Health Variations 2 Flashcards Quizlet 2 PDF

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Health Variations 2 Flashcards | Quizlet

Health Variations 2 Terms in this set (212) Chronic disease

long-lasting, non-communicable disease

irreversible presence, accumulation or latency of disease states or Chronic illness

impairments that involve the total human environment for supportive care and self-maintenance of function and prevention of further disability

1. complex causality, multiple factors leading to onset features of chronic illness

2. long development period, without symptoms 3. prolonged course of illness, leading to other health complications 4. associated functional impairment or disability

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- arthritis - asthma - back problems 8 most frequently occurring chronic

- cancer

diseases

- COPD - CVD - diabetes - mental health conditions

- tobacco smoking modifiable risk factors for chronic diseases

- excess alcohol use

(behavioural)

- physical inactivity - poor diet

modifiable risk factors for chronic diseases (biomedical)

- excess weight - high blood pressure - high blood cholesterol

- socio-environmental factors risk factors for chronic disease (possibly not

- early life factors

modifiable)

- psychosocial factors - political factors

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- age - gender non-modifiable risk factors for chronic diseases

- Indigenous status - ethnic background - family history - genetic make-up

- person-centred - team-centred - population health approach - primary care emphasis Chronic care model

- proactive, planned intervention - ongoing care - prevention/management focus - community setting, collaborative across primary and secondary - 1:1 or group contact through patient visit or health professional - support for self-management

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- disease-centred - doctor-centred - focus on individuals - secondary care emphasis - reactive, symptom driven Acute care model

- episodic care - cure focus - single setting - 1:1 contact through patient visit - diagnostic information provided

level of difficulty experienced in one or more of interconnected areas Definition of Disability

--> impairment of body function or structure --> limitations in every-day activities --> participation restriction in any area of life not just health

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- intellectual - physical - acquired brain injury - neurological impairment Types of disabilities

- deaf/blind - vision - hearing - speech - psychiatric - developmental delay

is a process aimed at enabling people to reach and maintain their Rehabilitation

optimal physical, sensory, intellectual, psychological and social functional levels. It provides disabled people with the tools they need to attain independence and self-determination.

Habilitation

support for a disabled person to attain new skills.

ICF Model

International Classification of Functioning, Disability, and Health

Biopsychosocial model of disability. It highlights how functioning and ICF explained

disability at the personal level are created through dynamic interaction between a person's health conditions and contextual factors.

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- body functions - body structures - impairments - activity Components of ICF

- activity limitations - participation - participation restrictions - environmental factors - personal factors

pancreatic alpha-cells

secrete glucagon --> hyperglycaemic

pancreatic beta-cells

secrete insulin --> hypoglycaemic

Glucagon effects

Insulin effects

Type 1 diabetes

breakdown of glycogen to glucose (glycogenesis)

enhanced membrane transport of glucose into most body cells (muscle, fat) and inhibits the breakdown of glycogen to glucose

autoimmune destruction of the insulin producing beta-cells of the pancreas

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increased thirst due to hyperglycaemia, which acts as an osmotic polydipsia

diuretic, the amount of glucose filtered by the glomeruli of the kidneys exceeds that which can be reabsorbed by the renal tubule, glycosuria results, accompanied by large amounts of water lost in the urine

increased hunger due to depletion of cellular stores of carbohydrates, polyphagia

fats and proteins results in cellular starvation and a corresponding increase in hunger

weight loss in T1DM

Diabetic Ketoacidosis (DKA)

NovoRapid

occurs because of fluid loss in osmotic diuresis and the loss of body tissue as fats and proteins are used for energy

increased metabolism of fats and proteins resulting in high levels of circulating ketones

Ultra short acting insulin

Actrapid

short acting insulin

Lantus

long acting insulin

Target Blood Glucose Level

4-8 mmol/L

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- genetic predisposition risk factors for T1DM

- environmental factors ( viral infection, chemical toxins)

• Heart rhythm abnormalities • Nausea, vomiting, abdominal pain Signs and symptoms of DKA

• Central nervous system depression, coma • Acetone breath • incr rate and depth of breathing

- Polydipsia clinical manifestations of T1DM

- Polyuria - Polyphagia - Weight loss

1. hyperglycaemic crisis > 11.1mmol/L OR Diagnosis of T1DM

2. fasting plasma glucose > 7.0 mmol/L OR 3. oral glucose tolerance test > 11.1mmol/L OR 4. Hemoglobin A1c > 6.5%

Humalog (Lispro): 0.25hrs - 1hrs - 4-5hrs Ultra-short acting insulin

NovoRapid (Aspart): 0-0.25hrs - 1-3hrs - 3.5-5hrs Apidra (Glulisine): 0-0.25hrs - 1hrs - 3-5hrs

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Protaphane (Isophane): 1-2.5hrs - 4-12hrs - 16-24hrs Intermediate (NPH) insulin

Long acting insulin

Hypoglycaemia cause

Hypoglycaemia symptoms

Humulin NPH (Isophane): 1-2.5hrs - 4-12hrs - 16-24hrs

Lantus (Glargine): 1-2hrs - none - 24hrs Levemir (Detemir): 3-4hrs - 6-8hrs - 12-24hrs

imbalance between insulin, carbohydrates and activity

- mild: tachycardia, pallor, sweating, tremors, hunger, restlessness - severe: seizures, coma, death

- Syringe (mostly used in hospital) - Insulin pen disposable (very common, easy to use) S/C insulin delivery devices

- Insulin pen reusable (sometimes preferred) - Insulin pump (more precise, better control and quality of life, less injections, basal and bolus delivery)

- DKA T1DM complications (short-term)

- Hyperosmolar hyperglycaemic nonketone syndrome (HHNS) - Hypoglycaemia

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- micro-vascular disease (renal and retinal disease) T1DM complications (long-term)

- macro-vascular disease (coronary heart disease, stroke, peripheral vascular disease) - neuropathies

T2DM pathophysiology

- insulin resistance (failure of target cells to react to insulin) - beta-cell destruction (hyperglycaemia destroys beta-cells)

- Obesity (decr number of insulin receptors) - Physical inactivity T2DM risk factors

- Diet (saturated fats decr function of insulin, simple sugars --> hyperglycaemia) - Genetic factors (genes that influence cellular response to insulin) - Age (more common over 40)

- recurrent infections (microorganism growth incr by high BGL - genital puritis (fungal growth encouraged by hyperglycaemia and glucosuria) T2DM manifestations

- visual changes (due to fluctuating water balance in eye --> retinopathy) - paraesthesias (feeling of pins and needles) - fatigue (due to poor use of food products)

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MOA: stimulate release of insulin from pancreas (- inhibiting glyconeogenesis in liver - incr number of receptors on target cell) DOES NOT: enhance insulin receptor binding Sulfonylureas (Gliclazide, Diamicron) (MOA, AE, CC)

AE: hypoglycaemia - allergic skin reaction - bone marrow depression - GI disturbance CC: regular BGL checks - take with food to decr risk of hypoglycaemia - best in combination with other oral meds or insulin

MOA: inhibiting glyconeogenesis in liver (- incr glucose uptake by incr insulin receptor binding - slowing absorption of glucose from gut) DOES NOT: incr number of insulin receptors on target cells AE: drug tolerance Biguanides (Metformin) (MOA, AE, CC)

- acidosis - short-term GI upset NOT: hypoglycaemia CC: take with meals to red GI upset - slow onset, glucose control could take up to 2 weeks - limit alcohol to decr lactic acidosis - monitor creatinine levels

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MOA: incr beta-cell insulin secretion (- red glucagon secretion - incr glucose uptake into cells) DOES NOT: inhibit DPP-4 Incretin agonists (Exenatide, Liraglutide)

AE: nausea, vomiting

(MOA, AE, CC)

- hypoclycaemia (when used with other oral meds) - decr appetite - headache CC: S/c injection 60 min before breakfast and dinner

MOA: prevents degradation of endogenous incretin hormone AE: hypoglycaemia - GI upset - headache DPP-4 inhibitors (Sitagliptin, Januvia) (MOA,

- UTI

AE, CC)

- nasopharangitis CC: less effective than sulfonylureas or biguanides - taken in combination if poorly controlled - do not affect weight - OD at same time with or without food

GLUT 4 transporter

insulin-regulated glucose transporter found primarily in adipose tissues and striated muscle (skeletal and cardiac)

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a group of hormones produced by the gastrointestinal system that Incretins

stimulate the release of insulin from the pancreas and help preserve the beta cells

1. free fatty acids circulation interferes with insulin signalling insulin resistance increased by obesity

2. inflammation through circulating cytokines and macrophages interferes with insulin signalling 3. brain impaired insulin signalling fails to suppress appetite

thyroid gland location

Thyroid gland function

2 main thyroid hormones

inferior to the larynx and anterior to the trachea - in throat below Adam's apple , is a bi-lobed butterfly shaped gland

produces hormones to regulate rates of cellular metabolic processes

thyroxin (T4) triiodothyronine (T3)

- 90% of thyroid hormone Thyroxine (T4) function

- converted into triiodothyronine at target tissue - incr rate of protein, fat, glucose metabolism --> incr metabolism, heat production, body temp

- 10% of thyroid hormone Triiodothyronine (T3) function

- incr sympathetic nervous system by incr number of adrenergic

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1. TRH is produced in the hypothalamus Regulation of thyroid hormone secretion

2. TRH triggers TSH release (from anterior pituitary) 3. TSH triggers production of T3 and T4 in thyroid 4. T3 and T4 feedback inhibit TRH and TSH release

Hyperthyroidism

incr thyroid hormone levels --> hypermetabolic state --> thyroidtoxicosis

tachycardia, palpitations, nervousness, insomnia, heat intolerance, moist thyrotoxicosis effects

skin, tremor, incr eye lid retraction, incr systolic BP, incr cardiac contractility, weight loss

- Graves's disease - toxic nodule Hyperthyroidism causes

- thyroiditis (subacute, postpartum, lympocytic) - rare causes (TSH secreting pituitary tumour, thyroid hormone ingestion)

an autoimmune disorder that is caused by antibody production against Graves disease

TSH receptors --> incr production of thyroid hormones --> incr gland size (goiter) and eye position and movement (eyeball protrusion)

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- incr T3 and T4 levels Hyperthyroidism diagnosis

- decr TSH - TSH antibodies present through blood test, thyroid scan, punction

MOA: prevents incorporation of iodine into peptide structure --> inhibiting thyroid hormone synthesis - blocking of peripheral conversion of thyroxine to triiodothyrodine AE: decr body temp, cold intolerance, red appetite, weight gain, depression, parasthesias, memory impairment, listlessness, hypoactive Carbimazole, Propylthiouracil (MOA, AE,

reflexes, decr HR and BP

CC)

CC: 3-4 weeks before thyroid hormone stores are depleated and effects will be notices - propylthioruracil better during pregnancy - high doses for 4-6 weeks to establish normal thyroid function then reduce to lowest dose possible - contact GP if fever, mouth ulcers, rash, sore throat

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MOA: in combination with other antithyroid agents - red vascularity and incr firmness of thyroid gland for easy surgical removal - adjunct in acute hyperthyroidism - high dose of iodide --> immediate inhibition of TH release, effect only 2 days Iodine (MOA, AE, CC)

AE: iodism - like head cold, metallic taste, burning sensation in mouth and throat, sore gums, sneezing, increased salivation CC: not recommended during pregnancy - incr risk of cancer development - wear rubber gloves when administering radioactive iodide

MOA: adrenergenic receptor blockers - adjunct in acute care of pts in hyperthyroid crisis - no effect on circulating levels of TH BUT block the effect of excess TH - propranolol also blocks peripheral conversion T3-->T4 AE: bradycardia beta-blockers (MOA, AE, CC)

hypotension constipation cold extremities headache fatigue sleep disurbances

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Hypothyroidism definition

insufficient secretion of thyroid hormone

1. congenital defect 2. defective hormone production resulting from autoimmune thyroiditis, Hypothyroidism causes

iodine deficiency or antithyroid drugs 3. iatrogenic loss of thyroid tissue after surgical or radioactive treatment of hyperthyroiditis

1. acute thyroiditis 2. subacute thyroiditis Primary hypothyroidism disorders

3. autoimmune thyroiditis (Hashimoto's disease) 4. painless thyroiditis 5. postpartum thyroiditis

Thyroiditis

Hashimoto's thyroiditis

primary thyroiditis pathophysiology

inflammation of thyroid gland causing fever, tenderness, enlargement of thyroid gland

an autoimmune disease in which the body's own antibodies attack and destroy the cells of the thyroid gland

loss of thyroid tissue --> decr production of thyroid hormone --> incr production of TSH --> size of thyroid tissue --> goitre formation

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- red energy metabolism & heat production - delayed neuromuscular processes - low basal metabolic rate, cold intolerance, lethargy, tiredness, thinning hypothyroidism clinical manifestetions

brittle hair, constipation, oedema around eyes, hands & feet, tongue thickens-->slurred speech, hoarseness

hypothyroidism diagnosis

- blood test: incr TSH, red T4 & T3 - clinical symptoms of hypothyroidism

MOA: thyroid hormone replacement therapy --> incr rate of metabolic activity AE: incr temp, heat intolerance, incr appetite, weight loss, hypertension, loss of muscle mass, irritability, restlessness, insomnia, tachycardia, diarrhoea, skin flushed thin & moist, nails soft & thin Thyroxine Sodium (Oroxine) (MOA, AE, CC)

CC: - life-long treatment - clinical responses are useful indicators of appropriate dose - check TSH levels 6 weeks after adjustment - metabolism of other drugs affected by hypothyroid state - if symptoms of hyperthyroidism occur during treatment: discontinue drug for 1 week and recommenced at lower dose - needs to be taken on an empty stomach 30 min before breakfast

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1. incr energy requirements 2. hypothalamus releases thyropropin releasing hormone 3. anterior pituitary releases thyroid stimulating hormone, binds to receptors on follicular cells 4. thyroid gland releases stored thyroid hormone thyroid hormone regulation

5. synthesis of thyroid hormone to 'restock', thyroglobulin is synthesized and discharged into follicle lumen 6. iodide is trapped and oxidized to iodine, iodine is attached to tyrosine 7. iodanated tyrosines are linked together to form T3 and T4

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