OCCT 3002 Exam Prep

Type 1 Diabetes

• Characterized by lack of insulin production

• Sometimes known as “insulin-dependent” diabetes

• Autoimmune condition which results in the destruction of cells responsible for insulin production

What are some risk factors for T1D?

• Age

• Race

• Genetics

• Environment/lifestyle (more people diagnosed in winter, consumption of cows milk too early as a child, stress)

• Physiological (exposure to microorganisms in childhood or viral exposures)

What is NOT a risk factor for T1D?

Gender

How can T1D be diagnosed?

• Urine testing

• Blood testing

• Ketone levels (measured by blood or urine)

T1D diagnosis: blood testing

Glucose levels in the blood can be tested after fasting to see if the patient has diabetes, impaired glucose tolerance (IGT), or impaired fasting glucose (IFG)

T1D diagnosis: urine testing looks at

Glucose, ketones and protein levels

What are some medications that can be used to treat T1D?

• Exogenous insulin

• Protective medications

What are some non-pharmacological treatments for T1D?

• Monitoring nutritional intake - ‘meal planning’

• Exercise

• Monitoring blood glucose levels

• Education

Glycated haemoglobin (HbA1c)

• A form of hemoglobin that has glucose molecules attached to it

• Key biomarker used to assess long-term blood glucose control

Beta cells

• Located in the islets of Langerhan

• Produce insulin

• Monitor for high blood glucose and release an appropriate amount of insulin to balance levels

Alpha cells

• Located in the islets of Langerhan

• Produce glucagon

• Release glucagon when blood sugar levels are low to stimulate conversion of glycogen (stored glucose) from liver

Bolus insulin vs basal insulin

• Bolus = rapid acting, taken before meals

• Basal = long acting, taken at regular intervals regardless of meal times

• Both generally administered via a fine needle, pen, or pump

How/where is insulin produced?

• By beta cells within the islets of Langerhans in the pancreas

• Beta cells trigger production and release of insulin when high blood glucose is detected

Type 2 Diabetes

• Characterized by insulin resistance, decreased insulin sensitivity, or decreased insulin secretion

• Body produces insulin but cannot use it effectively

• Non insulin dependent diabetes mellitus, aka adult onset diabetes

T/F People with T2D will never develop insulin deficiency requiring replacement therapy

False, 20% of people with T2D will develop insulin deficiency requiring replacement therapy

Prevalence of T2D/risk factors

• Increased prevalence with age

• Over-represented among Indigenous populations (Aboriginal and Torres Strait Islander people are over 4x more likely to have diabetes or pre-diabetes)

• Family history of diabetes or gestational diabetes

• Physical inactivity and high body weight

• High BP and cholesterol

How can T2D be prevented?

• 30 minutes of moderate intensity PA on most days

• Healthy diet

• ‘Normal’ BMI

• Regular health checks

Presentation of T2D

• Insidious onset

• Symptoms as listed in T1D

• Presentation

  • overweight/obese

  • High blood sugar levels

• Complications

How is T2D diagnosed?

• Via the same methods as T1D in addition to:

• Oral Glucose Tolerance Tests (OGTT)

• Glycated haemoglobin levels (HbA1c)

Pre-diabetes

Describes a state of impaired glucose tolerance

Physiology of Insulin/Glucose in a healthy body

• When we eat food, glucose is produced and enters the blood stream

• Pancreas senses higher blood glucose levels and produces insulin

• Insulin stimulates cells to take up the glucose from the blood

• Cells use the glucose to meet the body’s energy needs

• Unused glucose is converted to glycogen and stored in the muscle cells and liver

Which form of diabetes is most common?

Type 2 Diabetes is more common

Symptoms of diabetes

• Chronic fatigue

• Wounds that won’t heal

• Systemic weight loss

• Frequent urination

• Always thirsty and/or hungry

• Blurry vision

• Numbness or tingling in hands or feet

• Sexual problems

• Vaginal infections

Diabetic Ketoacidosis

• Major medical emergency due to low insulin levels and high blood sugar (hyperglycemia)

• Breakdown of fat stores for energy produces ketones as a by product (results in sweet acetone breath)

• Serious cause of morbidity

• Symptoms include vomiting, dehydration, polyuria, polydipsia, tachycardia, confusion, rapid breathing

Polydipsia

Excessive thirst and increased fluid intake

Signs of insulin resistance

• Hyperpigmentation (darkening of skin pigment particularly in the neck and axilla regions)

• Skin tags on the body or face

• Central obesity (defined by a high waist-to-hip ratio, waist-to-thigh ratio and waist circumference

• Hirsutism (excess facial and body hair, particularly on women)

What are some long-term complications of T1D and T2D?

Microvascular disease and Macrovascular disease

Diabetes complications: Microvascular disease

• Retinopathy: disease of the retina resulting in impairment or loss of vision

• Nephropathy: disease or damage to the kidneys

• Neuropathy: nerve damage resulting in numbness, pain, tingling, and muscle weakness

Diabetes complications: Macrovascular disease

• ‘Silent’ MI

• Peripheral vascular disease: conditions of the arteries outside of the heart and brain (ex. atherosclerosis)

• Stroke

Eye disease in diabetes

• Leading cause of blindness in Australian adults

• Includes

  • Non proliferate retinopathy

  • Proliferate retinopathy

  • Macular oedema (swelling of macula (responsible for central vision) due to fluid and protein leaking into retina)

Diabetic retinopathy types

• Non proliferate retinopathy (early stages of damage to blood vessels in retina due to hyperglycemia)

• Proliferate retinopathy (most advanced version, retina’s blood supply is compromised causing growth of abnormal, fragile new blood vessels (neovascularization) can lead to vision loss and retinal detachment)

Diabetic eye disease treatments

• Vitreal injection (medication inserted directly into vitreous humor of eye)

• Surgery including laser surgery

Diabetic eye disease patient experience

• Concerns include

  • Frustrations caused by driving restrictions

  • Impacts on social and work lives

  • Emotional states

  • Financial situation

Role of OT in diabetic eye disease

• Driving assessment

• Vision loss strategies and aids

• Supporting independence

• Compensating for visual loss

Peripheral neuropathy

• Damage to peripheral NS

  • loss of signals normally sent

  • inappropriate signals

  • errors that distort the messages being sent

• aka diabetic neuropathy, affects 50-70% of people with diabetes

Symptoms and presentation of peripheral neuropathy

• Muscle weakness and cramps

• Reduced ability to feel temp, vibration, and touch especially in hands and feet

• Loss of reflexes, balance, and/or joint position

• Neuropathic pain

• Commonly presents as numbness, tingling, or burning feet

• T1D: may present after many years of hyperglycemia

• T2D: may be part of the diagnosis of the condition

Foot complications and diabetes

• Associated with peripheral neuropathy and peripheral vascular disease

• Ulceration, infection, ischaemia, or neuro-arthropathy (breakdown of bones/joints)

• Leading cause of diabetes-related hospitalizations and amputations

Pathophysiology of peripheral neuropathy and resulting complications in the feet

• PN leads to insensitive foot, foot deformities, and altered gait

  • leads to high pressure in some areas → development of callus

  • further leads to abnormal loading → hemorrhage and ulceration

• Minor trauma to the foot (ie. ill fitting shoes, walking barefoot, or acute injury (ingrown nail, stubbing toe, blister))

  • causes ulcer

• Impaired wound healing especially if walking continues on injured foot

Diabetic foot problems prevention and management

• Wear footwear that fits and protects the foot

• Wear socks to reduce shear and friction

• Educate on importance of appropriate footwear

• Skin care and checking feet regularly

• Podiatrist involvement

Management of diabetic foot ulcers

• Relieve pressure and protect ulcer

• Restore skin perfusion

• Treat infection

• Metabolic control and treat comorbidity

• Local wound care

• Educate patient and relatives

• Prevent recurrence

Diabetic amputations occur due to:

Progression of poor healing ulcer due to diabetes-related atherosclerosis (poor arterial inflow) and peripheral neuropathy

Patient presentation of diabetic amputations

• Common in older people

• Co-morbidities

• Obesity

• May be progressive (eg. toe, partial foot, below knee, above knee over many years)

• Other leg may also be affected

Types of amputations

• Transfemoral

  • above knee amputation (AKA)

• Transtibial

  • below knee amputation (BKA)

Amputee treatment pathway (pre-op and acute/subacute)

• Pre-operative stage (decision to amputate)

  • monitoring, planning, preparation (when possible)

• Acute and subacute

  • Operative and Post-op medical care until stable

Amputee treatment pathway (rebab)

• Inpatient rehab

  • Pre-prosthetic and/or interim prosthetic rehabilitation

  • Wound healing

  • Functional independence for discharge

• Outpatient rehab

  • Pre-prosthetic and/or prosthetic rehab

  • Optimize independence

  • Support community participation

  • Secondary prevention

Amputee treatment pathway (management and support)

• Ongoing prosthetic review

• Services and rehabilitation may be required depending on changes throughout the participant’s lifespan

Role of OT in Diabetes

• Commonly encountered as a comorbidity to other conditions (stroke, amputations)

• Health promotion and chronic condition self management

• Fall prevention

• Home assessment and modifications

• Equipment prescription (wheelchair)

• Management of daily activities

• Sensory training, desensitization, pressure management, management of phantom limb pain

• Driver assessment and rehab

Lived experience of T1 and T2 Diabetes

• Adherence and understanding of treatment

• Chronic condition

• Depression

• Sexual dysfunction

• Employment

• Managing complications

• Disability

• Progression, uncertainty, and mortality

Impact on family of T2D

• Increased risk of developing diabetes

• Diet and lifestyle

• Change in roles

• Accommodating equipment or modifications

• Coping with deterioration and progression

Impact on society of T1 and T2 Diabetes

• Absenteeism

• Reduced productivity

• Early retirement

• Pharmaceutical scripts and medical care come with high costs

• T2D has most economic burden of all diabetes

• Financially: carer costs, productivity losses, health system costs, obesity

Impact on society of diabetes complications

• T1D has higher costs relating to micro and macro vascular complications

• Diabetic foot disease has a high cost to healthcare system

• Disability related to diabetes

  • Amputations and artificial limbs

  • Equipment

  • NDIS

The left side of the heart receives ____ blood from

Oxygenated blood from the lungs (via pulmonary veins) and sends it to the body (via aorta)

The right side of the heart receives ____ blood from

Deoxygenated blood from the body (via vena cava) and sends it to the lungs for re-oxygenation (via pulmonary arteries)

Leading cause of death globally

Cardiovascular diseases

Coronary heart disease (aka ischemic heart disease)

• Most costly heart disease in Australia

• Caused due to coronary artery clogs and narrowing as a result of plaque build up

• Main cause of premature death

• Slightly more common in men (1/3 vs ¼ women)

• Includes:

  • Stable angina

  • Acute Coronary Syndrome:

    • Unstable angina

    • Myocardial Infarction (MI)

Development of atherosclerosis

1. Irritants in blood damage endothelium

2. Cholesterol builds up under endothelium, causing fatty streaks

3. Oxidization of cholesterol → immune response of monocytes

4. Monocytes turn into macrophages, eat cholesterol until they die and become foam cells

5. Foam cells release cytokines which cause inflammation, more damage, more cholesterol deposits → plaque grows

6. Smooth muscle notices damage to artery, migrates and secretes to form a fibrous cap.

7. Cytokines signal for muscle to put calcium into the plaque

8. Plaque and calcium narrow and harden arteries, decreasing blood flow

Fatty plaque can also rupture, exposing thrombogenic material to blood and causing a clot

Unmodifiable risk factors for CHD

• Age

• Gender

• Ethnicity

• Family history

• Previous MI

Modifiable risk factors for CHD

• High BP

• High cholesterol

• Physical inactivity

• High body mass

• Smoking

• Diabetes

Protective factors for CHD

• Sufficient PA

• Low alcohol consumption

• High density lipoprotein

Stable angina

• Describes clinical symptoms rather than a disease

• Occurs due to partial blockage causing oxygen depletion

• EFFORT RELATED CHEST PAIN

• Relieved by rest

• Can be a symptom of other diseases so diagnosis is important

Analyzing symptomology of CVD chest pain

Location: center of chest is the centralizing point

Radiates to: neck, jaw, upper or lower arm, back

Character: dull, constricting, choking, squeezing, heavy, crushing, burning, aching NOT knife like or sharp

Onset: typically takes several minutes to develop

Acute Coronary Syndrome

• Includes unstable angina and MI

• Presents against background of stable angina or as a new phenomenon

• Symptoms occur during rest

• Evidence of myocardial damage through blood tests

Symptoms of acute coronary syndrome

• Chest pain

• Nausea

• Shortness of breath

• Light-headedness

• Sweating

• Vomiting

• Pain or discomfort in one or both arms, jaw, neck or back

• Claudication (muscle pain due to lack of oxygen)

 

Presentation of CVD/MI in males vs females

• Females:

  • Jaw pain

  • Shortness of breath

  • Backache

  • Extreme fatigue

• Males:

  • Sweating

  • Heartburn

  • Vomiting

• Both:

  • Chest pain or tightness

  • Nausea

Diagnosis/Investigation of CVD

• Routine:

  • Electrocardiogram (ECG)

  • Chest X-ray

  • Echocardiogram (echo)

  • Blood test

• Angiogram - cardiac catheterization

Treatment/Intervention of CVD

• CPR/Defibrillation

  • First line of treatment to shock the heart back into sinus rhythm

• Thrombolysis (clot-dissolving drugs)

• Angioplasty and stent implantation

• Bypass surgery (CABG)

• Medications

• Cardiac rehabilitation

Medications for CVD

• Anticoagulants

  • decrease clotting ability of blood

• Antiplatelet agents

  • prevent blood clotting

• Beta-blockers

  • decrease HR and CO → decrease angina

• Angiotensin-converting enzyme (ACE) inhibitor

  • vasodilator, decreases workload to the heart

• Statins

  • lower cholesterol

Cardiac rehabilitation

• Regular exercise

• Diet

• Reduce stress

• Medical therapy

• Stop smoking

Role of OT in Cardiac Rehab

• Conserving energy

• Retraining ADLs

  • Don't overexert heart

• Environmental adaptations

• Education

• Lifestyle modifications

• Medication management

• Improving muscle strength and heart endurance

CVD Prognosis

• Major determinants include extent and severity of atherosclerosis and ventricular dysfunction

• Prognosis better for ppl who receive immediate hospital treatment

• 5 year mortality double for people with unstable angina vs stable

• Mortality of ppl with MI double that of people with unstable angina

Complications of MI

• Arrhythmia (abnormal heart rhythm) →ex, Afib = atrial fibrillation

• Embolisms (blockage of blood vessel by travelling piece of material (embolus))

• Heart failure

Atrial Fibrillation

• Due to random chaotic electrical signals in the atria

• Causes heart to twitch rapidly and out of rhythm

• Short of breath, light-headedness, and feelings of rapid heart beat (palpitations)

Heart failure

• Occurs when heart is unable to maintain strong enough blood flow to meet the body’s needs

• Usually slow developing

• Can occur due to MI, hypertension, cardiomyopathy, or damaged heart valve

• Life threatening and associated with poor survival

Prevalence of heart failure

• 1 person hospitalized every 8 mins

• More deaths in females than males

• Rate is over 2x as high in indigenous populations in Australia

• Deaths have been decreasing over time

• Prevalence increases with age

Deaths in females/males from heart failures vs CHD/CAD

• More males die from CHD and CAD

• More females die due to heart failure

Risk factors for heart failure

• CHD

• High blood pressure

• Diseased heart muscle or valve

• Diabetes

• Obesity

Presentation of heart failure

• Chronic fatigue/tiredness

• Reduced ability to participate in PA

• Shortness of breath/Pulmonary oedema

• Peripheral oedema

• Distended neck veins

Prognosis of heart failure

Generally cannot be cured and is associated with poor survival rates. People who are hospitalized longer and have more frequent readmissions have a higher mortality rate

Treatments/Intervention for heart failure

• Diuretics - promote fluid excretion

• Beta blockers - lower HR

• ACE inhibitors - vasodilators

• Rest

• Surgery

• Pacemaker and internal defibrillator

• Cardiac rehabilitation

Impact on the person - CVD

• Fatigue and pain

• Reduced concentration

• Reduced confidence

• Role changes and changes to occupations

• Depression/Grief

Impact of CVD on families/carers

• Stress and anxiety

• Lowered QoL

• Increased risk of death of the partner

• Changes of roles and occupations

Infectious respiratory diseases

• Due to viruses, bacteria, or fungi

• Pneumonia and influenza

Obstructive respiratory diseases

• Due to damage to lungs or narrowing of passages

• COPD, asthma, cystic fibrosis

Restrictive respiratory diseases

• Lungs unable to fill with air due to restricted expansion

• Interstitial lung disease

COPD

• Umbrella term for a group of long-term chronic lung conditions unifying characteristics of obstruction to airflow

  • Emphysema

  • Chronic bronchitis

  • Chronic asthma

• Its unclear why some people develop one condition over the other

• Not fully reversible with use of bronchodilators. Also includes diseases of the alveoli

Emphysema pathophysiology

• Premature collapsing of airways causes air to be trapped in the alveoli (decreased expiratory airflow)

• Main symptom is breathlessness

• Disease of the alveoli → loss of alveoli

• Results in:

  • Obstructions to airflow

  • Lung hyperinflation due to loss of elasticity

  • Decreased SA for exchange of O2/CO2

Emphysema presentation

• Shortness of breath

• Less cough and sputum production than chronic bronchitis

• Less hypoxemic (low O2) and hypercapnia (high CO2) than CB until disease further advances

• ‘Barrel chested’ due to hyperinflation of lungs

• Flattened diaphragm - apparent in physical exam and x-ray

• ‘Pursed lips’ breathing

• ‘Hyper-resonant or drum like’ lungs

• Fatigue

Diagnosis - Pulmonary function tests (PFT)

• Spirometry testing measures:

  • FVC - Forced vital capacity

    • max amount of air that can be exhaled after a full inspiration

  • FEV₁ - Forced expiratory volume

    • volume exhaled in 1 second of forced expiration

• Peak flow meter

  • PEF - Peak expiratory flow

    • force of expiration

Emphysema X-ray looks for

• Flattened diaphragm

• Increased front to back diameter of the chest

• Increased air space behind the sternum

• Prominent or enlarged pulmonary arteries

• Elongated mediastinum

Emphysema treatment and intervention

• Smoking cessation

• Medications

  • Bronchodilators

  • Corticosteroids (reduce inflammation of airways)

  • Anticholinergics (relax airway muscles and help open airways)

• Long term home oxygen therapy

• Pulmonary rehabilitation

• Surgical intervention

Emphysema complications

• Pulmonary hypertension

  • Cor Pulmonale (pulmonary heart disease)

  • Right ventricle hypertrophy (due to high CO2 and low O2 in blood)

• Respiratory acidosis (due to high CO2 in blood)

• Bullae - air pockets/holes from stretched alveoli

  • Collapsed lung (pneumothorax) as a result of bullae rupture

Chronic bronchitis pathophysiology

• Disease of the airways

• Chronic irritation and inflammation of the airways.

• Inflammation due to bronchial mucous lining the bronchi

• Results of inflamm:

  • Hypertrophy of mucus glands

  • Smooth muscle hypertrophy and spasm

• Main symptoms are cough and increased secretions from the lungs such as mucus

• Hypoxemia and hypercapnia also occur

Chronic bronchitis presentation

• Chronic cough

• Sputum production

• Hypoxemia and hypercapnia likely

• Cyanosis

• Wheeze

Chronic bronchitis diagnosis

• Chronic cough or mucous production for at least 3 months of the year for 2 years

• Shortness of breath

• Wheeze

• Pulmonary function test

Chronic bronchitis treatment/intervention

• Smoking cessation

• Medications

  • Bronchodilators

  • Anticholinergics (can be in inhaler form)

  • Corticosteroids

• Long-term home oxygen therapy

• Pulmonary rehab

• Surgical intervention

Chronic bronchitis complications

• Pulmonary hypertension

  • Cor pulmonale (pulmonary heart disease)

  • Right ventricle hypertrophy

• Respiratory acidosis

Chronic asthma pathophysiology

• Affects small airways

• Muscles in airways tighten and lining of airways swell and produce sticky mucus → narrowing of airway

• Medicines do not fully open the airways - making it irreversible and characterized as chronic

Prevalence of COPD

• 4th leading cause of death worldwide and 5th in Australia

• More common in older populations

• Rates similar between males and females, depends on age group

Risk factors for COPD

• Tobacco and cannabis smoke

• Occupation (exposure to vapours, gasses, and fumes)

• Outdoor and indoor air pollution (low and middle income countries)

• Low birth weight (poor lung development)

• Lung growth

• Infections

• Low SES

• Nutrition

• Genetics

COPD symptoms

• Repetitive chronic cough that doesn’t get better

• Increased phlegm or mucous production

• Shortness of breath (dyspnoea)

• Fatigue (ppl with COPD use 25-50% more energy than healthy ppl)

• Chest infections