Semester Two - Regulation, Stress and Self Flashcards

1
Q

What are the 9 major endocrine glands?

A
  1. Hypothalmus
  2. Pituitary gland
  3. Pineal gland
  4. Thyroid gland
  5. Thymus
  6. Parathyroid gland
  7. Adrenal gland
  8. Pancreas
  9. Gonads - testes (male), ovaries (female)
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2
Q

What is an endocrine gland? What does it do?

A
  • Endocrine gland are ductless glands that release hormones directly in to the bloodstream.
  • Produce, control and modify release of these specific hormones.
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3
Q

How is the endocrine system and nervous system closely related?

A
  • They are both responsive to internal and external stimuli and together maintain homeostasis.
  • Can regulate each others activity to bring about change in the body’s function.
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4
Q

What glands are regulated by the hypothalamic-pituitary-target gland axis feedback mechanism and how does it work?

A
  • Thyroid gland
  • Adrenal gland
  • Gonads
  • The hypothalamus secretes releasing hormones which are transported via the blood to the pituitary gland
  • The releasing hormones induce the production and secretion of pituitary hormones that are transported by the blood to their target glands
  • Feedback from the target glands to the hypothalamus and pituitary gland regulates hormone levels/functions in the body
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5
Q

How does homeostatic regulation of hormones through negative feedback work?

A

Hormones released by target gland are detected by the hypothalamus turning off the response.

Example to help with understanding:

  1. The hypothalamus secrete thyroid releasing hormone (TRH)
  2. This stimulates cells in the anterior pituitary to secrete thyroid-stimulating hormone (TSH)
  3. TSH binds to receptors on the thyroid gland, stimulating synthesis and secretion of thyroid hormones
  4. When blood concentrations of thyroid hormones increase above a certain threshold- TRH-secretions by the hypothalamus are inhibited and stop secreting TRH
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6
Q

How does homeostatic regulation of hormones through a direct negative feedback loop work?

A

The secretion of hormones is dependent on the levels in the blood and not the action of any releasing-hormones

Example to help with understanding:

  1. Blood glucose levels rise stimulating beta cells in the pancreas to release insulin
  2. Insulin facilitates entry of glucose into the cells of the body and blood glucose levels fall and the stimulus for insulin release disappears and insulin is no longer secreted
  3. Additionally Glucagon works in opposition to insulin – both act to regulate blood glucose levels
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7
Q

How does homeostatic regulation of hormones through positive feedback work?

A

A stimulus causes hormone production to increase

Example to help with understanding:
1. Lactation - hormone levels increase in response to the baby suckling which causes milk production to increase
2. Prolactin is secreted from the pituitary gland in response to nursing/suckling by the baby – increases milk production
3. Suckling by the baby also stimulates the hypothalamus which signals the posterior pituitary gland to produce oxytocin
4. Oxytocin stimulates contraction of the milk ducts
The increased pressure causes milk to flow through the duct system and be released through the nipple

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8
Q

What are other organs that have a endocrine function?

A
  1. GI (digestive)
  2. Renal
  3. Thymus
  4. Adipose tissue
  5. Placenta (during pregnancy)
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9
Q

What are the three common causes of endocrine pathophysiology?

A
  • too much hormone (hypersecretion - graves disease: too much thyroxine)
  • too little hormone (hyposecretion - type 1 diabetes: too little insulin)
  • lack of response to target cell (type 2 diabetes: target cells insensitive to insulin)
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10
Q

What is the role of the thyroid?

A
  • Produces t4 and t3 which control the rate at which glucose is used to supply the body with energy. (BMR)
  • Regulates BMR - the minimum rate at which the body uses energy to stay alive.
  • Produces calcitonin (reduces blood calcium level)
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11
Q

How do the nervous system and endocrine system differ?

A

Nervous system

  • Performs short term crisis management
  • Electro-chemical communicator– action potential /neurotransmitters

Endocrine system

  • Acts slowly taking minutes, hours or days to produce regulating effects
  • Chemical communicator – hormones
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12
Q

What hormones are released by the hypothalamus? (2) How does this relate to the posterior pituitary gland?

A

These hormones are released by hypothalamus and then travel to posterior pituitary gland where they are released.

  • Antidiuretic hormone (ADH): main regulator of fluid in body
  • Oxytocin: uterus contractions in labor
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13
Q

What hormones are released by anterior pituitary gland? (6)

A
  • Thyroid stimulating hormone (TSH): travels to thyroid and stimulates T4 and T3.
  • Growth hormone (GH): stimulates growth of long bones
  • Prolactin (PRL): stimulates milk production
  • Follicle stimulating hormone (FSH): stimulates production of ova and sperm
  • Luteinizing hormone (LH): stimulates ovaries and testes
  • Adrenocorticotropic hormone (ACTH): stimulates adrenal cortex to secrete glucocorticoids.
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14
Q

What hormone is released by the parathyroid gland?

A

Parathyroid hormone (PTH): main function raises calcium level in blood

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15
Q

What hormones are released by the adrenal medulla (inner)? (2)

A
  • epinephrine
  • norepinephrine
    Major action is to raise BGL level, increase rate of metabolism, constrict certain blood vessels, fight or flight
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16
Q

What hormones are released by the adrenal cortex (outer)? (2)

A
  • glucocorticoids (cortisol): increase BGL

- mineralocorticoids (aldosterone): promote reabsorption of Na+ and excretion of K+ in kidneys

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17
Q

What hormones are released by the pancreas? (2)

A
  • insulin: reduces BGL
  • glucagon: raises BGL

Regulation of glucose in blood and cells.

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18
Q

What hormones are released by the gonads? (3)

A

Testes:
- androgens (testosterone): support sperm formation, development and maintenance of male secondary sex characteristics

Ovaries:

  • estrogens: stimulate uterine lining and growth, development and maintenance of female secondary sex characteristics.
  • progesterone: promotes growth of uterine lining
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19
Q

How do hormones communicate with cells?

A
  • Endocrine hormones are released then travel in the blood stream.
  • Hormones are received by very specific receptor sites on cells.
  • Similar to how a key fits a lock.
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20
Q

What other organs have an endocrine function? (5)

A
  • intestines
  • atria of heart
  • ventricles of heart
  • kidneys
  • thymus
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21
Q

What are the main steps of the HPA axis?

A

The hypothalamic pituitary adrenal axis:

  1. Stimulated by an environmental stressor the hypothalamus secrete corticotrophin-releasing hormone (CRH) and ADH (arginine-vasopressin/AVP)
  2. CRH is transported to the anterior pituitary, stimulating the secretion of ACTH (corticotropin)
  3. Leads to activity in adrenal gland resulting in the release of stress hormones including cortisol, epinephrine, norepinephrine resulting is stress response in body.
  4. ADH (vasopressin) increases reabsorption of water by the kidneys, vasoconstriction and the contraction of blood vessels - increases blood pressure
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22
Q

What regulates the release of cortisol?

A

The HPA axis

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23
Q

What are some of the functions of cortisol?

A
  • Regulates protein metabolism
  • Increases BGL by stimulating gluconeogenesis
  • Prevents cells from losing sodium and accelerates the rate of potassium excretion - regulate the action of cellular sodium-potassium pump
  • Helps regulate pH
  • Reduces immune response - cortisol blocks T-cells from proliferating and preventing interleukin signals
  • Reduces immune response - by inhibition of histamine secretion
  • Excess cortisol can cause atrophy of hippocampus - damage to memory (often reversible)
  • Chronic levels of high stress disrupt the feedback mechanism resulting in the failure of feedback inhibition to operate and the continued release of cortisol
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24
Q

What is the difference between physiologic and pharmacologic therapy?

A
  • The goal of Physiologic Therapy is to replace the natural adrenal steroid for example Addison’s disease
  • The goal of Pharmacologic Therapy is to relieve the symptoms of non hormonal conditions and diseases for example COPD, asthma, Rheumatoid Arthritis, Ulcerative Colitis
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25
Q

What are some common side effects of steroid medication? (there’s lots, just name a couple)

A
  • Dangerous to suddenly stop the medication as steroids override the body’s usual adrenal function
  • Fluid retention (oedema) and sodium retention
  • Thin skin and hair growth
  • Bruising
  • High or increased blood pressure
  • Susceptibility to infections
  • Weight gain and fat deposits face, between shoulders
  • Osteoporosis and osteopenia
  • Pathological bone fractures- particularly in the spine and ribs
  • Insomnia, mood changes (occasionally acute psychosis)
  • Alterations in blood glucose levels and potassium
  • Loss of muscle mass
  • Secondary sex characteristics of the other sex
  • Heart failure
  • GI ulceration
  • Poor growth in children and adolescents (hip bone deformity)
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26
Q

What is the best route of administration for steroid medication?

A

Local administration of steroids is always preferred over systemic routes for example:

  • Inhaled glucocorticosteroids for asthma and COPD
  • Applied topically for skin conditions
  • Injected directly into the joint for inflammatory joint conditions for example frozen shoulder
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27
Q

What causes adrenal insufficiency?

A
  • Adrenal crisis may occur due to adrenal insufficiency
  • Adrenal insufficiency can be primary or secondary

Addison’s disease -primary adrenal insufficiency:

  • the adrenal glands do not produce enough cortisol and aldosterone
  • 80% - autoimmune - primary adrenal insufficiency occurs when at least 90 percent of the adrenal cortex has been destroyed

Secondary insufficiency:

  • Stoppage of Corticosteroid Medication
  • Surgical Removal of Pituitary Tumors - ACTH-producing tumors of the pituitary gland that cause Cushing’s syndrome
  • Tumors (most commonly adenoma), infection in the pituitary
  • loss of blood flow to the pituitary (eg. post partum hemorrhage)
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28
Q

What are some signs and symptoms of adrenal crisis?

A
Dizziness or light-headedness 
Flank pain 
Headache 
High fever 
Joint pain 
Low blood sugar
Low blood pressure
Dehydration 
Confusion
Loss of consciousness
Coma 
Rapid heart rate 
Rapid respiratory rate (tachypnea)
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29
Q

What is the role of insulin in BGL regulation?

A
  • Glucose is stored as glycogen in the liver (reserve approx. 6 hours) and peripherally in skeletal muscle (in much smaller quantities)
  • Insulin allows glucose to move from the blood the cell
  • Insulin is released from the beta cells in the pancreas
  • Insulin stimulates protein synthesis and free fatty acid storage in adipose tissue (anabolic steroid) and facilitates the movement of serum glucose into the cells.
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30
Q

The stimulus for insulin secretions is a HIGH blood glucose level. True or false?

A

True.

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31
Q

The stimulus for glucagon is a HIGH blood glucose level. True or false?

A

False. The stimulus for glucagon secretion is a LOW blood glucose level

  • Glucagon is secreted by the alpha cells of the pancreatic islets in opposition to insulin
  • The effect of glucagon causes the liver to release the glucose it has which increases blood glucose
  • Glucagon causes the liver and muscles to produce glucose by utilizing protein and fat
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32
Q

What is GFR?

A

The glomerular filtration rate.
Glomerular filtration rate (GFR) is the volume of fluid filtered from the renal (kidney) glomerular capillaries into the Bowman’s capsule per unit time.

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33
Q

What is creatinine?

A

Creatinine - waste product from muscles, a more accurate marker of kidney function than urea.

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34
Q

What is the most accurate measure of renal function?

A

Estimated glomerular filtration rate (eGFR) - the eGFR is the most accurate measure of renal function.
Serum creatinine is used to estimate the eGFR using age, sex and race
eGFR calculated by computer and reported with the creatinine blood test
Electrolytes - sodium, potassium, chloride and bicarbonate usually measured.

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35
Q

What can cause a UTI?

A
  • E. coli
  • Sexual activity
  • Contraception – spermicide, diaphragm, condom
  • Catheterisation
  • People at high risk: women 50x greater than men – short urethra, spinal cord injury, people who have problems emptying bladder, enlarged prostate or kidney stones, diabetes, pregnancy, long term catheter (almost 90-100% more likely). Short term catheter (10-30%)
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36
Q

What investigations are used to identify a UTI?

A
  • Urinalysis test

- Urine culture

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37
Q

Signs and symptoms of UTI?

A
  • Urgency of urination
  • Frequency
  • Pain when urinating
  • Pressure in bladder
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38
Q

What is treatment for UTI?

A

Antibiotics - trimethoprim is first choice

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39
Q

How can a UTI be prevented?

A
  • 6-8 glasses of water daily
  • urinate regularly when urge arises
  • urinate shortly after sex
  • woman should wipe from front to back
  • cotton underwear
  • loose fitting clothes
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40
Q

What is pyelonephritis? What causes it?

A
  • Follows on from a UTI
  • Pyelonephritis is bacteria that invades the renal cortex and medulla
    Causes:
  • Untreated UTI
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41
Q

Signs and symptoms of pyelonephritis:

A
  • Intense pain
  • High fever
  • Loin pain
  • GI upset
  • Blood cells and pus in urine
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42
Q

What are the 8 types of incontinence?

A
  • Stress incontinence: associated with coughing sneezing, physical activity
  • Urgency incontinence: detrusor muscle over activity
  • Overactive bladder syndrome: more than 8x per day
  • Mixed incontinence: combination of stress and urgency incontinence
  • Overflow incontinence: obstruction at bladder neck or impairment of detrusor contractility, leakage. Can be caused by stroke ect.
  • Functional incontence: cognitive and physical impairment that stop you voiding independently.
  • Post void dribbling: little bit of leakage after void
  • Urogenital fistula: bladder/urethra/vagina rip. Due to complication from gynae surgery such as hysterectomy
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43
Q

What are some causes of incontinence?

A
  • Previous vaginal delivery
  • Obesity
  • Prostate surgery
  • Damage to CNS or nerve damage or external urethral sphincter
  • Infants
  • Elderly
  • 6x more common in females than males
  • Detrusor muscle problems
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44
Q

What can assist with the management of incontinence?

A
  • Bladder training
  • Pelvic floor exercises
  • Anticholinergics – oxybutynin (Ditropan), tolterodine (Detrol), darifenacin (enablex)
  • Triicyclic antidepressants – imipramine (tofranil) used to treat mixed urge/stress incontinence, duloxetine (cymbalta) used to treat stress incontinence
  • Pessary – ring inserted in vagina
  • Botox injection in to bladder muscle
  • Surgery or catheterisation
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45
Q

Benign Prostatic Hyperplasia (hypertrophy BPH), what is it?

A

Enlarged prostate, non-cancerous

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46
Q

What is the cause of Benign Prostatic Hyperplasia?

A
  • High levels of di-hydro testosterone (DHT) which stimulate growth of prostate
  • DHT synthesised by testosterone in the prostate gland
  • Testosterone levels decrease with age as oestrogen levels increase. Oestrogen stimulates prostate growth.
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47
Q

What are some signs and symptoms of Benign Prostatic Hyperplasia (hypertrophy BPH)?

A
  • Difficulty to start to void
  • Poor flow of urine
  • Need to strain to pass urine
  • Frequency
  • Stopping and starting/stuttering
  • Nocturia
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48
Q

What is an Acute Kidney Injury? (AKI)

A
  • The same thing as acute renal failure.
  • Defined as rapid or abrupt decline in renal filtration function
  • AKI often associated with acute illness, upper or lower resp tract infection. UTIs, Sepsis
  • It is a medical emergency, you must identify and treat the cause
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49
Q

What are the three main causes of Acute Kidney Injury?

A
  1. Prerenal (blood flow to kidney): interference with renal perfusion eg. Hypervolemia, GI bleeding, trauma, vomiting and diarrhoea, cardiogenic shock, MI, fluid volume shift, medication NSAIDS, ACE inhibiters and ARBs.
  2. Intra/intrinsic renal causes (inside kidney): characterised by direct damage to nephrons, may be secondary to another illness, acute tubular necrosis (death of epithelial cells), acute glomerulonephritis (acute inflammation of kidney), crush injury, severe transfusion reaction, infections
  3. Post renal causes (urine from kidney): interference with outflow of urine from kidney. Can be caused by blockage of flow of urine resulting in back pressure to kidney causing damage to nephrons. Obstruction in urinary tract. Renal calculi (kidney stones). Prostatic enlargement. Pelvic malignancy.
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50
Q

What are signs and symptoms of Acute Kidney Injury?

A
  • Decrease fluid output
  • Swelling/oedema
  • Drowsiness
  • SOB
  • Fatigue
  • Confusion
  • Nausea
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51
Q

What is Chronic Renal Disease? (CKD)

A
  • Term for chronic renal failure due to long term disease or damage to kidneys
  • Most people that with present with acute renal injury have some degree of chronic renal damage.
  • Higher prevalence in Maori and pacific due to high incidence of diabetes and hypertension
  • 5 stages (1 is mild, 5 is severe)
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52
Q

What are some causes/risk factors of Chronic Renal Disease? (CKD)

A
  • Diabetes
  • Hypertension
  • Cardio vascular disease
  • Other renal disease or abnormality including persistent protein or blood in urine
  • Family history of CKD or other renal disease
  • Long term use of medication – diuretics and lithium, ACE inhibitors, NSAIDs
  • CKD is an independent cardio vascular risk factor
  • More people with CKD die of cardio vascular disease than end stage renal disease
  • History of any risk factors mentioned above
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53
Q

What is End Stage Renal Disease? (ESRD)

A

CKD stage 5, caused by poor management of CKD

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54
Q

What are signs and symptoms and the very end of ESRD?

A
  • At very final stage – hiccups, uremic frost, coma, convulsions. Assess for renal replacement therapy: dialysis or renal replacement – some people are not suited to dialysis and some choose not to. Without dialysis – survival is generally 6 to 8 months.
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55
Q

What is haemodyalisis?

A
  • Surgical formation of an AV fistula connecting an artery to a vein
  • Three sessions a week that last four hours a week
  • Two cannula are inserted in to AV fistula which remove blood and transfer to dialysis machine
  • Dialysis machine is a series of membranes that act as filters and dialysate membranes filter waste which are passed in to dialysate fluid and then that fluid is pumped out of the dialyser and blood is passed back through a second needle
  • During haemodialysis, they have a very strict fluid intake because 2-3 days of fluid is removed in four hours
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56
Q

What is peritoneal dialysis and what are the two types?

A
  • Surgical incision in abdomen, just below navel, tenckhoff catheter is inserted in to incision. Dialysate fluid passes through the catheter in to the peritoneal cavity. After dialysis, the end of the catheter is sealed.
  • Two types
    1) continuous ambulatory peritoneal dialysis (CAPD) – this involves exchanging old dialysate fluid that contains waste products and excess fluid with new dialysate. Exchange of old dialysate in to a waste bag, new in to peritoneal cavity. Takes 30-40 minutes to complete. Requires 3-4 exchanges a day. As the blood passes through the peritoneum, the dialysate fluid draws out waste products and excess fluid from the blood in to the fluid.
    2) automated peritoneal dialysis (APD) – same principals to control drainage of fluid, exchange is over night, takes 8-10 hours, final exchange of the dialysate is in place throughout the day.
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57
Q

What is Addison’s disease?

A
  • Opposite of Cushing’s
  • Disorder of body producing insufficient hormones of adrenal glands. Not enough adrenal hormones (cortisol, aldosterone).
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58
Q

What is Cushing’s syndrome and Cushing’s Disease?

A
  • Syndrome is excessive levels of cortisol in blood - common cause by taking medication already high in cortisol – too much cortisol (steroid medication, inhalers, topical)
  • Disease caused by tumour in pituitary gland in which pituitary releases the hormone ACTH.
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59
Q

What is diabetes type 1?

A
  • Autoimmune condition
  • Insulin dependent *
  • Body attacks beta cells so body cannot produce insulin
  • absolute insulin deficiency
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60
Q

What is diabetes type 2?

A
  • Insulin resistance, issue at receptor sites on cell membrane
  • a deficiency of insulin, the body is unable to produce adequate insulin to meet the needs.
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61
Q

What is the role of insulin in normal function?

A

Normally, a rise in BGL after a meal triggers pancreatic beta cells to release insulin. Insulin works as a key and stimulates cells to take the glucose from the blood.

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62
Q

What does the HbA1c test?

A

It measures glycated haemoglobin - this is haemoglobin that has joined with glucose in the blood. It gives an overall picture of average BGL over a period of 4-6 weeks.

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63
Q

What is metabolic syndrome?

A
  • Group of features that are linked to the body’s metabolism
  • Fat distribution associated with altered metabolic profile
  • Causes of syndrome is associated with cortisol – chronic
  • Define syndrome of co-occurrence of three risk factors: high BP, dyslipidaemia and central obesity. Obesity –> insulin resistance –> metabolic syndrome
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64
Q

What is Diabetic Ketone Acidosis? (DKA)

A
  • Body burns fat because there is no glucose for energy
  • Acute
  • If you have high BGL, you take insulin to lower BGL, insulin releases glucose
  • Normally, glucose is used for energy from liver, in diabetics, body burns fats to use for energy.
  • Caused by a diabetic not taking insulin or eating.
  • Common prior to diagnosis – glucose not being released, don’t know what’s going on – not taking insulin.
  • Can be caused by infection or trauma.
  • Fatigue, weight loss, thirst, smelly, unconsciousness, coma, death
  • High BGL.
  • Treated with insulin
  • Acid base balance affected
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65
Q

What is the mode of action of metformin?

A
  • Reduction of gluconeogenosis
  • Stops liver releasing stored glucose
  • Increases insulin sensitivity improving glucose uptake in peripheral muscle and adipose tissue
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66
Q

What is the difference between an anion and a cation?

A

Positively charged ions = cations +

Negatively charged ions = anions -

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67
Q

Are bicarbonate, phosphorus and chloride anions or cations?

A

Anions

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68
Q

Are sodium, potassium, magnesium and calcium anions or cations?

A

Cations

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69
Q

Which electrolytes are intracellular?

A

Potassium, phosphorus, magnesium

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70
Q

Which electrolytes are extracellular?

A

Sodium, chloride, bicarbonate

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71
Q

Which electrolyte is equal in ICF and ECF?

A

Calcium

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72
Q

What is the normal range for blood pH?

A

7.34-7.45

73
Q

What is the difference between an acid and a base?

A
  • An acid is a substance that can donate H+ to a base. Examples include hydrochloric acid, nitric acid, ammonium ion, lactic acid, acetic acid, and carbonic acid (H2CO3).
  • A base is a substance that can accept or bind H+. Examples include ammonia, lactate, acetate, and bicarbonate (HCO3-).
  • pH reflects the overall H+ concentration in body fluids. The higher the number of H+ in the blood, the lower the pH; and the lower the number of H+, the higher the pH
74
Q

What are the three systems that regulate the body’s pH?

A

Chemical buffers, respiratory system and renal system

75
Q

How do you detect metabolic acid/base imbalance?

A

By reviewing serum HCO3 levels

76
Q

How do you detect respiratory acid/base imbalance?

A

By reviewing PCO2 or serum CO2 levels

77
Q

What is the normal level for PCO2?

A
  • PCO2 (partial pressure of carbon dioxide in the blood) is 35-45mmol/L
78
Q

What is the normal level for HCO3?

A
  • 22-26mmol/L
79
Q

If a pH is 7.2 and an HCO3 of 20, what does this suggest?

A

Metabolic acidosis

80
Q

If a pH is out of the normal range, what does it suggest?

A
Metabolic acidosis (low pH) or metabolic alkalosis (high pH) 
Respiratory acidosis (low pH) or respiratory alkalosis (high pH)
81
Q

Symptoms of low pH

A
  • Depressed cardiac contractions, hyperventilation, depression of myocaridial contractility, tachycardia, vasoconstriction, arrhythmia threshold.
  • Effects of hyperkalaemia on the heart
  • Cerebral vasodilation
  • Less than 6.8 - fatal
82
Q

Symptoms of high pH

A
  • Impaired muscular function
  • Arrhythmias
  • Depressed myocardial contractility
  • Cerebral vasoconstriction
  • Increased neuromuscular activity
  • Potassium shift in to cells (hypokalaemia)
  • More than 7.8 – fatal
83
Q

What can cause metabolic acidosis?

A
  • an increased production of ketones
  • chronic alcoholism
  • severe malnutrition
  • poor intake of carbohydrates
  • hyperthyroidism
  • severe infection with fever
  • renal insufficiency
  • diarrhoea, intestinal malabsorption
  • lactic acidosis (can cause it or can worsen it)
  • acidic drugs
84
Q

What can cause metabolic alkalosis?

A
  • A decrease in hydrogen production
  • Somebody will have a pH of over 7.45 and an HCO3 of over 26
    Causes:
  • Often associated with underlying conditions
  • ECG changes
  • Hypocalcaemia
  • Hypokalaemia
  • Excessive vomiting
  • NG suctioning
  • Thiazide and loop diuretics
85
Q

What can cause respiratory acidosis?

A
  • A compromise of ventilation, perfusion or diffusion
  • Unable to rid of excess CO2 – alveolar hypoventilation
  • Respirations or impaired gas exchange
  • Hypercapnia (increased CO2)
  • If above 45 – acidosis
  • Unable to get rid of CO2 resulting in an increase in acid
  • Hypoventilation due to neuromuscular disorders, CNS trauma or brain lesions, airway obstruction, medication such as opioids and anaesthesia
  • CO2 combines with H2O and forms carbonic acid and pH drops
86
Q

What can cause respiratory alkalosis?

A
  • Exact opposite of acidosis, not enough CO2
  • Increase in CO2 elimination
  • Blood gas under 35, pH over 7.45
    Causes:
  • Conditions which cause hyperventilation: pain, sepsis, asthma, fever, heart attack, panic attack
87
Q

What are some signs and symptoms of respiratory alkalosis?

A
  • Shallow sharp breathing
  • Hyper excitability of the CNZ, twitching, jerking, spasms
  • Convulsions
88
Q

What are some signs and symptoms of respiratory acidosis?

A
  • Headache
  • Altered LOC
  • Flapping tremor
  • Warm and flushed
  • Rapid, shallow resps
89
Q

What are some signs and symptoms of metabolic acidosis?

A
  • rapid and deep breathing
  • BP drops
  • Cardiac arrhythmias with hyperkalaemia
  • Warm and dry, peripheral dilatation
  • Cold and clammy as the shock develops
  • Diminished muscle tone and deep reflexes
  • Lethargy
90
Q

What are some signs and symptoms of metabolic alkalosis?

A
  • Initial hypoventilation
  • Neuromuscular excitability
  • Neurologic symptoms
91
Q

What is the role of sodium?

A
  • Normal function helps maintain acid/base balance
  • Activates muscle and nerve cells
  • Works with chloride to influence water distribution in the body
  • Support normal extracellular osmolality – this is a shift in NA concentration that will trigger a fluid volume change to restore normal water and solute ratios
92
Q

What is hyponatraemia?

A
  • Not enough sodium
  • This is where the ratio of water to sodium is too high
  • Either a sodium deficit or a water excess
  • The water moves out of the vascular space in to the interstitial space then in to the intracellular space causing oedema
93
Q

What are signs and symptoms of hyponatraemia?

A
  • dry pale skin, dry mucous membranes
  • tachycardia, hypotension, muscle weakness
  • nausea/vomiting/diarrhoea, abdominal cramps
  • headaches, lethargy, anxiety, confusion, convulsions, behavioural changes
94
Q

What is hypernatraemia?

A
  • excess in the extracellular level of sodium
  • excess of sodium or deficit of water
  • hyperosmolar state exists because the ratio of sodium to water is too high, this ratio causes an increase in the extracellular osmotic pressure pulling fluid out of the cells causing dehydration at a cellular level
95
Q

What are signs and symptoms of hypernatraemia?

A
  • Flushed, dry skin
  • Red dry tongue
  • Dry mucous membranes
  • Tachycardia
  • Increased muscle tone
  • Hyperreflexia
  • Nausea/vomiting
  • Anorexia
  • Polyuria
96
Q

What is the normal function of potassium?

A
  • Normal function: a cation (+ charged), intracellular
  • Regulates cell excitability
  • Affects cell electoral status by permeating cell membranes eg. Action potential
  • Helps to maintain cell osmolality
  • Intracellular fluid osmotic pressure
97
Q

What is hypokalaemia?

A
  • Normal range of extracellular potassium is narrow; the slightest increase or decrease can cause serious life threatening effects on physiological function
  • A reciprocal relationship exists between sodium and potassium
  • A large sodium intake = an increased loss of potassium and vice versa
  • When potassium is lost from the cells, sodium will enter the cells
98
Q

What are some signs and symptoms of hypokalaemia?

A
  • Constipation
  • Decrease in gut motility
  • Nausea, vomiting
  • Polyuria
  • Lethargy
  • Confusion
  • Disorientation
  • Shallow rapid respirations
  • Tachycardia
  • Decrease in peripheral pulses
  • Postural hypotension
  • Generalised muscle weakness
  • Hyporeflexia
99
Q

What is hyperkalaemia?

A

High potassium

100
Q

What are some signs and symptoms of hyperkalaemia?

A
  • GI upset
  • Muscle weakness
  • GI cramps
  • Bradycardia = cardiac arrest
  • ECG results
  • Ventricular tachycardia
  • Never give as a push? (slow administration of treatment)
101
Q

What is the normal function of calcium?

A
  • Cation
  • Equal in ICF and ECF
  • Found in cell membranes, helps cells adhere to each other and supports shape of cell membrane
  • Effects cell membrane operability and cell membrane firing
  • Is an enzyme activator within cells eg. Action potential, muscle contraction
102
Q

What is hypocalcaemia?

A

Low calcium level

  • The stable serum calcium is maintained by endocrine negative feedback system
  • Phosphorus is inversely related to calcium and inhibits calcium absorption from the diet
103
Q

What are some signs and symptoms of hypocalcaemia?

A
  • Anxiety, irritability, convulsions
  • Tingling and numbness of fingers
  • Abdominal and muscle cramps
  • Contraction of facial muscles (chvosksteks) and tetany – condition characterised by spasm of the hands, feet, cramps and spasm of the larynx.
  • CVD – will decrease stroke volume
  • ECG changes
  • Decrease in prothrombin and elevated serum phosphorus
104
Q

What are signs and symptoms of hypercalcaemia?

A
  • GI upset
  • Anorexia
  • Constipation
  • Polyuria
  • Depression
  • Lethargy
  • Decrease in muscle tone
  • Osteoporosis
  • Heart block
  • Cardiac arrest
  • Hypercalcaemia crisis
105
Q

Magnesium normal function:

A
  • A cation (positively charged)
  • Intracellular
  • It is a important component of protein synthesis
  • A catalyst for enzyme reactions
  • Aids in the function of the sodium potassium pump
  • Modifies nerve impulse transmission and skeletal muscle response at the neuromuscular junction
106
Q

What are symptoms of hypermagnesaemia?

A
  • Lethargy
  • Drowsiness
  • Coma
  • Muscle weakness
  • Decrease in resps. and BP
  • Bradycardia
  • Prolonged QT interval
107
Q

What are symptoms of hypomagnesaemia?

A
  • Vertigo
  • Irritability
  • Disorientation and confusion
  • Tremors
  • Increased tendon reflexes
  • Positive signs of chvosteks (facial muscles),
  • Increased BP
  • Tachycardia
  • Dysrhythmias
108
Q

What is the normal function of phosphorus?

A
  • An ion (negatively charged)
  • Intracellular
  • Promotes energy storage
  • Promotes metabolism of protein, fat and carbohydrate
  • Acts as a hydrogen buffer
109
Q

What are some signs and symptoms of hypophosphataemia?

A
  • Anorexia
  • Memory loss
  • Seizures
  • Muscle pain
  • Weak pulse
  • Hyperventilation
110
Q

What are some signs and symptoms of hyperphosphataemia?

A
  • GI upset
  • Anorexia
  • Muscle weakness
  • Hyperreflexia
  • Tachycardia
  • QT interval is shortened
111
Q

What is the normal function of bicarbonate?

A
  • Is an ion
  • Extracellular
  • Main compensatory chemical buffer in the body
  • Regulates acid/base balance
112
Q

What is bicarbonate deficiency?

A

Metabolic acidosis

113
Q

What is it called when there is too much bicarbonate?

A

Metabolic alkalosis

114
Q

What is the normal function of chloride?

A
  • An ion (-)
  • Extracellular
  • Affects body pH and plays a massive role in acid base balance eg. Combines with hydrogen ions to produce hydrochloric acid
  • Helps to maintain extracellular fluid osmolality
115
Q

What is called when the body has too much chloride?

A

Hyperchloraemia

116
Q

What is it called when the body has too little chloride?

A

Hypochloraemia

117
Q

What is it called when the body has too little chloride?

A

Hypochloraemia

118
Q

What are the five types of trauma?

A

Acute – a single one off event eg. a natural disaster
Complex – this is an ongoing and interpersonal eg. domestic violence
Neglect – first three years of development eg. orphanages
Historical – wounding over a lifespan eg. racism, jews
Sanctuary/harm betrayal – placed somewhere for safety, abuse happens in this safe place

119
Q

What factors can impact reactions to trauma?

A
  • Context
  • History
  • Your current emotional state
  • Age
  • Abilities
  • Circumstances
120
Q

What are the three Es of trauma?

A

Event
Experience
Effects

121
Q

What is the ACE study?

A

Adverse Childhood Experiences study

  • There is an association between childhood maltreatment and later life health and well-being.
  • Experiences = social, emotional and cognitive impairment = health risks behaviours = early death
  • ACE is a scoring system, if you have a high ACE score it means you may be more vulnerable when you are older, scored 1-10. Based on neurological, biological, psychological and social factors.
122
Q

What are some symptoms of trauma?

A
  • Triggers (reminders of the event)
  • Physical stress responses
  • Hyper vigilance
  • Dissociation
  • Avoidance
  • Flash backs
  • Difficulty in trust
  • Self-injury
  • Guilt and shame
123
Q

What are some long term impacts of trauma?

A
  • Substance abuse
  • Depression
  • Liver disease, COPD (health alterations)
  • Smoking
  • Obesity
  • Suicide attempts
  • STDs
124
Q

What is acute stress disorder?

A
  • Transient anxiety response to severe trauma eg. car accident, getting mugged
  • Symptoms: anxiety, disassociation, disturbance of thoughts, flashbacks
  • For diagnosis, must last between 2-31 days and then if it’s longer than 1 month it becomes PTSD
125
Q

What is post-traumatic stress disorder?

A
  • Long lasting anxiety response following and traumatic or catastrophic event eg. violent assault, torture, war, accident
  • Develops at least a month after a traumatic event, can show up years later.
  • People are more vulnerable if they have a first degree history of it
  • Symptoms: flash backs, intrusive memories, depression, amnesia, social withdrawal, concentration difficulties, nightmares
126
Q

What is complex/chronic trauma?

A
  • Long lasting anxiety response following prolonged or repeated events
  • Develops from PTSD
127
Q

What are the three clusters of personality disorder?

A
  • Three clusters:
  • Cluster A) odd or eccentric
  • Cluster B) dramatic, erratic and emotional
  • Cluster C) anxious and fearful
128
Q

What is borderline personality disorder?

A
  • Struggles with irrigation of emotion
  • All triggered from trauma
  • Border-line between neurosis and psychosis
  • Emotional dysregulation disorder with strong anxiety components
  • DSM is only diagnosis that includes self-harm as a criteria
  • Symptoms: five or more for 1 year to be diagnosed. Fear of abandonment, relationship problems, identity disturbance, paranoia and disassociation, self-harm, intense mood swings, difficulty controlling anger
129
Q

What are some signs and symptoms of emotional dysregulation?

A
  • Clinging
  • Depression, rage, and defended by acting out
  • Detachment and withdrawal
  • Blame
  • Behaviour is a defense against a fear of loneliness
  • Fear of loss of control
  • Overwhelmingly sense of emptiness
130
Q

What are the three key factors that contribute to personality development?

A
  • Innate temperament – this is what you are born with, your own personal personality
  • Quality of early relationships – nurturing or neglect from parents/caregivers
  • Early life experiences and environments stress
131
Q

What are some key principals of informed services?

A
  • Asking what is wrong, not what happened
  • Appreciate many problem’s behaviours began as attempts to cope
  • Strive to maximise choices for the individual
  • Understand each person’s experiences
  • Cultural background
  • Acknowledge, assess, respond
  • Set a negotiated treatment plan
  • Avoid re-traumatising people, being aware
  • Responding to disclosure: listening, validating experience, normalising responses, acknowledging courage, showing empathy, non-judgemental approach
132
Q

What are the two main stress response pathways?

A
  • Short term response: Sympathetic nervous system (noradrenaline & adrenaline release)
  • Longer term response: Hypothalamus-pituitary-adrenocortical (HPA) axis (cortisol secretion)
133
Q

What is the long term impact of stress on mental health?

A

Difficulties with problem solving
Avoidance behaviours
Difficulty functioning, and new problems arise
Unable to relax
Feel out of control and may think we are ‘going mad’
May become severely depressed

134
Q

What are the types of anxiety disorders?

A
  • Generalized anxiety disorder (GAD)
  • Phobic disorders
  • Panic Disorder
  • Obsessive Compulsive Disorder (OCD)
135
Q

What are some characteristics of GAD?

A
Excessive worry & anxiety
Difficulty controlling the worry
Restlessness
Fatigue & irritability
Decreased ability to concentrate
Indecision
Muscle tension
Disturbed sleep
136
Q

What are the three phobic disorders?

A
  1. agoraphobia
  2. social phobia
  3. specific phobia
137
Q

What is a panic attack?

A
  • A distinct period of intense fear in the absence of real danger
  • Acute stress response (fight or flight), with abrupt onset, it reaches a peak in 10 minutes or less
  • An instantaneous surge in sympathetic nervous system activity is essential for mobilizing fast action
  • The physiological changes are primarily triggered by activation of adrenal pathways in the brain, which act on the heart, blood vessels, respiratory centres, and other sites.
138
Q

What are the characteristics of a panic disorder?

A
  • Recurrent unexpected attacks
  • Persistent worry about having further attacks
  • Apprehension about routine activities
  • Fear that attacks indicate a life-threatening illness
  • Devastating loss of self-confidence
  • Possible development of associated agoraphobia
139
Q

What are some nursing considerations for a patient experiencing a panic attack?

A
  • Stay with the person
  • Stay calm - anxiety is contagious
  • Communicate that you will not let anything happen to the person
  • Encourage slow breathing
  • Allow person to express their feelings and acknowledge their discomfort
  • The person may feel smothered if touched
  • Remember the attack will begin to subside in 10 minutes
  • Post-attack teaching plan – ongoing education on the nature of panic attacks, and slow breathing techniques
  • Medications: Antidepressant, and possible prn sedative/hypnotic
140
Q

What is OCD?

A

Persons with OCD know their thoughts are irrational, but cannot control them due to the significant anxiety and distress they experience if they try to resist acting out their obsessions

Obsessions and compulsions are so severe and time consuming they interfere with normal occupational and social functioning

141
Q

What is used in treatment for anxiety?

A
  • Antidepressants
  • Benzodiazepines
  • Buspirone (non benzodiazepine anxiolytic, does not have addictive properties, may augment antidepressant use)
  • Beta-adrenergic antagonists (betablockers)
  • Best treatment combination of psychological and pharmacological therapy
142
Q

What is a benzodiazepine?

A
  • Most common in MH: clonazepam, lorazapam; diazepam for treatment of withdrawals
  • Recommended not for long term use as addictive in nature. However many patients are on them for years.
143
Q

What is the mode of action for benzodiazepines?

A
  • Binds to benzodiazapine GABA- chloride receptor complex
  • Enhance the effect of the neurotransmitter gamma-aminobutyric acid (GABA) at the GABAA receptor, resulting in sedative, hypnotic (sleep-inducing), anxiolytic (anti-anxiety), anticonvulsant, and muscle relaxant properties
144
Q

What are the functions of the liver?

A
  • Breaks down toxins absorbed from the intestine or manufactured in the body and modifies them so they are no longer harmful excretes them in to bile.
  • Stores fat soluable vitamins
  • Synthesises cholesterol
  • Metabolises or stores sugars and processes fat
  • Assembles amino acids in to various proteins
  • Key functions: synthesis and storage of amino acids, proteins, vitamins and fats
  • Dexification
  • Blood circulation and filtration
  • Bile drainage
  • Blood glucose regulation
145
Q

What are the three types of Steatosis?

A

1) non-alcoholic fatty liver disease – this is accumulation of high amounts of fat in the liver highly associated with obesity, diabetes, metabolic syndrome, hyperlipidaemia, triglycerides, hypertension. Asymptomatic. Isolated fatty liver in which there is only an accumulation of fat.
2) Non-alcoholic steato hepatitis (NASH) – fatty liver inflammation and damage to hepatocytes. May produce symptoms: abdominal discomfort, anorexia, nausea, in more advance cases the liver may be enlarged. Progresses to cirrhosis. Treatment: lifestyle changes, weight loss.
3) Alcoholic fatty liver – the earliest stage of alcohol related liver disease. Abstaining from alcohol for 6 weeks will result in the fat decreasing. If alcohol use is continued, cirrhosis may develop.

146
Q

What is Cirrhosis of the liver?

A
  • Loss of hepatocytes
  • Irreversible scarring of the liver – an amount of tissue is not functioning
  • Chronic
147
Q

What can cause Cirrhosis of the liver?

A
  • Alcohol
  • NAFLD – non-alcoholic fatty liver disease
  • Hepatitis B and C
  • Other causes: hemochromatosis, primary bilary cirrhosis, fibrosis (scarring of connective tissue)
  • Cytokines are involved in the initiation and progression of fibrosis and cirrhosis, activated kupffer cells destroy hepatocytes and stimulate the activation of other mediators, hepatocytes undergo repeated cycles of damage and regeneration which contributes to the scarring.
148
Q

What is portal hypertension?

A
  • portal hypertension leads to oesophageal varices which leads to haemorrhage
  • two important factors are: vascular resistance and blood flow
  • the portal vein carries blood from the small and large bowel, spleen and stomach TO liver. About 1500ml of blood per minute. Obstruction of this flow results in increased venous pressure. Increased venous pressure is a compensatory mechanism, the development of collateral circulation (when blood re-routes) occurs and diverts the obstructed blood flow to the systemic veins.
  • Liver disease produces an increase in portal vascular resistance eg. Cirrhosis
149
Q

What are the three groups of causes for portal hypertension?

A
  • Causes come under pre-hepatic, intrahepatic, post-hepatic:
  • Pre-hepatic causes of increased resistance: portal vein thrombosis, splenic vein thrombosis, congenital atresia, stenosis (narrowing) of portal vein, tumours.
  • Intrahepatic: occurs when there is compression of the hepatic venules, by regeneration nodules, primary biliary cirrhosis, polycystic disease, hepatic metastasis, tuberculosis.
  • Post-hepatic resistance: thrombosis of inferior vena cava, right sided heart failure, constrictive pericarditis, severe tricuspid regurgitation, arterial venous portal fistula
150
Q

What are Oesophageal Varicies?

A
  • Abnormally enlarged veins in oesophagus
  • CONTRIBUTING FACTOR TO OESOPHAGEAL VARICES is due to the re-routing (usually re-routes to oesophageal vein) of the blood flow in the portal vein due to obstruction causing enlarged veins in oesophagus.
  • Portal hypertension causes oesophageal varices
  • Leads to oesophageal haemorrhage
151
Q

What is ascities and what can cause it?

A
  • The accumulation of fluid in the peritoneal cavity
  • Associated with portal hypertension and low levels of albumin
    Caused by:
  • Liver disease/failure
  • Hep C or B infection
  • Alcoholic cirrhosis
  • Cancer in colon, ovaries, uterus, pancreas and liver
  • Portal vein thrombosis
  • Congestive heart failure
  • Acute/chronic pancreatitis
  • Renal failure and dialysis
152
Q

What is Cholecystitis?

A
  • Acute cholecystitis is inflammation of gall bladder usually caused by calculi (gall bladder)
  • Role of gall bladder is to store and concentrate bile
153
Q

What is the cause of Cholecystitis?

A
  • When cystic duct gets blocked by gall stone or biliary sludge (a mixture of bile and small crystals of cholesterol and salt) results in a build-up of bile in gall bladder, increasing pressure causing the gall bladder to become inflamed and swollen. This can trigger gangrenous cholecystitis.
154
Q

What are some signs and symptoms of cholecystitis?

A
  • Severe, sharp and constant pain in upper right abdomen
  • Worse when breathing deeply
  • Pain in right shoulder or shoulder tips
  • Fever of 38+
155
Q

What is acute pancreatitis? How is it caused?

A
  • Gall stones cause acute pancreatitis by: gall stones pass through the common bile duct to enter the small intestine via the ampulla of vater.
  • The main pancreatic duct joins or lies immediately next to the common bile duct. Stones lodge and obstruct common bile duct and impinge in the main pancreatic duct causing an obstruction of the normal flow of pancreatic fluid.
  • Auto digestion occurs due to activated pancreatic enzymes leading to pancreatic injury.
  • Backflow of bile into pancreatic duct leads to pancreatic injury.
  • Inflammation of pancreas
156
Q

What are some signs and symptoms of acute pancreatitis?

A
  • gradual and sudden pain in upper abdomen that extends to the back
  • initial pain may be mild but worse after eating
  • when the pain intensifies it is severe and constant
  • look and feel very ill
  • needs immediate attention
  • swollen and tender abdomen
  • nausea and vomiting
  • fever
  • rapid pulse
157
Q

What are some investigations for acute pancreatitis?

A
  • medical history
  • physical examination
  • blood test for amylase or lipase which are pancreatic enzymes. During acute pancreatitis these will be elevated 3x the normal level.
  • Ultrasound scan
  • CT scan
  • Risk scoring tool predicting who is more likely to develop severe pancreatitis
  • BGL
158
Q

What are some treatments for acute pancreatitis?

A
  • uncomplicated cases require hospitalisation for 3 to 5 days for close monitoring, pain control and IV fluids
  • fluid resuscitation
  • nutritional support – nil by mouth to rest pancreas and bowel for first 48 hours, following this you can provide nutrition.
  • Pain control – opiates
  • Treatment depends on underlying conditions, treat underlying cause
159
Q

What is CBT?

A
  • Cognitive Behavioural Therapy
    How our thinking influence our mood and behaviour, which influences our further thinking
  • Primarily used to treat people with depression or anxiety but has been developed to treat most other mental disorder and addictions
  • Based on the assumptions that individuals can construct their own reality.
160
Q

What is DBT?

A

Dialectical Behavioural Therapy

  • When they cannot tolerate emotional distress and they get overwhelmed – self harm often used as a way to deal with emotions
  • DBT encourages individuals to consult themselves – find ways to deal with emotions appropriately and encourages them to tolerate the emotions
  • Use strategies to gain mastery to regulate emotions
  • DBT involves individual therapy and skill-based groups
161
Q

What is Motivational Interviewing?

A
  • Used for addictions, chronic health conditions such as eating disorders, obesity and diabetes
  • Deprived from CBT, looks to assist people to change unhealthy behaviours
162
Q

What are the five principals of motivational interviewing?

A
  1. Express empathy
  2. Avoid argument
  3. Supports self-efficiency
  4. Role with resistance – new perspectives, conflict resolution
  5. Develop discrepancy – awareness of consequences, looking at long term
163
Q

In regards to motivational interviewing, what is intrinsic and extrinsic?

A
  • Promotes intrinsic thinking – important good decision making
  • The goal of motivational interviewing is to improve intrinsic thinking
  • Avoiding blame of outside (extrinsic) factors, encouraging the internal will-power to self-fulfil goals.
164
Q

What is an attachment disorder?

A
  • Occurs when an attachment is disturbed in some way, when this occurs to children, they don’t develop the skill necessary to build meaningful relationships and struggle to connect with people.
  • Affects an infant’s ability to express emotions
165
Q

What is fetal alcohol syndrome? What effects does it have on a child?

A

This includes a range of effects on a child because of alcohol consumption during pregnancy

  • The effects include: poor growth/small size, facial abnormalities, failure to thrive, heart defects, brain damage, developmental delay eg. seizure disorders, fine motor skills – poor gait, social, emotional, behavioural and mental disabilities.
  • Socially very outgoing and socially engaging but frequently seen by others as intrusive, overly talkative and unaware of social cues. Poor judgement and socialisation skills.
  • Hyperactivity, short attention span
166
Q

Why do mental health symptoms usually show in late teenage years to early adulthood?

A

This is shown because of the crucial development of this age. Development domains, major changes are occurring, outcomes in adult hood. These processes have a major long term stress on the person. Eg. study, buying a car, new relationships, family.

167
Q

What does a HEEADSSS assessment consist of?

A

Home, education, employment, activity, drugs, suicide, safety, self harm, spirituality

168
Q

What are symptoms of cystic fibrosis?

A
  • Meconium ileus (bowel obstruction), this appears at birth
  • Salty tasting skin
  • Greasy bulky and fowl smelling poo
  • Poor growth/weight gain despite good apatite
  • Chronic coughing at times with phlegm
  • Frequent lung infections
169
Q

What are some treatments for cystic fibrosis?

A
  • Bronchial airway drainage
  • Oral enzymes
  • Better nutrition – high calorie diet, special vitamins and pancreatic enzymes
  • Lung transplant
170
Q

How can you test for cystic fibrosis?

A
  • A genetic analysis – a new-born screening called the Guthrie test
  • Sweat test – measures sodium or chloride. This is not reliable on new-borns
171
Q

What is cystic fibrosis?

A
  • It is a defective gene related to protein involved in chloride ion transport
  • The body produces thick sticky mucous that is trapped in the lungs
  • Chronic infections
  • Obstructs pancreas resulting in malnourishment and malabsorption
  • Located on 7th chromosome
172
Q

What does PLISSIT stand for?

A

Permission (P) – to talk about sexuality

Limited Information (LI)- answer questions/give info/ resources

Specific Suggestions (SS)- refer on

Intensive Therapy (IT)-refer on

173
Q

What is sensory modulation?

A

A clinical intervention that utilises environment, equipment and activities to regulate a persons sensory experience and optimise wellbeing.

174
Q

What is the optimal arousal state in sensory modulation?

A

The ‘calm alert’ state

175
Q

What things would you assess in a client prior to using sensory modulation?

A
Allergies
Diagnostic considerations
Respiratory precautions
Medication changes or side effects
Environmental (e.g. lighting, background noise)
Seizure history
Trauma history
Cardiac precautions
176
Q

What are some warning signs of suicide?

A

Direct or indirect threats kill/hurt self
Questions about death and dying
Obsessing about death
Talking or writing about death and dying
Looking for means to kill/hurt self
Saying goodbye, giving personal effects away
Isolating from family/friends
Hopelessness, worthlessness, feeling trapped
Rage, angers, seeking revenge
Reckless or risky behaviour (increase in drug or alcohol use)
Dramatic changes in mood or behaviour

177
Q

How do you determine the risk of a suicidal person? What does SLAP stand for?

A

Ask about how (the plan)
Ask about the means for suicide (Remove the means if possible)
Ask about the timeframe

S pecific (how specific is the plan)
L ethality (means)
A vailability (of means)
P roximity (of help)
178
Q

What are the three steps of haemostasis?

A
  1. Vasoconstriction
  2. Platelet activation (temporary plug formation)
  3. Coagulation (cascade occurs here) Prothrombin to thrombin, thrombin converts fibrinogen to fibrin. Fibrin sticks to everything as a mesh resulting in stable clot = healing.
179
Q

What is thrombosis?

A

Local coagulation or clotting of blood in circulatory system, disrupting blood flow.