Unit 3: Package 2 - Thyroid Dysfunction
Anatomy and Physiology - Thyroid hormone regulates the rate of cellular glucose and fat breakdown (catabolism), therefore energy, heat and waste production.
T3 (triiodothyronine) and T4 (thyroxine)
- regulate energy metabolism and growth and development
- regulates the speed at which cells are functioning; stimulates cells to speed up/do things
- temperature; nervous system development; how fast nutrients are being broken down; stimulates production of enzymes
| Characteristics | Hypothyroidism | Hyperthyroidism |
| Metabolic Rate | - decrease; apathy and lethargy; emotional dullness | - increase; restlessness; heightened wakefulness |
| Energy Production | - decreases | - increases; hyperactive |
| Temperature tolerance | - intolerance to cold - decreased sweating | - intolerance to heat - diaphoresis |
| Mental state | - apathy; inability to stay alert | - nervousness; inability to concentrate or focus |
| Appetite | - decreased | - increased; can’t gain weight |
| Weight | - weight gain | - weight loss |
| Bowel function | - decreased; constipation | - increase; sometimes diarrhea |
| Heart rate | - decreased rate and force | - bounding, rapid pulse; palps |
| Blood pressure | - low; hypotension | - high; HTN |
| T3 and T4 serum levels | - decrease in circulating levels | - excess circulating levels |
Drug Classification(s): Thyroid Replacement Therapy
Drug Name(s): levothyroxine (Synthroid, Eltroxin)
Nursing considerations
Assessment
- History: Allergy to active or extraneous constituents of drug, thyrotoxicosis, acute MI uncomplicated by hypothyroidism, Addison's disease, lactation
- Physical: Skin lesions, color, temperature, texture; T; muscle tone, orientation, reflexes; P, auscultation, baseline ECG, BP; R, adventitious sounds; thyroid function tests
Interventions
- Administer oral drug as a single daily dose before breakfast with a full glass of water.
- Arrange for regular, periodic blood tests of thyroid function.
- WARNING: Most CV and CNS adverse effects indicate that the dose is too high. Stop drug for several days and reinstitute at a lower dose. (tremors, headache, nervousness, insomnia; palpitations, tachycardia, angina, cardiac arrest)
Teaching points
- Take as a single dose before breakfast with a full glass of water (increases absorption; some foods affect metabolism of drug)
- This drug replaces an important hormone and will need to be taken for life. Do not discontinue without consulting your health care provider; serious problems can occur.
- Wear a medical ID tag to alert emergency medical personnel that you are using this drug.
- Arrange to have periodic blood tests and medical evaluations.
- Report headache, chest pain, palpitations, fever, weight loss, sleeplessness, nervousness, irritability, unusual sweating, intolerance to heat, diarrhea (indicates dose is too high)
- Replacement therapy taken at bedtime may result in early awakening and sleep disorders
Thyroid hormone replacement is used to treat hypothyroidism. Usually thyroid replacement needs to be taken for the rest of the client’s life. If thyroid replacement hormone has been effective, we should see the client’s weight - decrease; pulse rate - increase; stabilize
Drug Classification(s): anti-thyroid agents - thioaminde derivative
Drug Name(s): propylthiouracil (PTU), methimazole (Tapazole)
| Action/Effects/Uses | Adverse Effects |
| · stops/blocks the absorption of iodine by the thyroid; thyroid uses iodine to make thyroid hormones · blocking ability of iodine to combine with tyrosine to form T4 & prevents formation of T3 · Graves; goiter; cancer; thyroiditis; hyperthyroidism | · tingling/prickling/numbness of skin · inflammation of blood vessels · rash · itching · GI upset · signs of hypothyroidism Liver and bone marrow toxicity - a major adverse effect of anti-thyroid medications
|
Unit 2: Package 1 - Types of Immunity and Immunizing Agents
Antigen
- a substance, usually a protein, that the body recognizes as foreign; stimulates the body to make antibodies; some cause illness; some don’t
- Allergy is a type of antigen;
T and B cells (Lymphocytes)
- made in bone marrow; grow up/mature in thymus gland
- some stay in the thymus gland; some migrate to lymph nodes; other migrate to the spleen
T cells - directly attack and destroy foreign cells (antigens); kill antigens
- produced in the bone marrow
- mature in the thymus gland
- after maturation, present in blood and lymph nodes
- Helper-T’s, Suppressor T-Cells, NK-T cells (Natural Killer - specifically kill cancer)
B cells - protect body by producing plasma cells/daughter cells that secrete antibodies (and memory cells) in the blood; render antigens impotent
- give rise to plasma cells which produce antibodies (immunoglobulins)
- antibodies directly attach themselves to antigens, inactivating the antigens and making them susceptible to destruction
Specific immunity? (aka. Adaptive Immunity)
- Immunity against a specific antigen or disease
- cells of the body (B cells) when they encounter an antigen they specifically make antibodies specific for that antigen
Antibody responses to an antigen occur in two phases, a primary and secondary response.
Primary response:
- occurs with the first exposure to the antigen causing antibody production
- may take a few days to develop
- triggers not just the production of antibodies (from B cells), but also memory cells; and cold symptoms
Secondary response:
- occurs years later
- activation of the memory cells (B cells) by the reappearance of their antigens
- more rapid than the primary response as the memory cells are ready to spring into action
- quick defence
Antibodies inactivate their antigens by attaching themselves to their antigens and labelling them as non-self. Collectively, they are known as ANTIGEN-ANTIBODY REACTIONS.
Immunization
Immunity is defined as:
Active or passive (according to whether or not the body’s immune mechanisms are actively involved in making antibodies against antigens)
Natural or artificial (according to how one acquires the immunity, naturally or by artificial means)
Natural Active - body naturally makes antibodies against antigens; actively making antibodies
Natural Passive - someone else is “giving you” immunity (antibodies); from mother via placenta/breast milk; temporary
Active Artificial - needles; immunizations - e.i. the flu shot (recumbent or dormant virus in vaccine);
Passive Artificial - needles; “we are giving you the antibodies”; temporary; immunoglobulins
Differences between active and passive immunity as to the source of antibodies
Active - a form of long-term, acquired immunity; protects the body against a new infection as the result of antibodies that; actively made by B Cells
- develop naturally after an initial infection
- artificially after a vaccination
Passive - a form of acquired immunity resulting from antibodies that are transmitted naturally; not permanent and does not last as long as active immunity; come from the blood of someone else who has already made them
- through the placenta to a fetus
- through the colostrum to an infant
- artificially by injection of antiserum for treatment or prophylaxis
Explain why passive immunity provides only temporary immunity
- does not involve white blood cells- it is only antibodies
- their lymphocytes have “not been activated” to make antibodies
Artificial acquired immunity, either active or passive, requires the administration of an injection preparation.
Immunological preparations:
vaccines and toxoids
- preparation contains a weakened or killed form of an antigen
- stimulates the body's immune system to recognize the antigen as foreign, destroy it, and "remember" it
gamma globulin and antitoxins
- more commonly known as antibodies
- usually given in an attempt to temporarily boost a patient's immunity against disease
- often given as a preventive against possible infection when a person has been exposed to a dangerous disease
We require booster injections of immunological agents
- to ensure adequate immunity for specific diseases
Examples of booster injections
- Diphtheria
- Tetanus
- Polio
- Whooping Cough (Pertussis)
- Hepatitis B
- MMR
Unit 2: Package 2 - Immunological Disturbances: Hypersensitivity and Auto-Immunity
Allergens stimulate the body to produce:
- ANTIBODIES
The resulting antigen antibody response can damage body cells. Histamine and leukotrienses are released from special cells found near blood vessels called mast cells.
Histamine causes
- vasodilation
- bronchoconstriction
- capillary permeability
- increase mucus gland secretion
Asthma is an inflammatory reaction of the lungs, sometimes precipitated by an allergic response. If triggered by allergens such as dust or pollen it is called extrinsic asthma. Also may be intrinsic; no external cause; clients with asthma have a mixture of both types.
status asthmaticus
- an acute, severe, and prolonged asthma attack
- caused by critically diminished airway diameter resulting from ongoing bronchospasm, edema, and mucous plugging
- hypoxia, cyanosis, and unconsciousness may follow, and the attack may be fatal
- treatment includes supplemental oxygen given to correct hypoxemia, bronchodilators given intravenously or by aerosol inhalation, corticosteroids, mechanical ventilation, sedation, frequent therapy, and emotional support
Each of the following symptoms may occur in anaphylactic shock
hives and pruritus
- when tons of histamines are being dumped into system, histamine will go into blood vessels of skin causing vasodilatation; causing skin damage
drop in blood pressure
- histamines cause vasodilatation
respiratory distress
- histamines cause bronchoconstriction
INHALED CORTICOSTEROIDS
- steroids are powerful anti-inflammatory drug
- commonly used in asthma therapy to prevent attacks
Health teaching information about inhalation steroids to prevent throat irritation and fungal infection of the mouth and throat which may occur with the use of inhaled steroids
- adequate oral hygiene to minimize the overgrowth candidiasis (thrush)
- rinse mouth with water after using the inhaler
- spacer device can greatly reduce how much medication stays in mouth
- clean outside of inhaler with warm water and air dry on regular basis
ORAL CORTICOSTEROIDS
Work to relieve the symptoms of an acute episode of asthma by suppression of inflammation and modification of the normal immune response
A potentially serious side effect from long-term administration of steroids is suppression of adrenal gland activity with eventual immuosuppression. To minimize this, steroids are usually administered for only short periods of time and/or locally, if possible.
Common adverse effects from prolonged administration of steroids include
- adrenocorticoinsufficiency
- weight gain
- edema
- hypertension
- loss of muscle mass
- osteoporosis
- mood swings
- insomnia
- gastric ulceration - wear away at the lining of the stomach
- immunosuppression
State why each of the following nursing considerations are important when administering steroids, or providing health teaching about steroids to clients
take oral steroids during or immediately after a meal
- reduce GI upset
watch closely for signs of infection
- immunosupression
take medication exactly as ordered, decreasing dosage as per schedule when withdrawing from the drug
- abrupt stoppage can exacerbate or worse asthmatic symptoms
avoid taking any OTC drugs, especially NSAIDs, at the same time as steroids without consulting a physician first
- can cause drug interactions and toxicity
monitor client for signs of fluid retention
- adverse affect of steroids
BRONCHODILATORS
Physiological mechanism of how bronchodilation relieves the symptoms of asthma
- Stimulate beta cells in bronchial smooth muscle
- Smooth muscle cell receptors stimulate/icrease the production of a type of energy; this energy increases broncho-dialation
- block the action of Ach
Bronchodilators can be produced in a variety of ways. Therefore, drugs are classified according to how they produce bronchodilation. One way of classifying these drugs is as follows:
Sympathomimetics - i.e. epinepherince, albuterole sulphate (Ventolin);
These drugs mimic the sympathetic nervous system thus causing bronchodilation. Another name for them is adrenergic.
Anti-cholergenics - i.e. ipatropium bromide (Atrovent); (same thing as sympathetic; adrenergic)
These drugs block the effects of the parasympathetic nervous system
Common side effects of bronchodilators are related to, in many cases, how they achieve their action and in some cases, how they are administered.
Drug Classification(s): bronchodilator; sympathomimetic/adrenergic
Drug Name(s): Ventolin, epinephrine
Action/Effects/Uses
Indications
- control and prevent reversible airway obstruction
- blocks & mimics the sympathetic nervous system
Action
- Relaxation of airway smooth muscle with subsequent bronchodilation
Therapeutic Effect(s):
- Bronchodilation
Unit 4: Package 1 - Hypoxia: Causes and Effects on Cell Functioning
Difference between the following terms:
Hypoxia - inadequate oxygen tension at the cellular level; oxygen deficiency in the cell; leads to ischemia
Hypoxemia - an abnormal deficiency in the concentration of oxygen in arterial blood; oxygen deficiency in the blood
Ischemia - a focal deficiency of blood to a part of the body; diminished blood supply; decreased blood supply to a specific area
The following are possible factors affecting oxygenation. These changes may contribute to hypoxia
- inflammation of the respiratory tract
- affects the diffusion of oxygen into across the alveolar membranes into the bloodstream; less oxygen is able to diffuse; inhibits gas exchange
- airway narrow so less O2 goes in; narrowing of the lumen
- number of erythrocytes in the bloodstream
- less RBC means less binding locations for oxygen to attach to hemoglobin that is on RBSs
- decreased O2 to the periphery of the body
- blood vessel patency (state of being open) throughout the body
- ability for blood to flow through vessels
- vasoconstriction decreases O2 flow to periphery
- cardiac output
- decreased output means decrease O2 to periphery
If disturbed the circulatory system, cardiac cycle, and coagulation may cause impairment leading to hypoxia or ischemia.
CARDIAC CYCLE
Recall
- cardiac cycle - sequence of events that occurs when the heart beats; one heart beat is one cardiac cycle; one cardiac cycle is completed when the heart fills with blood and the blood is pumped out of the heart
- systole - pressure the heart exerts against arteriole walls during contraction of heart beat; the ventricles contract and pump blood to the arteries
- diastole - pressure the heart exerts during arteriole walls during relaxation of heart beat; heart ventricles are relaxed and the heart fills with blood
- cardiac output - is the volume of blood being pumped by the heart, in particular by a left or right ventricle in the time interval of one minute; Cardiac Output (Q) = SV × HR
- stroke volume - the volume of blood pumped from one ventricle of the heart with each beat; SV = EDV − ESV
The sequence of events during one cardiac cycle, considering the cardiac chambers, cardiac valves and specific blood vessels
Cardiac Cycle
4 chambers
- right and left atria
- right and left ventricles
4 valves
- tricuspid
- mitral/bicuspid valve
- pulmonic valve
- aortic valves
4 blood vessels
- superior/inferior vena cavae
- pulmonary veins
- pulmonary arteries
- aorta
Path of Oxygen in the body from the Lungs
1. lungs
2. pulmonary veins
3. left atrium
4. mitral/bicuspid valves
5. left ventricle
6. aortic valve
7. aorta
8. body
9. superior/inferior vena cavae
10. right atrium
11. tricuspid valve
12. right ventricle
13. pulmonic valves
14. pulmonary arteries
*think of the heart as two pumps; a left pump and the right pump
- right pump - blood is going to the lungs and coming right back
- left pump - when blood leaves the heart, its left the body…left to go to the periphery
A significant cause of ischemia is blood flow obstruction which can occur as a result of:
- narrowing of blood vessels from vasospasm
- atherosclerosis
- formation of a thrombus
A thrombus can form from blood clotting (coagulation), a chain of reactions which begins with damage to the lining of the blood vessel.
Two blood proteins most responsible for coagulation and where they are manufactured
- Prothrombin - Liver
- Fibrinogen - Liver
*always a little bit being secreted in the blood stream (inactivated)
Vitamin necessary for coagulation; where it is manufactured; its role in blood clotting
- Vitamin K; fat soluble
- produced in large intestines by natural body flora; stored in liver; extra in adipose tissue
- necessary for Prothrombin synthesis
Function of Calcium in coagulation and food sources
- combines with other substances released from damage tissue as well as Vitamin K and clotting factors
- bony fish
- animal products
- sesame seeds
- spinach
***Calcium + Vitamin K + clotting factors + substances from damaged tissue = Prothrombin Activator
Thrombus
- a clot which forms in an unbroken blood vessel and remains stationary
Describe the three steps in coagulation considering:
thrombocytes
- rush to area of damaged tissues; clump and stick to the damaged area; creates a plug
blood vessels
- at the same time, blood vessel starts to spasm; an attempt for the system to try and close off blood supply; vasospasm
clotting proteins
- at the same time clotting factors/clotting cascade is happening
- calcium is coming into contact with substances being released from damaged area
- mixes with Vitamin K and clotting factors in blood stream
- makes Prothrombin Activator
- converts Prothrombin to Thrombin
- Thrombin converts Fibrinogen to Fibrin
- Fibrin creates clot meshwork
Unit 4: Package 2 - Pathophysiology: Cardiovascular Disease
Coronary Artery Disease (CAD), also called Arteriosclerotic Heart Disease (ASHD), is the most common form of heart disease. Coronary artery occlusion may lead to myocardial ischemia resulting in angina, myocardial infarctions, dysrhythmias and heart failure (HF) which is also known as congestive heart failure (CHF).
Disease Process: these disorders develop due to tissue ischemia and the clinical behaviours result from cellular hypoxic changes related to the cardiovascular system.
Atherosclerosis and hypertension (HTN) are major risk factors in both CAD and stroke/cerebral vascular accident (CVA). A major risk factor for atherosclerosis is HTN and vice versa.
ATHEROSCLEROSIS
| Term | Definition |
| atheroma | - an abnormal mass of fat/lipids, as in a sebaceous cyst or in deposits in an arterial wall |
| atherosclerosis “athero” - “plaque” | - a common disorder characterized by yellowish plaques of cholesterol, other lipids, and cellular debris in the inner layers of the walls of arteries |
| arteriosclerosis | - a common disorder characterized by thickening, loss of elasticity, and calcification of arterial walls; hardening of the arteries |
Atherosclerosis plaques in blood vessels are dangerous because they may:
- weaken the vessel wall
- narrow the vessel lumen thus:
- increasing blood pressure
- decreasing local blood flow
- have the potential to become thrombi or emboli
For each of the following branches of the aorta, the organs/areas of the body whose blood supply would be interrupted by blockage of the arteries and consequences:
coronary arteries
- heart; CAD; branch right off the aorta to the heart
common carotids
- head, neck, and brain: stroke or TIA
femoral
- lower extremities (pelvis (reproductive/urinary)/legs/feet); Peripheral Vascular Disease
Following condition may cause hypertension
Activation of the renin-angiotensin mechanism
- Kidney baroreceptors sense low BP
- Release hormone called renin
- Angiotensinogen is in the blood stream
- Renin stimulates/binds Angiotensinogen to convert to Angiotensin I
- Lungs sense that Angiotensin I is in the blood and releases Angiotensin Converting Enzyme (ACE)
- ACE then converts Angiotensin I to Angiotensin II
- Angiotensin II is a powerful vasoconstrictor thus raising BP
- an altered renin-angiotensin mechanism may contribute to the development and maintenance of HTN
- ACE Inhibitors prevent convertion of Angiotensin I to Angiotensin II
Atherosclerosis and HTN are risk factors for CAD and stroke. Risk factors are either modifiable or non-modifiable.
| Risk Factor | Why is it a risk? | Unmodifiable or modifiable? |
| Aging | - arteries loose elasticity; heart valves calcify | unmodifiable |
| Alcohol intake | - increase in fluid retention - decrease in HDL | modifiable |
| Diabetes Mellitus | - glucose molecules damage blood vessels | modifiable |
| Diet (obesity) | - leads to atherosclerosis which leads to arteriosclerosis
| modifiable |
| Gender | - CAD and stroke more prevalent in women (37% women; 35% men) | unmodifiable |
| Genetic predisposition |
| unmodifiable |
| Hyperlipidemia/ Hypercholesterolemia (1) | - narrows the blood vessel lumen = hypoxia and ischemia | modifiable |
| Hypertension (2) | - increases the rate of atherosclerotic development | modifiable |
| Oral contraceptive use | - estrogen causes increase level of clotting factors | modifiable |
| Race | - increase in black people | unmodifiable |
| Sedentary lifestyle (3) | - hemostatis | modifiable |
| Smoking (4) | - generalize vasoconstriction | modifiable |
| Stress | - stimulates the SNS - increased levels of epinephrine, norepinephrine which increases HR/force of contraction, vasoconstriction | modifiable |
ANGINA
- insufficient oxygen to the heart muscle; partial blockage or spasm
- clinical manifestation of reversible ischemia
- either an increased demand for oxygen or decreased supply of oxygen
DYSRHYTHMIAS
If the infarct involves the conduction system of the heart, cardiac dysrhythmias can occur. Basically, dysrhythmias reduce the efficiency of the cardiac pump, and cause changes in cardiac output.
Examples of dysrhythmias
SA Node: bradycardia, tachycardia (not as severe as AV blocks)
70-83 beats/minute
- bradycardia - “fires” too slowly (at a rate less than 60 beats/minute) causing a slow heart beat
- tachycardia - “fires” too quickly (at a rate greater than 100 beats/minute) causing a fast heart beat
Atrial Conduction defects: atrial fibrillation
40-60 beats/minute; can take over fro SA node
- disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction
- atrial rate may be as high as 350 to 600 beats/minute
- ventricular rate can vary from as low as 50 beats/minute to as high as 180 beats/minute
AV Node: Heart block
- every impulse is conducted to the ventricles but the duration of AV conduction is prolonged
- after the impulse moves through the AV node, it is usually conducted normally through the ventricles
Client experiencing a dysrhythmias might exhibit:
- irregular apical and radial pulses
- vertigo (dizziness) (r/t decreased CO)
- hypotension (r/t decreased CO)
***because chaotic qualities of the rhythm
Assessment findings are indicative of a valve disorder
Depends on which valve and the degree of damage to the valve
- decrease in CO
- change in pulse rate
- dyspnea due to reduced lung compliance
- fatigue and palpitations from atrial fibrillation
HEART FAILURE/CONGESTIVE HEART FAILURE (HF/CHF)
Signs and symptoms of left-sided HF (goes to the body - came from the LUNGS - blood will back up in the LUNGS):
- cough
- crackles on auscultation
- dyspnea
- orthopnea
*** The inability of the left side of the heart to pump into the systemic circulation. Back-up behind the left ventricle causes accumulation of fluid in the lungs.
Progressively, back-up of blood from the left side affects right ventricular function due to pulmonary hypertension, and right-sided HF occurs.
Signs and symptoms of right-sided HF (goes to the heart - came from the BODY - blood will back up in the BODY):
- peripheral edema
- ascites
*** The inability of the right side of the heart to adequately pump venous blood into the pulmonary circulation. This causes a back-up of fluid in the body, resulting in swelling and edema.
Treatment of HF, in many cases, is related to treating the underlying cause of the heart’s inability to pump effectively. However, HF is the end result of many cardiac and respiratory conditions. Pharmacological intervention can stabilize the condition, and with medication, people can continue to carry on productive lives.
CARDIAC ARREST
Cardiac arrest can occur with a MI, dysrhythmias or HF
- cessation of cardiac activity
- cardiac stand still; no contractions
- #1 cause of sudden death in Canada
- most occur in the home or out in public; in the morning
