HF some notes for exam PDF

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https://amhonline-amh-net-au.ezproxy-b.deakin.edu.au/chapters/rheumatologicaldrugs/immunomodulating-drugs/rheumatoid-arthritis#antirheumatics-table

HF The heart is not pumping enough, sufficient blood for the rest of the body. Or the heart muscle loss its function to pump as much amounts blood as body needed. Congestion HF Heart ventricle pump the blood and then send blood to tissues or organs, atrium Left HF

Right HF

Systolic HF

Diastolic HF

Pain pathways. Hurt --- specific neuro cells nociceptors --- spinal cord--- brain grey matter--- cortex Obesity is defined as abnormal and excess accumulation of adipose fat. When BMI >= 30kg/m2 can be defined as obesity. When body produce excess adipose tissue, fatty acids boosts, hepatic glucose increase, inhibit glucose utilisation and insulin secretion. Insulin resistance has been found present in obesity and diabetes. Obesity put much more stress and pressure on ability to use insulin properly control BSL, and more likely to develop to diabetes. Role of insulin: A chemical messenger essential for glucose entry into the cells. When BGL rise, body release insulin, triggers removal of blood glucose into cell from the blood. T2DM A abnormal, metabolic disorder, that causes glucose or sugar accumulation in the blood rather than as an useful fuel to the cells in the body.

Hyperglycaemia Fatigue, dizziness, excessive hunger, thirst, frequency urination, DKA ketoacidosis, fruitysmelling breath, diabetic coma, dry, parched mouth, peripheral neuropathy, autonomic neuropathy, diabetic retinopathy. Hypoglycaemia Fatigue, pale skin, shakiness, seizures, anxiety, irritability, sweating, blurred vision, slurred speech, irregular heart rhythm, loss of consciousness Motivational interviewing Amis to be empathic A brief method of communication 1-2 sessions Designed to move individuals in the direction of change Toward change Two main phases Increase motivation for change Consolidating the commitment to change Principles Collaboration, non judgement, non adversarial, guide rather than direct Expressing empathy, developing discrepancy, rolling the resistance, supporting self-efficacy. Self-management Providing information, specific skill, behaviours, problem-solving skills, person centred care, mental health care, regular follow up, active in own care.

Over uncontrolled high BGL hyperglycaemia --- damage the liner lining of blood vessels, arteries response by layering plaques --- narrows and harden the arteries. --- reducing blood supply to tissue --- causing conditions --- peripheral vascular disease --- coronary artery disease --- peripheral neuropathy

Over uncontrolled hyperglycaemia --- damage blood vessels liner lining --- arteries response by layering plaques --- narrow the arteries--- harden the arteries Reducing supply blood to tissue Causing some further conditions --- peripheral vascular disease, peripheral neuropathy, coronary artery disease

Stroke: Blood supply to brain blocked or reduced that can happen (a blood clot, narrowing vessels, or blood vessel rupture leading to bleeding) L) HF Occurs when the left ventricle is not pumping blood adequately Resulting in deficiency of oxygen-rich blood that is pumped from heart to body Leads to right heart failure SOB, coughing pink and foamy mucus, fatigue, pale skin, lung congestion, cyanosis, dyspnoea

Systolic HF The heart is unable to pump adequate amounts of blood throughout the body during this contraction

R) HF Right ventricle is not pumping adequately Blood pooling in the right Atrium Blood flow back into body Reduce/ decrease blood in the lungs. Fluid build-up in veins or oedema (leg ankles) Oedema, weight gain, peripheral vessel pressure increasing, peripheral oedema, ascites, jugular vein extended, GI distress

Diastolic HF The heart muscle is unable to relax fully between contractions and allow enough blood to enter the ventricles Left ventricle lose its ability to relax normally The heart muscle becomes stiffer than normal Results in fluid build-up and congestion in the lungs

RA Rheumatoid Arthritis Autoimmune disorder Body mistakenly send WBC attack the synovium, leading to inflammatory response. The WBC of the immune system move into the joint, release a kind of chemicals called cytokines, it can attack synovial membrane, leading to synovial membrane release other substance, grow new vessels, form a thickened area called pannus. Pannus may destroy and invade the cartilage or bone inside of the joint. Inflammation causes fluid build-up in the joint making the joint swell. Without treatment, the space of joint may narrow, joint may come together, occur stiffness, ankylosis, loss ability to movement. Stage 1 Joint pain, stiffness, swelling. Synovia reacts invading WBC, grow up new cells in a rapid pace. New cells lead to smooth synovium to develop to rough grooved surface, excess fluid, swell joint, warm to touch, redness on the skin surface. Pain relief and control inflammatory. NSAIDs (inhabit the production of prostaglandins by block COX enzymes 1 and 2. Side effects: GI distress, N&V, renal impairment Stage 2 Synovia continues to thicken, abnormal tissue (pannus) formed over the ends of joint bone surface, damage to the joint cartilage, pain, loss of mobility Control inflammatory, pain relief, anti-rheumatic, given cytokine modulators injection NSAIDs, Standard DMARD, Steroids. Retard progressive joint destruction, reduce long-term disability. Reduce long-term non-controlled inflammatory cause long-term damage to the joint. Stage 3 Severe. Damage extends to bone. Pannus released enzyme lysosomes damages cartilage, bone, soft tissue, bone space narrow, joint rub together, ankylosis occurs. When symptoms mid to severe, cartilage and bone damages, given DMARDs to slow joint damage. Long-term taking hydroxychloroquine reduce pain, stiffness, joint swelling. Often taking with methotrexate. Stage 4 No inflammatory. Cartilage lost. Reduced muscle strength. Joint destroyed. Bone fused together. Other rheumatoid nodules coming underneath the skin. Combine with non-pharmacological (psychotherapy, occupational therapy, surgical) Can also given pain relief.

ACE inhibitor Ramipril Inhibiting the conversion of angiotensin I to angiotensin II, causing blood vessels dilate and then decrease BP. Also, reducing angiotensin II-induced vasoconstriction, sodium retention. Side effects – non-productive cough, hypotension, dizziness, fatigue, renal impairment Beta blockers Metoprolol Block beta receptors in the heart. Reducing heart rate, BP, the heart ability of contract Inducing antihypertension effect by reduction in cardiac output. Reduce pressure on the heart. Side effects Dyspnoea, hypotension, bradycardia Loop diuretics Frusemide Inhibiting reabsorption of sodium and chloride in the ascending of limb of loop of Henle. Dehydration, renal impairment, hypotension, gout, dizziness Digoxin Reduce heart rate by reduce the electric conductivity in the heart. Increase strength of the each heart beat by releasing intracellular calcium Side effects Narrow therapeutic range, digoxin toxicity, may worsen arrhythmia

RAAS Kicks in when BP low, sodium low Strat in liver, liver release angiotensinogen, kidney release enzyme renin Angiotensinogen + enzyme renin = angiotensin I Angiotensin I released in blood stream, when goes into lungs, lungs then release ACE Angiotensin I + ACE = Angiotensin II Angiotensin II works in adrenal glands and kidney Angiotensin II goes to adrenal glands and then create Aldosterone. Aldosterone help BP regulation, increase reabsorption of sodium, decrease K+, Vasoconstriction in arterioles, then BP increase.

HF Heart is unable the provide sufficient blood to meet body’s need. The impairment of heart function including: inability to pump --- during systole called systolic HF Inability to fill --- during diastole called diastolic HF Systolic HF Systolic dysfunction: heart ventricle contract poorly, or empties inadequately. Increased ventricle pressure, decrease cardiac output/ ejection function. Heart ventricle is not pumping effectively, can not provide sufficient blood for body to use. May due to heart muscle weakness, or due to other conditions leading to ventricle loss its ability to contract. Most common reason: hypertension (systolic pressure > ventricle pressure --- aorta valve not open) Dilated Cardiomyopathy --- heart ventricle wall thin and weak Coronary artery disease --- plaque build narrows of the coronary artery --- reduce blood supply. Valvular disease --- valve damage cannot open normally, blood cannot pump out through ventricle to atrium. The effectiveness of systolic function can using ejection function EF= ejected / filled normally 50-70% When systolic dysfunction, ejected reduce, cardio output reduce, then EF reduce.

Diastolic dysfunction Ventricle fills poorly Decrease end-diastolic volume Increase end-diastolic pressure Diastolic HF Left ventricle cannot relax as normal, muscle stiffer than normal Heart ventricle unable relax fully between contract and allow enough blood to enter the ventricle. Resulting in blood and fluid build-up in lungs. (Congestion in lungs) Common reason: Hypertension: ventricle try harder and increase it pressure to pump out due to systolic high pressure, then heart muscle may thicken, reduce space in ventricle, then small volume to fill up blood. L) HF Occurs when left ventricle is not pumping adequately --- deficiency of oxygen-rich blood pumped from heart to body and tissue. --- leads to R)HF S&S SOB, cough pink foamy mucus, dyspnoea, pale skin, cyanosis R) HF Occurs when right ventricle is not pumping adequately, blood pooling in the right atrium and back flow into the body. Decrease blood in lungs, increase build-up fluid in body. Oedema in

lower place (feet, ankles) usually as directly result of L)HF, and can be due to severe lung disease, or right valve disease. S&S Oedema, weight gain, ascites, peripheral venous pressure increase, peripheral oedema, distended jugular veins....