Progression to diabetes among those with prediabetes is not inevitable. Studies show that people with prediabetes who lose at least 7% of their body weight and engage in moderate physical activity at least 150 minutes per week can prevent or delay diabetes and even return their blood glucose levels to normal. For persons with prediabetes who did not lose weight and engage in moderate physical activity, 11% progressed to diabetes annually. |
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Metabolic Syndrome
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Syndrome X
3 or more of 5 following risk factors: Central obesity High blood pressure high triglycerides Low HDL Insulin resistance People with the metabolic syndrome are at increased risk of coronary heart disease, stroke, peripheral artery disease (PAD), and type 2 DM. Estimated that over 50 million in US have metabolic syndrome. The dominant underlying risk factors for metabolic syndrome: •abdominal obesity •insulin resistance Metabolic syndrome is also called insulin resistance syndrome. Some people are genetically predisposed to insulin resistance. Environmental factors, such as excess body fat and physical inactivity, can elicit insulin resistance and the metabolic syndrome in genetically predisposed people. Most people with insulin resistance have abdominal obesity. The biologic mechanisms at the molecular level between insulin resistance and metabolic risk factors are not fully understood. Refer to p 489 Prediabetes – pay attention to difference in following terms: •Prediabetes •Insulin resistant syndrome •Metabolic syndrome – includes central obesity, insulin resistance (the “prediabetes” component) and dyslipidemia. |
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Two Major Components of Blood are examined:
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1. Plasma
2. Formed elements • Erythrocytes – red blood cells – transport oxygen to body tissues & exchanges for carbon dioxide (role of hemoglobin) • Most numerous of the circulating blood cells • Leukocytes – white blood cells – defense against disease, injury & harmful microorganisms/foreign substances; removes debris from injured tissue and aids in tissue repair & healing process • Thrombocytes – platelets – mechanisms for blood coagulation |
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Disorders of Erythrocytes
Disorders of Leukocytes Disorders of Thrombocytes – Disorders of Hemostasis Hemoglobinopathy – |
Disorders of Erythrocytes
Will briefly discuss Anemias in class Disorders of Leukocytes Neoplastic Disorders of Blood and Lymph Systems Will cover Leukemias, Lymphomas in class Disorders of Thrombocytes – Disorders of Hemostasis Will cover haemostatic disorder in class – Hemophilia Hemoglobinopathy – Condition that results from abnormality in formation of hemoglobin - Sickle Cell Disorders |
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Hemolytic Anemia
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Hemolytic anemia is a condition in which there are not enough red blood cells in the blood, due to the premature destruction of red blood cells.
There are many types of hemolytic anemia, which are classified by the reason for the premature destruction of red blood cells. The defect may be in the red blood cell itself (intrinsic factors), or outside the red blood cell (extrinsic factors). Sickle cell disease results in sickle cell anemia. Has both intrinsic factor (defect in RBC) and extrinsic factor (Blood clots in small blood vessels). Both contribute to clinical manifestation of SCD. |
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Anemias
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Anemias
Reduction in oxygen-carrying capacity of blood because of abnormality in quantity or quality of erythrocytes (RBCs). WHO defines anemia based on level of hemoglobin Less than 14g/dL ♂ 100ml = 1 dL (deciliter) Less than 12g/dL ♀ Anemia is not a disease, but a symptom of many other disorders such as: • Acute or chronic blood loss (iron deficiency), could be 2ndary to chronic NSAID use •Dietary deficiency (referred to as nutritional anemia). Malabsorption syndrome, B12, iron • Congenital defects of hemoglobin (sickle cell diseases) • Diseases of bone marrow • Chronic inflammatory, infectious or neoplastic diseases (RA or SLA, or TB or AIDS, or Cancer) • Or any disorder that upsets balance between blood loss through bleeding or destruction of blood cells & production of blood cells TUMOR. May be malignant or benign. • Exposure to industrial poisons (eg radiation) • Will learn blood lab values and exercise guidelines in Medical Therapeutics and Cardiopulmonary Therapeutics later in the curriculum. |
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In men and postmenopausal women,
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anemia is usually caused by gastrointestinal blood loss associated with ulcers, the use of aspirin or nonsteroidal anti-inflammatory medications (NSAIDS), or certain types of cancer (esophagus, stomach, colon).
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Etiology – Causes (Table 14-3, p 686 Causes of Anemia by Category)
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Etiology – Causes (Table 14-3, p 686 Causes of Anemia by Category) 1. Excessive blood loss - Hemorrhage
• Trauma, wound • GI cancers • Bleeding ulcer • Excessive menstruation • Bleeding hemorrhoids 2. Destruction of Erythrocytes (RBCs) – Hemolytic Anemia • Autoimmune conditions • Immune system produces antibodies that clump (agglutinate) a person’s own RBCs together • Immune system thinks the clumps are foreign bodies & destroys them (phagocytosis) • Hemolytic anemia – associated with SLE, leukemias, lymphomas • Sickle cell diseases – hemoglobinopathy-related anemias as result of destroyed erythrocytes 3. ↓ production of RBCs • Chronic diseases (RA, SLE, TB, cancer) may decrease production of RBCs • Characterized by moderate decrease in RBC survival; bone marrow cannot compensate for decreased RBC life span • Nutritional deficiency (iron, Vit B12, alcohol abuse, folic acid deficiency) • ↓ bone marrow stimulation (hypothyroidism) • Bone marrow failure (leukemias) 4. Faulty hemoglobin production – ie Thalassemia an inherited chronic anemia, initially found among Mediterranean peoples, resulting from faulty hemoglobin production |
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Clinical Manifestations of Anemia
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Figure 14-1: Normal nail on the right compared with nail on the left is referred to as koilonychia and sometimes called spoon-shaped nails or spoon nails. They are thin, depressed nails with lateral edges turned up and are concave from side to side. They may be idiopathic, congenital, or a hereditary trait and are occasionally due to iron deficiency anemia.
Hematocrit is a blood test that measures the percentage of red blood cells found in whole blood. This measurement depends on the number of red blood cells and the size of red blood cells. Hemoglobin is a protein in red blood cells that carries oxygen. A blood test can tell how much hemoglobin you have in your blood. Both are determined as part of a complete blood count. Mild anemia: • Minimal & vague symptoms of fatigue Once hemoglobin and hematocrit fall below 1⁄2 of normal, symptoms progress and are quite obvious: • Weakness • SOB on exertion • Easy fatigue •P allororyellownessofskin,especiallypalms,fingernails,mucosa, conjunctiva • Changes in nails • Tachycardia • Increased angina in pre-existing CAD Severe anemia: • Sensory neuropathy – moderate pain or paresthesias of extremities, especially feet, loss of proprioception • Loss of motor function – usually symmetrical • Heart failure, hypoxic damage to liver & kidneys Vague symptoms until hematocrit and hemoglobin fall below half of normal |
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Medical Management and Prognosis for Anemia
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Critical to determine cause to guide treatment
Prognosis: nutritional deficiency - good hemolytic - poorer Aplastic - serious form that can be deadly Modern medical treatment for Anemia depends on etiology, examples: • Pharmacological – EPO (Epogen, recombinant human erythpoetin for treatment of anemia related to chronic disease • Bone Marrow transplant • Vitamin B12, folic acid or iron supplementation for nutritional deficits • Many, many others • Hemolytic anemia - anemia caused by excessive destruction (as in chemical poisoning, infection, or sickle-cell anemia) of red blood cells |
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PT implications - Anemia
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Impact of anemia on functional recovery in acute care setting or rehabilitation setting and risk for increased morbidity and mortality not thoroughly investigated. (increased incidence of disease and increased death rate)
• Need further study to examine implications of anemia on functional recovery and cardiopulmonary complications during acute care and rehabilitation. Current Guidelines (until proven protocols are developed) 1. Exercise for patient, or any person, with anemia should be approved first by the individual’s physician. 2. Increased physical activity will increase oxygen demand, which may not be adequate in circulating blood in persons with anemia. • Diminished exercise tolerance • Easy to fatigue • Use pacing and exercise that distributes workload over time to promote physiologic recovery • Extreme caution with exercise testing • VO2max is at least 20% lower for anemic client • Can still exercise if severely anemic, but at lower intensity |
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Signs of Anemia
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One of most common seen clinically – GI blood loss associated with NSAID use worsens suddenly precipitating crisis in therapy setting.
• Vomiting blood, passing blood in stool • Patients with severe bleeding may present with signs of shock (eg, tachycardia, tachypnea, pallor, diaphoresis, oliguria, confusion). • Patients with severe bleeding may faint (syncope) • Patients with underlying ischemic heart disease may develop angina or MI because of hypoperfusion. 2. Bleeding under the skin and easy bruising of skin may result when platelet count is low (thrombocytopenia) secondary to some types of anemia (hypoplastic or aplastic anemia) • Extreme care with manual techniques or equipment to avoid injuring skin 3. Decreased oxygen delivery to tissues results in impaired healing • To skin – loss of elasticity, delayed healing • Delayed wound healing • Delayed healing of musculoskeletal injuries 4. PNS & CNS affected by pernicious anemia (2° to vit B12 deficiency) • Paresthsias, esp. numbness mimicking carpal tunnel syndrome • Gait disturbances • Extreme weakness • Spasticity • Abnormal reflexes • Responds well to therapy, but in extreme cases where intervention has been delayed neurologic damage is unresponsive to vitamin B12 therapy. Vital Signs – Resting cardiac output normal in persons with anemia, but as anemia progresses resting CO will increase and exercise tolerance progressively decreases until dyspnea, tachycardia and palpitations occur at rest. |
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ne·o·plasm n.
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An abnormal new growth of tissue that grows by cellular proliferation more rapidly than normal, continues to grow after the stimuli that initiated the new growth cease, shows partial or complete lack of structural organization and functional coordination with the normal tissue, and usually forms a distinct mass of tissue which may be either benign or malignant.
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Hematologic cancers include
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diseases in any hematologic and lymphatic tissues (spleen, bone marrow, lymph nodes), that arise from single cell mutations producing malignant clones (genetically identical cells) and metastases to bone marrow where clones have a growth advantage over normal cells in the bone marrow
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Neoplastic Disorders
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The Leukemias - Malignant neoplasm of blood-forming cells 2. Lymphomas - Cancer affecting lymphatic system (ie lymph nodes & spleen) 3. Multiple Myeloma - excessive growth and malfunction of plasma cells in the bone marrow.
• The growth of these extra plasma cells interferes with the production of red blood cells, white blood cells, and platelets. This causes anemia, susceptibility to infection, and increased tendencies toward bleeding. • Complications include hypercalcemia and spinal cord compression 4. Myeloproliferative Disorders - increased production of bone marrow elements, such as erythroid, myeloid and platelet cells • Polycythemia Vera • Polycythemia vera is an acquired disorder of the bone marrow that causes the overproduction of all three blood cell lines:, primarily red blood cells, white blood cells and platelets. • Develops slowly, and most patients do not experience any problems related to the disease after being diagnosed. However, the abnormal bone marrow cells may begin to grow uncontrollably in some patients leading to acute myelogenous leukemia. • Increased tendency to form blood clots that can result in strokes or heart attacks. Some patients may experience abnormal bleeding because their platelets are abnormal. PT must be alert to signs of DVT. |
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Neutrophils –
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most numerous circulating leukocyte, very important for body protection • Granules stain with a neutral dye, resulting in lilac color • Motile, highly phagocytic, ingest & devour bacteria • First cell to appear at site of injury or infection
• If serious deficiency of this cell type, person will die despite protective responses of other body defenses. |
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Eosinophils –
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protect body from animal parasite infestations • Granules stain with red acidic dye called eosin • Protect body by releasing substances that neutralize toxic compounds
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Basophils –
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important role in inflammatory response to tissue damage • Granules readily stain with purple alkaline (basic) dye
• Release histamine – initiates inflammatory response by increasing blood flow to carry in additional nutrients, immune substances & cells to help contain and repair damage • Release heparin – anticoagulant, prevents blood from clotting as injury site. |
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Agranulocytes –
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also arise in bone marrow from stem cells, nuclei do not form lobes, also called
mononuclear leukocytes. |
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Monocytes –
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chief role in many activities associated with specific immunity
• mildly phagocytic when within blood vessels, but they remain in vascular channels only a short time. When exit circulatory system, transform into macrophages, avid phagocytes that ingest pathogens, dead cells & debris at site of inflammation. |
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• Lymphocytes –
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immune response • B cells, T cells – specific immune response; humoral & cellular immunity
• NK cells – generalized response whenever potentially dangerous or abnormal cell. Highly effective against cancer cells & cells harboring pathogens. |
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Leukemia
Oncological disorder of blood forming organs, characterized by |
an overgrowth (proliferation) of blood cells
• With rapid proliferation of malignant/leukemic cells, bone marrow becomes overcrowded with WBCs, or leukocytes, which then spill over into peripheral circulation – thus the name Leukemia. • Crowding of bone marrow by leukemic cells inhibits normal blood cell production. • Replacement of bone marrow by malignant clones of lymphocytes or bone marrow cells results ultimately in bone marrow failure. • |
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Leukemia Classified by
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Classified by type of leukocytes affected (myelogenous or lymphocytic). Further
classified as chronic or acute. Lymphocytic forms involve lymphocytes and lymphoid organs Myelogenous leukemia involves hematopoetic stem cells that differentiate into myeloid cells • Acute forms – cells are highly embryonic (blastic) with few mature forms, resulting in severe anemia, infections and bleeding disorders. • Life threatening forms • Chronic forms – proliferation of blastic cells but usually enough mature cells to carry on functions of the various cell types. |
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Three main symptoms of “infiltration and replacement”: in Leukemia
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Three main symptoms of “infiltration and replacement”:
1. Anemia • Reduced tissue oxygenation from decreased erythrocytes 2. Infection • Leukemic cells are functionally unable to defend body against pathogens 3. Bleeding tendencies • Decreased platelet production – platelets play a key role in normal blood clotting. • During the clotting process, platelets clump together to plug small holes in damaged blood vessels |
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Adult and childhood leukemias
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Adult Leukemia
Leukemia is one of the ten most common types of cancer diagnosed, and there seems to be a slightly higher occurrence in men than in women. CLL (100% adults; AML – 80% adults; CML - ~95-98% adults) Childhood Leukemia Leukemia is the most common cancer diagnosed among children and young adults, equal to one third of all cases of cancer in children under 15 years old, and one fourth of all cancer cases in patients under 20. This year, 2600 children will be diagnosed with Leukemia, 70% with ALL (Acute Lymphocytic Leukemia) and 20% with AML (Acute Myelogenous Leukemia). Chronic Leukemia is very rare among children. (CML only ~2% or less) Most childhood Leukemia patients are diagnosed between the ages of 3 and 7 years old. overview p. 693 |
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Figure 14-2: Pathologic basis for the clinical manifestations of leukemia. Leukemia is not limited to bone marrow and peripheral blood.
Infiltration and replacement with nonfunctional leukemic cells in other tissues in the body affects multiple organ systems |
Epistaxis - nose bleed
Ecchymosis –bleeding into the skin or mucous membranes, aside from the common bruise, which shows up on skin but bleeding may come from other deeper tissues as well as skin. Petechiae - Bleeding that consists of pinpoint dots of blood Purpura - Larger flat areas where blood has collected under the tissue, up to a centimeter in diameter Hyperuricemia - presence of high levels of uric acid in the blood. The upper end of the normal range is 530 micromol/L (6 mg/dL) for women and and 619 micromol/L (7 mg/dL) for men. [1] Hyperuricemia is caused either by accelerated generation of uric acid through purine metabolism or by impaired excretion in the kidney |
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Definition of ALL
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Acute lymphocytic leukemia is a common, progressive, malignant disease characterized by large numbers of immature white blood cells that resemble lymphoblasts. Acute lymphocytic leukemia results when cancerous cells lose their ability to mature. These cancerous acute lymphocytic leukemia cells multiply and start to overtake the normal cells. As your normal blood cells start to reduce in number, you can become more susceptible to bleeding and infection. These types of cells can be found in bone marrow, blood, lymph nodes, spleen, and other organs.
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Causes, incidence and risk factors for ALL
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Causes, incidence, and risk factors
It is believed that ALL accounts for approximately 80% of all the acute childhood leukemias. Most cases appear between the ages 3 and 7. Acute lymphocytic leukemia also occurs in adults. Adult acute lymphocytic leukemia makes up approximately 20% of all adult leukemias. Of the 4000 cases diagnosed each year, 2/3s occur in children and 1/3 in adults. 1500 annual deaths, almost 2/3s of these in adults. •M ost cases seem to have no apparent cause. However, radiation, some toxins such as benzene, and some chemotherapy agents are thought to contribute. Abnormalities in chromosomes may also play a role in the development of acute leukemia. •R isk factors for acute leukemia include Down syndrome, a sibling with leukemia, and exposure to radiation, chemicals, and drugs. The disease strikes 6 out of every 100,000 people. |
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Acute Myelogenous Leukemia
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There are 11 categories of AML, categorized as M0 to M7, based on which blood cells are abnormal.
Starts inside bone marrow - in stem cells that would normally differentiate Stem cells lose ability to mature and specialize - malignant cells multiply rapidly, replace normal cells Bone marrow failure occurs Picture of skin lesions with Acute Monocytic Leukemia. •T hese lesions are a common finding in acute forms, rarely found in chronic leukemia. •L esions appear as small solid rounded red bumps red on skin, or small flat red bumps on the skin or red, thick skin covered with silvery scales. • The lesions may be itchy. |
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Causes, incidence, and risk factors
of AML |
Causes, incidence, and risk factors
Acute myelogenous leukemia (AML) may occur at any age, but it primarily affects adults (80%) and young children (20%). In this condition, hematopoetic stems cells (that differentiate into monocytes, granulocytes, erythrocytes and platelets) which grow in the bone marrow, lose their ability to mature and specialize (differentiate). •T hese cells multiply rapidly and replace normal blood cells. •B onemarrowfailureoccursasmalignantcellsreplacenormalbonemarrow. Patients with AML are susceptible to bleeding and infection as the normal blood cells lose their ability to fight microorganisms and decrease in number. Most cases have no apparent cause. However, radiation, some toxins such as benzene, and some chemotherapy drugs (including etoposide and drugs known as alkylating agents) are thought to cause some kinds of leukemia, including AML. Genetic abnormalities may also play a role in the development of this condition. |
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Chronic Lymphcytic Leukemia
Causes, incidence, and risk factors |
Causes, incidence, and risk factors
Usually the symptoms develop gradually, staging used to indicate severity of progression. The incidence is about 2 per 100,000 (25-30% of all leukemias) and increases with age (~100% of cases are found in people over 50). Many cases are detected by routine blood tests in people with no symptoms. The cause of CLL is unknown. Some correlation with exposure to farming pesticides and chemical warfare pesticide Agent Orange, conclusive evidence lacking Some groups may have genetic predisposition – including people with 1st degree family member with CLL Mean survival, 10-14 years (survival ranges from 8 – 25 years) |
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Chronic Lymphocytic Leukemia - CLL
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Common adult leukemia
Causes a slow increase in number of mutated B lymphocytes in bone marrow Cancerous cells spread to blood and can affect lymph nodes and other organs CLL causes bone marrow to fail and weakens immune system |
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Causes, incidence, and pathology of Chronic Myelogenous Leukemia
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Causes, incidence, and pathology
•More than 90% of cases associated with a single specific genetic mutation in chromosome called the Philadelphia chromosome. • Exposure to severe ionizing radiation is one possible trigger for this chromosome abnormality. Such exposure could occur from a nuclear disaster or from treatment of a previous cancer, like thyroid cancer or Hodgkin's lymphoma. • However, the vast majority of people treated for cancer with radiation do not go on to develop leukemia. •C ML accounts for 20% of all leukemias affecting adults. It typically affects middle-aged adults. Uncommonly, the disease occurs in younger individuals. Younger patients may present with a more aggressive form of CML, such as in accelerated phase or blast crisis. Uncommonly, CML may appear as a disease of new onset in elderly individuals. • CML affects 1 to 2 people per 100,000 and accounts for 15% to 20% of all leukemias. • CML progresses through 3 phases: chronic, accelerated, and blast. • • • In the chronic phase of disease, mature cells proliferate; can last for months or years, many have few or no symptoms during early chronic phase. Eventually progresses to more dangerous accelerate phase in the accelerated phase, additional cytogenetic abnormalities occur; luekemic cells grow more quickly, may show sxs of fever, infection, bone pain & enlarged spleen Approximately 85% of patients are diagnosed in the chronic phase and then progress to the accelerated and blast phases after 3-5 years. Difficult to treat, Bleeding and infection may occur due to bone marrow failure. •The diagnosis of CML is based on the histopathologic findings in the peripheral blood and the Philadelphia chromosome in bone marrow cells |
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Chronic myelogenous leukemia (CML),
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Chronic myelogenous leukemia (CML), also known as chronic myeloid leukemia, is a myeloproliferative disorder characterized by increased proliferation of the granulocytic cell line without the loss of their capacity to differentiate. Consequently, the peripheral blood cell profile shows an increased number of granulocytes and their immature precursors, including occasional blast cells.
Neoplasm of Hematopoetic Stem Cell Causes rapid growth of blood-forming cells in bone marrow, and increased granulocytes , typically basophils and eosinophils |
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Special implications for PT for Leukemias
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p 700
Patient may be weak from abnormal blood counts and/or cancer treatments Interventions: Strength training gently according to blood value guidelines Cardio and stretching education Safety and fatigue management Joint involvement: Arthralgias or arthritis leukemic infiltrates of periosteum, synovium, periarticular bone Very painful, transient ROM exercise, stretching Manual therapy, massage |
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More special implications for PT for leukemias
precautions |
Preferred Practice Pattern depends on clinical signs & response to medical interventions or other treatments
1. Remission - highly susceptible to spontaneous hemmorhage and infection - Specific precautions for infection control, be aware of signs - exercise precautions like anemia 2. Side effects of medications - fatigue, loss of appetite - mood changes -depression -irritability |
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Two distinct groups of Lymphoma.
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Hodgkin’s disease usually affects young adults, though children & older adults may be affected (prognosis is poorer for older adults)
NHL – less common (3-5% of all malignancies in US), most common neoplasm of adults between ages 20-40 In the past 5 years, research has progressed and the distinction in the two types is beginning to obscure. More useful to categorize lymphomas according to clinical behavior – indolent or aggressive – and chromosomal features. HL – Characteristic type of cell – Reed-Sternberg cell All other forms of lymphoma are categorized as NHL. |
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Definition, causes, incidence, and risk factors of Hodgkin lymphoma
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Definition
Hodgkin's lymphoma is a malignancy (cancer) of lymph tissue found in the lymph nodes, can spread to spleen, liver, bone marrow and lungs. Causes, incidence, and risk factors The first sign of this cancer is often an enlarged lymph node which appears without a known cause. The disease can spread to nearby lymph nodes and later may spread to the lungs, liver, or bone marrow. Reed-Sternberg cell is primary finding in lymph nodes. • Part of tissue macrophage system • Twin nuclei & nucleoli with appearance of owl eyes The cause is not known. Most cases 20-30 or over 55, only 10% cases younger than 16 |
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Symptoms of Hodgkin Lymphoma
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Symptoms
Usually begins with a painless enlargement of lymph nodes, typically on one side of the neck, chest or underarm; occasionally groin. Fatigue Fever and chills Night sweats Weight loss Loss of appetite Generalized itching – pruritis (severe itching) Progressive anemia |
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More signs and symptoms of Hodgkin Lymphoma
(map of body) |
Pruritus (severe itching)- A sensation that the patient instinctively attempts to relieve by scratching or rubbing. Common early sign
Irregular fever Hepatosplenomegaly Anemia Pulmonary symptoms including nonproductive cough, stridor, dyspnea, chest pain, cyanosis, and pleural effusion Stridor - is an abnormal, high-pitched, musical breathing sound caused by a blockage in the throat or larynx, It is usually heard when inhaling. A significant sign of airway obstruction, can be obstructed by an object, by swelling of the tissues of the throat or upper airway, or by spasm of the airway muscles or the vocal cords. Superior vena cava syndrome (SVCS) is characterized by gradual, insidious compression/obstruction of the superior vena cava (SVC). SVCS is associated chiefly with malignancy. Currently, more than 90% of patients with SVCS have an associated malignancy as the cause. Dyspnea is the most common symptom, followed by trunk or extremity swelling. Facial swelling, Cough, Orthopnea, Headache, Nasal stuffiness, Light-headedness. Alcohol-induced pain in bone, in lymph nodes, or around the mediastinum occurs immediately after drinking and lasts 30-60 min invasion of pericardium bone pain paraplegia from spinal cord compression |
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Ann Arbor Staging Classification for HD
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1. Stage I–involvement of a single lymph node, group of nodes, or a single extra lymphatic (outside the lymph nodes) site (eg spleen, thymus) except liver and bone marrow
2. Stage II indicates involvement of 2 or more lymph node regions on the same side of the diaphragm (for example, both sides of the neck) or an extra lymphatic site and its regional lymph nodes with or without lymph nodes on the same side of the diaphragm. 3. Stage III indicates lymph node regions on both sides of the diaphragm(for example, groin and armpit). 4. Stage IV involves the spread of cancer outside the lymph nodes (for example,to bone marrow, lungs, liver, skin). • Treatment varies with the stage of the disease; treatment is highly effective • Radiation & chemotherapy important interventions • Bone marrow transplants • The best treatment for an individual patient depends on many factors, and should be discussed in detail with a doctor who has experience treating this disease. • Chemotherapy can cause low blood cell counts, which can lead to an increased risk of bleeding, infection, and anemia. Stage I and II have several treatment options Stage III and IV just treated with chemotherapy further classification: A = without symptoms B = with Considered one of the most curable forms of cancer |
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Non-Hodgkin Lymphoma
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Definition
Non-Hodgkin's lymphomas are cancers of lymphoid tissue (lymph nodes, spleen, and other organs of the immune system) – present as solid tumors. Classified as either B cell or T cell lymphomas. The latest lymphoma classification, the 2008 WHO classification, largely abandoned the "Hodgkin" vs. "Non-Hodgkin" grouping. Instead, it lists over 70 different forms of lymphomas in four broad groups. Causes, incidence, and risk factors Non-Hodgkin's lymphomas can be slow-growing (low-grade) or rapidly growing (high-grade) cancer. For most patients, the cause is unknown, but lymphomas often develop in people with suppressed immune systems. 95% with non-Hodgkin's lymphomas are adults. Average age of onset between 60-70 years of age. Over 67,000 develop NHL each year – 5th most common cancer in US. Symptoms Enlarged lymph nodes (such as an armpit lump), isolated or widespread Fever Excessive sweating, with night sweats Unintentional weight loss Treatment Treatment depends upon the stage of the disease. Low-grade disease may just need to be observed with no treatment until it causes problems (early treatment is not more effective). When treatment becomes necessary, chemotherapy or radiation therapy may be used. Patients with more aggressive or resistant disease may require more intensive treatment. High-dose chemotherapy with bone marrow transplantation may be a treatment option in selected cases. Expectations (prognosis) The average survival is 6 to 8 years for patients with low-grade lymphoma. The outcome for patients with high-grade lymphoma depends upon the response to chemotherapy or other treatment, and the type of high-grade lymphoma. About 30% of adults with high-grade lymphoma are permanently cured. About half of people survive 10 years |
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Implications for PT - lymphoma
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p. 706, 709
PT may find enlarged painless lymph nodes during routine cervical spine, shoulder or hip examination. • Normal lymph nodes that can be palpated usually 1 cm in diameter, soft to firm consistency, move freely and easily without tenderness •S uspiciousifgreaterthan1cmindiameter,firmandrubbery and/or tender • Enlarged lymph nodes associated with infection are more likely to be tender than slow-growing nodes associated with cancers. •A nychangesinsize,shape,tendernessandconsistencyshould raise red flag. •C ommon metastatic sites: • Lung, breast, testicular cancer – supraclavicular nodes •T umors in legs, perineum, prostate, genitals – inguinal nodes • If patient has past medical history of cancer, immediate medical referral. And if family history of HL – refer as soon as possible. Non-Hodgkin’s Lymphoma – association between use of methotrexate in RA and development of NHL •Uncommon, but has been reported. If patient is receiving methotrexate for RA complains of back pain accompanied by constitutional symptoms and/or GI symptoms and/or enlarged lymph nodes are found at any nodal sites – make medical referral. Monitor vital signs and lab values Considerations: physical deconditioning, weakness Decreased endurance Decreased balance impaired mobility Respiratory Impairment lymphedema side effects of chemo and/or radiation |
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Hemostasis –
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a series of interlinked reactions, each requiring a specific factor. If any of the factors are absent, a clot will not form.
• See movie file on BbLearn for hemostasis reactions • Initially blood vessel constricts & platelets become “sticky” • Platelets aggregate at injury site & provide barrier to contain blood loss. • Clotting factors in platelets & injured tissue release thromboplastin, substance that initiates clot formation. • Final step of coagulation – fibrinogen (a soluble blood protein) becomes insoluble & forms fibrin strands acting like a net, entrapping blood cells. This mass of blood cells & fibrin = blood clot or thrombus. |
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Definition Hemophilia
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•Hemophilia is a hereditary bleeding disorder in which it takes a long time for the blood to clot and abnormal bleeding occurs.
Cause •Hereditary bleeding disorder of specific blood clotting factors. • Approximately13differentclottingfactorsinadditionto calcium and several proteins The disorder is sex-linked; caused by an inherited X-linked recessive trait, with the defective gene located on the X chromosome., found most commonly in males. Women are carriers. • An autosomal recessive trait , which means it occurs in someone who has inherited the mutant sickle hemoglobin gene from both parents. |
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Definition Sickle Cell Disease & Anemia
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•Sickle cell disease is an inherited disease in whichRBCs,normallydisc-shaped, become crescent shaped.
• Sickle cell disease is much more common in certain ethnic groups, affecting approximately one out of every 500 African Americans. As a result, the RBCs function abnormally and cause small blood clots. These clots give rise to recurrent painful episodes called "sickle cell pain crises." Cause •SicklecellanemiaiscausedbyanabnormaltypeofhemoglobincalledhemoglobinS. • Hemoglobin is a protein inside red blood cells that carries oxygen. Hemoglobin S, however, reduces the amount of oxygen inside the cells, distorting their shape. |
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For most of history, people who had hemophilia frequently died or were disabled by joint- or organ-damaging bleeding. Today, the prognosis for people with hemophilia has vastly improved because of
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identification and development of clotting factors.
The identification of the clotting factors in the 1960s and the ability to treat people with clotting factors drawn from donated blood led to longer, healthier lives. However, in the late 1970s and early 1980s, many people with hemophilia were infected with viruses that were transmitted through blood donations, including hepatitis and HIV, the virus that causes AIDS. •I n the early 1980s, about half of the people with hemophilia contracted HIV through blood products and many of them died, according to the National Hemophilia Foundation. • Blood screening for HIV & hepatitis viruses began in 1985, which has essentially stopped this form of transmission. In 1992, researchers were able to synthesize blood clotting factors in laboratory proteins, without the need of human blood. |
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Types and severity of hemophilia
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Hemophilia A “Classic Hemophilia – 80% have this type; 60% severe hemophilia
Hemophilia B “Christmas Disease” – 15% have this type Mild - 5-50% clotting factor, 25% have this type Moderate - 1-5% clotting factor, 15% Severe - less than 1%, 60% of all cases Two main types of hemophilia: 1. Hemophilia A (also known as classic hemophilia or factor VIII deficiency). Clotting factor VIII is low or missing in the patient. About 90 percent of people with hemophilia have this type. • About 80 percent of the patients with this type of hemophilia have severe hemophilia. 2. Hemophilia B (also known as Christmas disease or factor IX deficiency). Clotting factor IX is low or missing in the patient. About 15 percent of people with hemophilia have this version of the disorder. Christmas disease refers to the first patient with hemophilia B who was studied in detail, Stephen Christmas. 3. Hemophilia C. Clotting factor XI is low or missing in the patient. This type of hemophilia is extremely rare in the United States and symptoms are typically mild. Degree of the deficiency varies from mild to severe. Mild symptoms • Nosebleeds • Easy bruising • Bleeding from gums Severe symptoms • Areas of blood seepage within joints (hemarthosis), muscles (hematoma) • Uncontrolled bleeding leading to shock & death |
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Hemathrosis –
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bleeding into a joint space, one of the most common clinical manifestations of hemophilia; typically synovial joints:
• Knees •A nkles •E lbows • H i p s • Shoulders • Wrist (in order of most common occurrence) • Bleeding in joint space leads to pain and possibly permanent deformity. Classification schemes, also using MRI methods for scoring joints changes. US, Canada, the Netherlands, and Sweden working jointly to develop an international joint evaluation scale to identify and quantify early changes in hemophilia joint disease. |
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Medical treatment of hemophilia
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Medical Treatment
• Medical management consists of IV administration of deficient factors. • Amount of factor replaced depends on seriousness of hemorrhage & amount of blood lost. • Stop bleeding episodes & IV infusion of missing clotting factors until bleeding stops • May infuse bleeding factors prior to minor surgery or dental work • Permanent prophylaxis of regularly scheduled infusions to maintain blood factor levels widely accepted. |
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Special Implications for PT - hemophilia
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p. 724
Interventions: Reduce bleeding episodes with preventative strengthening of joints Muscle re-ed and progressive weight-bearing and movement Gait training client education Acute episodes - factor replacement, pain management, RICE, pain free movement, maintain positioning and prevent joint deformity Specific exercise guidlines - p 724 |
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Sickle Cell Disease:
Causes, incidence, and risk factors |
•T he fragile, sickle-shaped cells deliver less oxygen to the body's tissues, and can break into pieces that disrupt blood flow.
• Although sickle cell disease is present at birth, symptoms usually don't occur until after 4 months of age. First three years of life – highest risk for severe morbidity and mortality. • May become life threatening . Blocked blood vessels and damaged organs can cause acute painful episodes, or "crises.” •R BC lifespan normally 120 days, then rupture, release hemoglobin and cell fragments. •H emoglobin breaks into iron compount called hemosiderin & several bile pigments. •H emosiderin returns to bone marrow & reused to manufacture new blood cells. • Liver excretes bile pigments, ie bilirubin. |
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Sickle cell disease
hand foot syndrome |
Figure 13-9: Dactylitis. Painful swelling of the hands or feet can occur when a clot forms in the hands or feet.
This problem, known as hand-and-foot syndrome, occurs most often in children affected by SCD. From Gaston M: Sickle cll anemia, NIH Pub No 90-3058, Bethesda, Md, 1990, National Institutes of Health. Occurs when micro-infarction (clot) occludes blood vessels supplying metacarpals & metatarsals – causing ischemia. May be infant’s 1st problem caused by SCD. Fairly common phenomenon seen almost exclusively in infants & young children. Presents with: •L ow grade fever •P ainful,symmetrical,diffuse,non-pittingedemainhands&feet,often extending to fingers & toes Self-limiting & bones heal without permanent deformity. |
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Clinical manifestations and possible complications associated with SCD.
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Figure 14-17 Clinical manifestations and possible complications associated with SCD.
These findings are a consequence of: •i nfarctions •A nemia •h emolysis, and •r ecurrentinfections. Pa O2 = Partial Pressure of Oxygen in Arterial Blood PaO2, or oxygen pressure, helps determine oxygen adequacy in the blood Hypoxia - PaO2 <70 to 80 mmHg Enuresis - bed-wetting during sleep. Hyposthenuria- Excretion of urine of low specific gravity due to an inability of the tubules of the kidneys to produce concentrated urine. Pyelonephritis – kidney infection Atelectasis - collapse of part or all of a lung by blockage of the air passages (bronchus or bronchioles). 45 |
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Sickle cell trait
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Sickle cell trait is a condition in which there is one gene for the formation of sickle hemoglobin and one for the formation of normal hemoglobin. Sickle cell trait occurs in 1 out of every 12 African Americans. Usually, people with sickle cell trait do not have any symptoms and they can lead normal lives. They do not usually develop sickle cell disease.
• Symptoms may occur with conditions associated with marked hypoxia and at high altitudes. • General anesthesia has no increased risk. • There have been a small number of cases of sudden death in athletes with sickle cell trait when engaged in strenuous, high-heat activities (such as military boot camp or demanding football practices). Indeed, new research suggests that taxing training conditions can exacerbate the danger of sickle cell trait. • Recommendations for athletes with SCT to comply with general guidelines for fluid replacement and acclimatization to hot conditions and altitudes. |
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Upper GI system:
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Aids in digestion
1. mouth 2. Esophagus 3. Stomach 4. Duodenum Table 16-1 p. 829 |
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Lower GI system:
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Digestion, absorption, storage, elimination
5. Jejunum 6. Ileum 7. Colon 8. Rectum |
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Hiatal Hernia
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Aka Diaphragmatic hernia
Figure 16-3 Hiatal hernia. A, Sliding hiatal hernia. Approximately 90% of esophageal hiatal hernias are sliding hernias. The stomach and gastroesophageal junction are displaced upward into the thorax (i.e., the stomach and gastroesophageal junction slide up into the thoracic cavity, following the usual path of the esophagus through an enlarged hiatal opening in the diaphragm). B, Rolling hiatal hernia. The remaining hiatal hernias are rolling or paraesophageal hernias. The gastroesophageal junction stays below the diaphragm, but all or part of the stomach pushes through into the thorax. Causes, incidence The cause is unknown, but hiatal hernias may be the result of a weakening of the supporting tissue. • Congenital & acquired Hiatal hernias are very common • 5 per 1000 • Increases with age, 60% in people over age 60 Symptoms • Heartburn, worse when bending over or lying down • Swallowing difficulty • Chest pain • Belching A hiatal hernia by itself rarely causes symptoms -- pain and discomfort are usually due to the reflux of gastric acid, air, or bile. A person may have reflux of gastric acid and not have a hiatal hernia. Treatment • Reducing the backflow of stomach contents into the esophagus (gastroesophageal reflux) will relieve pain symptoms. • Medications that neutralize stomach acidity, decrease acid production, or strengthen the lower esophageal sphincter may be prescribed. Other measures to reduce symptoms include: • Avoiding large or heavy meals • Not lying down or bending over immediately after a meal • Reducing weight and not smoking Failure to control the symptoms by general or medical measures, or the appearance of complications, may require surgical repair of the hernia. Expectations (prognosis) Most symptoms are alleviated with treatment without surgery. |
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PT implications for hiatal hernias
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NOT TO DO For clients with known hiatal hernias, during therapy intervention:
• Flat/supine position • Valsalva maneuver (increases intraabdominal pressure) • TO DO Instructions for clients: • Warn against activities that cause increased intraabdominal pressure (such as Valsalva, lifting, and especially doing both together) • Give safe lifting instructions |
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Gastroesophageal Reflux Disease
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The inner lining of the stomach has several mechanisms to resist the effect of gastric juice on itself, but the mucosa of the esophagus does not. The esophagus is normally protected from these acids by a one- way valve mechanism at its junction with the stomach. This one-way valve is called the esophageal sphincter (ES), and prevents gastric juice from flowing back into the esophagus.
Causes, incidence • Wide range of foods & lifestyle factors can contribute (Table 16-3) • Often associated with hiatal hernia – diaphragmatic hernia • Correlation between GERD and increasing incidence of esophageal cancer • Common condition that often occurs without symptoms after meals. • 10% of population has daily symptoms • 1/3 of population has symptoms monthly Symptoms • Heartburn • Involves a burning pain in the chest (under the breastbone) • Increased by bending, stooping, lying down, or eating • Relieved by antacids • More frequent or worse at night • Belching - eructation • Regurgitation of food • Sore throat • Hoarseness or change in voice • Difficulty swallowing - dysphagia • Nausea and vomiting • Cough or wheezing – has been linked to increased symptoms in those with asthma |
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Medical Management of GERD
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Acid suppressing inhibitors (Protein Pump Inhibitors - PPIs)
• 1st line of treatment – heals erosive GERD • Maintains healing by shutting off chemical pump that transports acids into stomach • Proton pump inhibitors (such as omeprazole (Prilosec), lansoprazole (Prevacid) or esomeprazole (Nexium) 2. Lifestyle modifications - don't lie down right after eating -sleep with head elevated -weight reduction - avoid fatty, acidic, chocolate, peppermint - avoid caffeine, alcohol, and nicotine 3. OTC - Antacids & Histamine blockers • • Antacids –neutralize stomach acid, goal of quick symptom relief Mylanta (calcium carbonate-magnesium carbonate) Maalox (magnesium hydroxide-aluminum hydroxide) Histamine blockers – prevents acid secretion, goal of long-term cure Pepcid Tagamet Zantac 4. There are also new two minimally invasive surgical procedure approved by FDA that can be performed through an endoscope (a flexible tube passed through the mouth into the stomach) for reflux • Results promising for stopping all medications, including PPIs 5. Anti-reflux operations (Nissen fundoplication-hiatal hernia repair) may help a small number of patients who have persistent symptoms despite medical treatment. |
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Implications for PT - GERD
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Gastroesophageal Reflux Disease
Clients with GERD often treated in therapy practice or rehabilitation setting for orthopedic and other problems. People with GERD may have trouble exercising because physical activity can worsen symptoms. •G ERDinducedbystrenuousexerciseextremelycommoninathletes. • Strenuous exercise inhibits both gastric and small-intestine emptying which can contribute to GERD • Avoid high-calorie meals or fatty foods (or other triggers) immediately before exercising to avoid or minimize exercise- related GERD. •D egree of reflux greater in activities with more body agitation • Eg More in running, aerobics than swimming, biking Monitoring GI status and medication responses is essential in conjunction with the individual’s response to therapy intervention. Anyone with GI dysfunction is at risk for impaired metabolism due to evacuation of medication, improper absorption or both. Polypharmacy – use of multiple medications for a single disorder or for co- morbidities. |
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Helicobacter pylori (H. pylori)
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Helicobacter pylori (H. pylori) is a spiral shaped bacteria that lives on gastric epithelium under the mucus layer of stomach & duodenum.
•D amages mucus layer (protecting coating) in stomach & duodenum, affecting the natural protection from gastric acids. •R esponsible for many cases of chronic gastritis (inflammation of the stomach) and most ulcers. Interestingly, many people have H. pylori in their gastrointestinal tract but don't get gastritis or an ulcer. It seems that other factors must also be present for the damage to take place. |
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Gastritis
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Acute Gastritis
• Most likely to occur in association with serious illness/physiologic stress or medications such as aspirin and NSAIDs Chronic Gastritis • Type A – associated with pernicious anemia, less common •V itamin B-12 cannot be produced by the human body, and must therefore be obtained from diet. Normally, dietary vitamin B-12 can only be absorbed by the ileum when it is bound by the intrinsic factor produced by parietal cells of the gastric mucosa. In pernicious anemia, this process is impaired because of loss of parietal cells, resulting in insufficient absorption of the vitamin, which over a prolonged period of time ultimately leads to vitamin B-12 deficiency • Type B – caused by chronic bacteria infection from Helicobacter pylori Less common causes are: •E xcessgastricacidsecretion(suchasfromphysiologicstress)–acuteerosivegastritis associated with hospitalization for serious life-threatening illness or injury, such as CNS injury like SCI or trauma, particularly burns Symptoms •E pigastric(abdominal)pain-uppermiddleregionoftheabdomen • Feeling of abdominal distention “bloating” •L oss of appetite • nausea & vomiting - vomiting blood or coffee-ground like material • Dark stools Treatment Some of the causes will resolve over time. One to two weeks of antibiotics (like clarithromycin and amoxicillin) along with a proton-pump inhibitor (PPI) such as Prilosec, Prevacid or Nexium is generally the treatment regimen to get rid of H. pylori and treat symptoms present including an ulcer or gastritis. Prognosis The outlook depends on the cause, but is usually good for acute & chronic gastritis |
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Treatment of H. Pylori conditions
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Signs and tests
Simple blood, breath, and stool tests can determine if you are infected with H. pylori. • The most accurate way to diagnose H. pylori, however, is through upper endoscopy of the esophagus, stomach, and first part of the small intestines (duodenum). Because this procedure is invasive, it is generally reserved for people at high risk for ulcers or other complications from H. pylori, like having stomach cancer. • Once diagnosed and treated, the breath and stool tests are used to determine if you have been cured of the infection. Treatment The treatment regimen to get rid of H. pylori and treat symptoms present including an ulcer or gastritis. • One to two weeks of antibiotics (like clarithromycin and amoxicillin) along with a proton-pump inhibitor (PPI) • Such as omeprazole (Prilosec), lansoprazole (Prevacid) or esomeprazole (Nexium) is generally Prognosis Once the H. pylori bacteria are eliminated, recurrence rates are very low in the United States. Still, there is not immunity from the bacteria once infected. Working on development of vaccine to provide lifelong immunity from H. pylori bacteria |
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Peptic Ulcer Disease
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Definition
A peptic ulcer is erosion in the lining of the stomach or duodenum (the first part of the small intestine). The word “peptic” refers to pepsin, a stomach enzyme that breaks down proteins. • 500,000 new cases per year in US • 4 million recurrences per year Causes Normally, the lining of the stomach and small intestines have protection against the irritating acids produced in your stomach. For a variety of reasons, the protective mechanisms may become faulty, leading to a breakdown of the lining. This results in inflammation (gastritis ) or an ulcer. The most common causes: • Infection of the stomach with a bacterium called Helicobacter pylori (H.pylori). •M ost people with peptic ulcers have this organism living in their gastrointestinal (GI) tract. • On the other hand, many people have this organism living in their GI tract but they don't get an ulcer. Other factors can make it more likely for you to get an ulcer, including: • Using aspirin, ibuprofen, or naproxen • D rinking alcohol excessively •Smokingcigarettesandusingtobacco Duodenal more common than stomach up to 10% will get one in their life |
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Will stressing give you an ulcer?
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Many people believe that stress causes ulcers. Evidence is inconclusive.
While critically ill patients who are on a breathing machine are at risk of so- called “stress ulceration,” everyday stress at work or home doesn't appear to cause peptic ulcers. • Physiologic stress ulcers (or acute erosive gastritis) thought due to ischemia of gastric mucosa, which has high oxygen requirements |
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Symptoms and diagnosis of Peptic Ulcer Disease (PUD)
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Symptoms
Epigastric pain is the classic symptom but it may not always be present. The abdominal pain from peptic ulcers can differ a lot from person to person, and some people have no symptoms at all. For example, the pain may get better or worse after eating a meal. • Burning, gnawing, cramping or aching near the xiphoid • Pain comes in waves that last several minutes • Pain may radiate to the back • Perforation of posterior duodenal wall produces steady midline thoracic spine pain from T6-T10 Other possible symptoms include: • Nausea, vomiting • Weight loss • Fatigue • Heartburn, indigestion, belching • Chest pain • Vomiting blood • Bloody or dark tarry stools To diagnose an ulcer, your doctor will order one of the following tests: • An upper GI -- a series of x-rays taken after you drink a substance called barium. • An esophagogastroduodenoscopy (EGD) -- a special test performed by a gastroenterologist in which a thin tube is inserted through your mouth into the gastrointestinal tract to look at your stomach and small intestines. • During an EGD, the doctor may take a biopsy from the wall of the intestines to test for H. pylori. • Stool guaiac cards to test for blood in your stool • Hemoglobin test to check for anemia |
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Treatment of PUD (peptic ulcer)
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Treatment
Treatment often involves a combination of medications to kill the Helicobacter pylori bacteria, reduce acid levels, and protect the GI tract, may include: • Antibiotics to kill Helicobacter pylori - clarithromycin and amoxicillin • Antacids –neutralize stomach acid, goal of quick symptom relief Mylanta (calcium carbonate-magnesium carbonate) Maalox (magnesium hydroxide-aluminum hydroxide) • Histamine blockers – prevents acid secretion, goal of long-term cure Pepcid Tagamet Zantac • Proton pump inhibitors • • • omeprazole (Prilosec) lansoprazole (Prevacid) esomeprazole (Nexium) .An actively bleeding ulcer may also be cauterized (blood vessels are sealed with a burning tool) during a Gastroscopy procedure. Prognosis Peptic ulcers tend to come back if untreated or if stop taking meds before finishing. If take all meds, Helicobacter pylori infection will be eliminated and much less likely to get another ulcer. Symptoms will also improve if you follow some preventive lifestyle steps. Can lead to emergency situations - perforation |
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Special Implications for PT - Peptic Ulcer Disease
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- older and/or medical history of painful musculoskeletal conditions, eg arthritis
- monitor for signs and symptoms of bleeding (pallor, exercise tolerance, fatigue, vital signs) - Peptic ulcers on posterior wall of stomach can perforate and hemorrhage with back pain only symptoms (relieved by antacids) Urge clients to take prophylactic medications and instructions as prescribed by physician and/or advised by pharmacist: •Steroidstakenwithmilk,food or antacids to reduce stomach irritation •Antacids takenbetweenmealsandatbedtime |
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Special Implications for PT - Gastritis
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- 50% with chronic use of NSAIDs have gastritis, often asymptomatic
- Monitor for symptoms and need medical referral (nausea and vomiting, hematemesis, if GI bleeding seek medical attention) - Urge clients to take prophylactic medications and instructions as prescribed by physician and/or advised by pharmacist: •Steroidstakenwithmilk,food or antacids to reduce stomach irritation •Antacids takenbetweenmealsandatbedtime |
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Pyloric Stenosis
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Pyloric stenosis - narrowing of the outlet from the stomach to the small intestine (called the pylorus)
Hypertrophic pyloric stenosis - occurs in infants. One of most common surgical disorders of early infancy. Causes, incidence, and risk factors This condition is caused by a thickening of the muscles of the pylorus. This prevents the stomach from emptying into the small intestine. The cause of the thickening is unknown, although genetic factors may play a role. It occurs more commonly in boys than in girls and is rare in patients older than 6 months. Approximately 2 to 3 of every 1,000 infants has pyloric stenosis. Longitudinal surgical division of muscle down to the submucosa or the placement of an expandable stent (not shown) establishes an adequate passageway. |
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Clinical manifestation (what's most common?) and symptoms of pyloric stenosis
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Clinical Manifestation
Regurgitation, then projectile vomiting (1+ ft in supine, 3-4 upright or sidelying) Leads to dehydration, lethargy with rapid progression to complete obstruction and complications of malnutrition, weakness, wasting, weight loss, fluid & electrolyte imbalance Symptoms Symptoms generally appear several weeks after birth and include: •V omiting • Usually mild regurgitation and vomiting at first, becoming progressively more forceful within one half hour of feeding •P rojectilevomiting–forciblevomitingthatejectsvomitus1footormorewhen in a supine position and 3-4 feet when upright or side-lying •I nfant appears constantly hungry •D iarrhea (loose green stools) •W ave-like motion of the abdomen shortly after feeding and just before vomiting occurs • Dehydration (becoming more profound with the severity of the vomiting) •F ailure to gain weight or weight loss Diagnosed with ultrasound Surgical repair (endoscopic balloon dilations, or pylorotomy and pyloroplasty with high success rates. Placement of stents at site of obstruction gaining popularity as alternative intervention. |
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Inflammatory Bowel Disease (IBD)
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Inflammatory Bowel Disease
1. Crohn's disease, also called regional enteritis, is a chronic inflammation of the intestines which is usually confined to the terminal portion of the small intestine, the ileum. Although may see in other segments. 2. Ulcerative colitis is a similar inflammation of the colon, or large intestine. 3. Antibiotic associated colitis – normal bacterial flora in lumen of intestine are suppressed by antibiotics, allows yeasts and molds to flourish • Other microrganisms may replace normal GI flora, Clostridium difficile, most common cause of this type of colitis with antibiotic associated diarrhea • Produces toxins that damage colonic mucosa, producing inflammatory plaques • Also called psuedomembranous enteritis, if in small intestine • IBDs (inflammatory bowel disease) have been linked with an increased risk of colorectal cancer. |
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Crohn's Disease
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Crohn's disease is an inflammation of the intestines caused by immune response to an infection.
The inflammation of Crohn's disease is nearly always found in the ileocecal region. • The ileocecal region consists of the last few inches of the small intestine (the ileum), which moves digesting food to the beginning portion of the large intestine (the cecum). • However, Crohn's disease can occur anywhere along the digestive tract. Lining of intestine may ulcerate forming channels of infection, called fistulas Fistulas tunnel from area of ulceration, creating a hole which may continue until reaching surface of organ, such as lymph tissue, or surface of nearby skin These holes typically spread infection that creates them, Life-threatening conditions such as peritonitis (inflammation of lining of abdomen) may occur |
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Ulcerative Collitis
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Chronic, episodic, inflammatory disease of the large intestine and rectum characterized by bloody diarrhea.
•U sually begins in rectal area and may eventually extend through entire large intestine. • Repeated episodes of inflammation lead to thickening of the wall of the intestine and rectum with scar tissue. • Death of colon tissue or sepsis may occur with severe disease. Causes, incidence The cause is unknown. It may affect any age group, although there are peaks at ages 15 to 30 and then again at ages 50 to 70. The incidence is 10 to 15 out of 100,000 people. Symptoms •D iarrhea, from only a few episodes to very frequently throughout the day (blood and mucus may be present) • Abdominal pain and cramping that usually subsides after a bowel movement Additional symptoms that may be associated with ulcerative colitis include the following: •N ausea and vomiting •J ointpain • Gastrointestinal bleeding Treatment The goals of treatment are to control the acute attacks, prevent recurrent attacks, and promote healing of the colon. Hospitalization is often required for severe attacks. Corticosteroids may be prescribed to reduce inflammation. Surgery to remove the colon will cure ulcerative colitis and removes the threat of colon cancer. Patients may need an ostomy or an ileal pouch-anal anastomosis, a procedure that connects the small intestine to the anus to help the patient gain more normal bowel function. Prognosis The course of the disease generally varies, with remissions and exacerbations over a period of years. Sometimes ulcerative colitis can be a fulminant (quickly progressing) disease. A permanent and complete cure is unusual. |
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Antibiotic Associated Collitis
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Causes, incidence
Almost any antibiotic can cause pseudomembranous colitis. The bacterium Clostridium difficile, which is normally present in the intestine, may overgrow when antibiotics are taken. The bacteria release a powerful toxin that causes the symptoms. The lining of the colon becomes raw and bleeds. Symptoms Tests •W atery diarrhea •A bdominalcramps • Low-grade fever • Bloody stools • An immunoassay for C. difficile toxin • A colonoscopy or flexible sigmoidoscopy showing pseudomembranous colitis (a characteristic appearance of the colon) Treatment The antibiotic causing the condition should be stopped. Anti-microbial agents Metronidazole is usually used to treat the disorder, but Vancomycin may also be used. Rehydration with electrolyte solutions or intravenous therapy may be needed to replace fluids lost with diarrhea. Prognosis If there are no complications, the outlook is generally good, although up to 20% of infections may recur and need additional treatment. PT needs to be alert for joint and/or muscle involvement – patient may develop reactive arthritis – acute, aseptic, inflammatory arthropathy arising after an infectious process, but at site remote from primary infection. •T ypically involves large and medium joints in LE • Manifests 1-4 weeks after infection |
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Special Implications for PT - Inflammatory Bowel Disease
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25% have migratory arthralgias, arthritis, sacroilitis
- joint pains may manifest 1st or with articular symptoms, but often disregarded - If LBP, hip pain, or SI pain of unknown origin, PT must screen for medical disease (question about family history, intestinal symptoms, relief of joint pain after passing gas) Medications -Alert for 1st signs of side effects and alert MD (prolonged high dose steroid therapy, low bone mineral content, high prevalence osteoporosis) Emotional stresses precipitate or exacerbate symptoms - stress reduction and management techniques |
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Irritable Bowel Syndrome - causes, incidence and risk factors
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Most common disorder of GI system
Group of symptoms often worsened by emotional stress Not the same as inflammatory bowel disease! (functional, not structural, disorder. No relationship between IBS and cancer) Causes, incidence, and risk factors Irritable bowel syndrome involves a combination of abdominal pain and alternating constipation and diarrhea. There are many possible causes. • For instance, there may be a problem with muscle movement in the intestine or a lower tolerance for stretching and movement of the intestine. •T here is no problem in the structure of the intestine. Irritable bowel syndrome (IBS) can occur at any age, but often begins in adolescence or early adulthood. It is more common in women. Risk factors may include a low-fiber diet, emotional stress, use of laxatives, having had infectious diarrhea, or other temporary bowel inflammation. Irritable bowel syndrome is extremely common, but only a small number of people seek treatment. |
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IBS - symptoms
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Symptoms
•C hronic and frequent diarrhea, usually accompanied by pain •C hronic and frequent constipation, usually accompanied by pain •A bdominalpainortenderness •F ollowing meals • Relieved by bowel movement •I ntermittent • Abdominal fullness, gas, bloating •A bdominaldistention •N ausea and vomiting •L oss of appetite |
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Irritable Bowel Syndrome Management
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Signs and tests
•T ests usually reveal no problems. • Irritable bowel syndrome, by contrast, is not an inflammatory condition, but the symptoms may be very similar to those of inflammatory bowel disease. •P atientsoverage50shouldbescreenedforcoloncancer. Treatment The goal of treatment is to relieve symptoms. •C hanges in diet may help relieve symptoms in some patients. No diet works for all patients. •I ncreasing dietary fiber and avoiding items that stimulate the intestines, such as caffeine, may help. Other possible treatments may include: •A nxiety-reducingmeasures,suchasregularexercise • Counseling (in cases of severe anxiety or depression) •A nti-diarrhealmedications •L ow-dose antidepressants Prognosis Irritable bowel syndrome may be a life-long chronic condition, but symptoms can often be improved or relieved through treatment. |
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Special Implications for PT - IBS
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Regular physical activity relieves stress and assists in bowel function
Be alert for breath-holding patterns or hyperventilation in response to stress Correlation between history of emotional or sexual abuse and GI disorders - more needed to offer PT guidelines and intervention management skills when abuse part of patient history Victims of domestic violence account for a significant number of women (and also increasing numbers of men) who use health care services, and the nature of domestic violence injuries will often necessitate physical therapy and rehabilitation. The rapport that a physical therapist or physical therapist assistant develops with a patient may facilitate the revelation of abuse by that patient—it could even save a life. APTA guidelines give needed background on the issue and the role that physical therapists have in identifying, treating and advocating for women and any others who are abused by a current or former intimate partner. |
