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PBL Notes > PBL 12- Osteoporosis > Flashcards

PBL 12- Osteoporosis Flashcards

1
Q

What is the first line treatment for depression in the elderly?

A

• First line = SSRI
○ Monitor for hyponatraemia and serotonin toxicity
○ Avoid paroxetine- anticholinergic
○ Avoid fluoxetine: long half life
• Second life : SNRIs
○ Venlafaxine
○ Mirtazapine- less likely to cause hyponatraemia
• ECT -safe and effective in the frail aged
• Third line = tricyclics

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2
Q

How does bipolar present differently in the older aged?

A
  • More irritable than euphoric
    • Paranoid rather than grandiose
    • May have dysphoric mania
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3
Q

What is the treatment for bipolar in the older person?

A

Lithium
○ May have decreased renal clearance and neurotoxic effects more common
○ Valproic acid is also helpful for behavioural disturbances

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4
Q

How common is psychosis in older people?

A
  • up to 23% of the older adult population will experience psychotic symptoms at some time
    • Main contributing factor is DEMENTIA
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5
Q

What are the risk factors for older people developing a psychosis?

A
  • age related changes in the frontotemporal cortices
    • Social isolation
    • Sensory deficits
    • Cognitive decline
    • Polypharmacy
    • Medical comorbidities
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6
Q

What are the diagnosis’ that account for 80% of psychotic older patients?

A
  • Dementia
    • Delirium
    • Depression
    • Organic
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7
Q

What is the First line medication choice for psychosis in older people?

A

• Haloperidol

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8
Q

What is used in the behavioural and psychological symptoms of dementia?

A

Risperidone

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9
Q

What is the DSM criteria for Dementia?

A
  • Declining cognition, functional decline for at least 6 months duration
    • Amnesia

PLUS 1 or more of the following:
• Aphasia
○ Impairment of language, affecting the production of comprehension of speech and ability to read or write
• Apraxia
○ Difficulty with the motor planning to perform tasks or movements
• Agnosia
○ Inability to process sensory information
• Executive function
○ Goal formation, planning, self monitoring, attention, response inhibition

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10
Q

What is the pathology found in Alzheimer’s disease?

A

• Damage in the medial temporal lobe (hippocampus)
○ Intracellular damage (neurofibrillary tangles)
○ Extracellular deposits (amyloid plaques)
• Spreads to effect cortical structures
• Memory and later language affected
• Both subserved by cortical structures

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11
Q

What is the treatment for dementia?

A 
• Biological treatments 
		○ Cholinesterase inhibitors for AD
		○ Aspirin for Vascular dementia
		○ There are no disease modifying agents at this time.
	• Functional issues addressed 
		○ Home care
		○ Residential placement
	• Legal issues
	• Carer support
	• Family issues ie genetic counselling
	• Behavioural and psychological symptoms of Dementia
		○ Often need psychogeriatric input
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12
Q

How is bone mass normally maintained?

What regulates this?

A

Balance between activity of:
• Osteoblasts which produce matrix and bone mineralization
• Osteoclasts which break it down (degrade the matrix and cause resorption)

Process is tightly regulated by local endocrine factors
	• Hormones
	• Vitamins 
	• Stress
	• Inflammation
	• Growth factors
	• cytokines
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13
Q

What factors affect formation and resorption by osteoblasts/clasts?

A 
• Glucocorticoids
		○ Inhibits osteoblasts 
	• Estrogen 
		○ Inhibits osteoclasts and stimulates osteoblasts
	• Thyroid hormones
		○ Stimulates osteoclasts
	• Growth hormone nd IGF1 
		○ Stimulates osteoblasts
	• Calcitonin 
		○ Inhibits osteoclasts
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14
Q

What things can shift bone turnover to favour resorption?

A
  • Decrease in sex hormones
    • Drugs- glucocorticoids
    • Hyperparathyroidism
    • Cushings Syndrome
    • Kidney disease
    • GIT absorptive issues
    • Genetic causes- affect enzymes that regulate bone metabolism
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15
Q

What is Osteoporosis?

A

· Systemic condition characterized by low bone mass and deterioration in bone microarchitecture
· Leads to increased bone fragility and increased fracture risk

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16
Q

Where is the bodies calcium usually stored?

Why is this clinically important?

A

· 99% is stored in the bone as ca hydroxyapatite
· 1% is dissolved in blood and ECF
• Bound to plasma proteins, small organic molecules (Phosphate) and free ions
· This means that If the body needs calcium, it needs to come from this store

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17
Q

Why is calcium homeostasis important?

A

· It is essential for key cellular processes
• Heart and muscle contraction
• Nerve conduction
• Exocytosis
• Activity of enzymes
· There is a tight control of extra and intracellular calcium levels via transporters, pumps and binding proteins
· If there is a dietary deficit in calcium it will be resorbed from the bone

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18
Q

What are the clinical consequences of high or low blood calcium?

A 
· Hypercalcaemia
	• Fractures due to excessive resorption of bones making them prone to break after minor trauma
	• Formation of renal stones
	• Proximal myopathy
	• Pancreatitis
	• Mental changes
	• Usually due to primary hyperparathyroidism
· Hypocalcaemia
	• Paraesthesia
	• Cramps
	• Tetany
	• Agitation
	• Seizures
19
Q

What are the key players in calcium homeostasis, and how to they interact?

A

Parathyroid hormone
• Fast acting
• Responsible for the minute to minute control of serum calcium concentration
· Calcitriol
• Slow acting and maintains day to day control of serum calcium concentration

20
Q

What are the main target organs in calcium homeostasis?

A

· Intestine
· Kidney
· Bone

21
Q 
Parathyroid hormone:
What is its role?
Where is it produced/Secreted?
What regulates this ?
What does it target and what are the effects?
A

Role:
· The most important regulator of blood calcium and phosphate
· Primary hormone regulating bone metabolism/remodelling

Produced and secreted:
· Parathyroid gland
· Synthesized as a preprohormone

Regulation:
· Secretion is dependent on serum calcium
• Calcium binds to a Calcium sensing receptor (CaR)
• This is a GPCR expressed on many cells
• Signalling cascade leads to SUPPRESSION of PTH secretion and cell proliferation
· Inhibited by - high plasma Ca
· Stimulated by- low plasma ca

Targets:
· Bone
• Causes resorption via increased osteoclast activity
• Increased calcium mobilisation
· Kidney
• Increased calcium reabsorption
• Decreased calcium excretion in urine
• Increased production of active vitamin D
○ This acts on the small intestine to increase calcium absorption from the diet

Effect:
· Increased blood calcium

22
Q

What is the Ca/PTH axis feedback loop?

What is the clinical significance of this?

A

· PTH is the principal modulator of plasma ca levels
· ECF Ca levels are the primary determinant of PTH secretion
· Comparing calcium and PTH levels can show where there is a problem in the axis
· Examples
• Low calcium with low PTH = PTH not responding ? Hypoparathyroidism
• High Calcium with High PTH = Gland producing too much PTH ? Hyperparathyroidism
• Low calcium with high PTH = response is correct- need to evaluate for non parathyroid problem

23
Q

Calcitonin
Where is it produced/Secreted?
What regulates this ?
What does it target and what are the effects?

A

Produced:
· Thyroid C cells (main source)
· Also in other tissues (lung, intestine and mammary gland)

Targets:
· Kidney
	• Increases excretion of calcium
· Bone
	• Increases deposition in bone by inhibiting osteoclasts
	• Prevents resorption
· Intestine
	• Decreases uptake

Aim:
· Decrease blood calcium levels

24
Q

Vitamin D2/D3
What are the different forms?
Where is it produced?
Solubility/trasnport?

A

Vitamin D2 = ergocalcigerol
• Sourced from plan and yeast

Vitamin D3 = Cholecalciferol
• Most is produced by the skin in photochemical synthesis
• Exposure of the precursor to UV radiation
• Some is ingested in small amounts in fish

Activity:
· In the D2 or D3 form it is a pro-hormone with little significant biological activity
· Needs to be metabolised to an active form

· Lipid soluble steroid hormone
· Transported in the blood by transcalciferin
• Vitamin D binding protein
• Long half life - 5-12 hours

25
Q

Calcitriol:
How is it synthesized?
What are its actions?
Solubility/binding?

A

· Vitamin D3 must be metabolised within the body to become the active form - calcitriol
• Liver forms the intermediate form - Calcidiol
• Kidney transforms this into the active form calcitriol under the stimulation of PTH

· The lipid soluble hormone Binds to intracellular Vitamin D receptors
· Effects gene expression to cause protein synthesis

Acts on
· Bone:
	• Regulates bone remodeling
· Gut
	• Inreases calcium and phosphate absorption
· Muscle
	• Increases growth , strength and contraction
· Increases immune function
· Decreases inflammation
· Epithelial cells
	• Increases differentiation
	• Decreases proliferation
	• Causes apoptosis
26
Q

What happens to calcium absorption when there is a vitamin D deficiency?

A

· It is not efficiently absorbed

· Calcitriol controls synthesis of genes and increases expression of proteins that promote transcellular transport of ca

27
Q

What happens when blood Calcium levels fall?

A

PTH
· Low calcium causes stimulation of PTH secretion
· PTH acts directly on bone to induce osteoclastic resorption from bone
· PTH increases synthesis of Calcitriol by the kidney
· PTH increases reabsorption of calcium from the glomerular filtrate preventing loss in the urine

Calcitriol
· Calcitriol increases intestinal absorption of calcium
· Calcitriol can stimulate osteoclasts indirectly by stimulating osteoblasts to release factors that stimulate differentiation
• Not as potent as PTH
• Slow acting
• Role in normal bone remodeling

28
Q

What do PTH , calcitriol and calcitonin do In the case of normal calcium levels?

A

PTH
· Inhibition of PTH synthesis
· Decrease in PTH levels
· Less mobilization of calcium from the bones

Calcitriol
· Enhances absorption of Ca and phosphorus from the small intestine
· This helps to maintain a proper balance that assists Calcitonin to mineralize the bone matrix

Calcitonin
· Reduces osteoclastic bone resorption and allows excess calcium to deposit in bones
· Decreases PTH synthesis

29
Q

How common is Vitamin D deficiency?
What are the effects of a mild/Moderate deficiency?
What are the effects of a s

A

· More than 40% of the world is vitamin D deficient
· 1 in 5 children

· Can be due to :
	• Reduced intake
	• Age related factors
	• Decreased sun exposure
	• Sunscreen use
	• Decline in renal function

· Mild to moderate deficiency
• Decreased calcium absorption resulting in decreased serum calcium
• Increased PTH causing increased tubular resorption of calcium and bone resorption
• Decreased bone density
• High bone turnover
• Increased fracture risk in older people

· Severe Vitamin D deficiency
• <15 nM
• Blood calcium below normal
• Can cause secondary hyperparathyroidism
○ PTH also causes phosphorus loss via the urine leading to a decreased serum phosphate
○ This imbalance causes a defect in bone mineralization
• Children get rickets
• Adults get Osteomalacia

30
Q 
Phosphorus-
How abundant is it?
Where is it stored?
What do cells use it for?
Dietary sources?
A

· It is the most abundant mineral after calcium
· The bulk is stored in bone (85%) as mineralized hydroxyapatite ECM giving the bone strength
· Every cell contains phosphate anions
• Complexed to proteins or lipids
• Nucleic acids in DNA and RNA
• Needed for energy production
• Used as a chemical buffer in serum and urine
· Most unprocessed food has it

31
Q

How is phosphate balance maintained- ie ?

A

Renal cotransporter:
• There are sodium- phosphate co transporters in the proximal renal tubular cells
• If there is low dietary phosphate intake there is an increase in expression of transporters leading to increased renal phosphate absorption
• In excess intake the opposite occurs and there is less transporters expression and more phosphate is excreted in urine

FGF-23
· FGF 23 = 23 fibroblast growth factor (phosphaturic hormone)
· Secreted from bone
· Works on the kidney
· Secreted in response to HIGH dietary intake or serum phosphate levels
· It works on the Sodium phosphate cotransporter to decrease expression of transporters
· Causes:
• Inhibition of phosphate reabsorption (Similar to PTH)
• Increased excretion of phosphate (Similar to PTH)
• Decreases calcitriol synthesis resulting in decreased gut phosphate absorption (Opposite to PTH)
· Aim:
• To decrease serum phosphate level

32
Q

What happens if the FGF-23 is excessively elevated?

What causes it?

A

· Phosphate levels will become too decreased
· Linked to rare forms of hereditary hypophosphataemic rickets and osteomalacia
· Most often found in chronic kidney disease
• Decreased glomerular filtration
• Decreased kidney phosphate excretion
• Increased FGF 23 secretion from bone
• Decreased calcitriol through inhibition of hydroxylase in the kidney
• Low blood calcium
• Secondary hyperparathyroidism

33
Q

Very broadly what are the effects of the following on ca and phosphate levels?
PTH
Calcitriol

A

PTH :
· Increases Calcium
· Decreases Phosphate

Calcitriol
· Increases Calcium
· Increases Phosphate

34
Q

What are some causes of hypercalcaemia?

What is the reference range?

A 
·  > 2.6
· Hyperparathyroidism 
	• Primary, secondary, tertiary
· Increased absorption of calcium
· Malignancy
· Vitamin D intoxication
· Thiazide diuretics
· Renal insufficiency
· Thyrotoxicosis
· Familial hypocalciuric hypercalcaemia
· Sarcoidosis
35
Q

What are the effects of Hypercalcaemia?

A 
· Neurological:
	• Confusion
	• Lethargy
	• Headaches
	• Depression
	• Coma
· Abdominal:
	• Nausea and vomiting
	• Abdominal pain
	• Polyuria, polydipsia
	• Pancreatitis
	• Kidney stones
· Other:
	• Dehydration
	• Bradycardia
	• Renal failure
	• Muscle fatigue
36
Q

What are some causes of hypocalcaemia

What is the range?

A 
·  < 2.25
· Osteomalacia : vitamin D deficiency
· Chronic renal failure
· Hypoparathyroidism
· Alkalosis
· Hypomagnesaemia
· Acute pancreatitis
· Alcoholism
· Chronic diarrhoea
· Hyperventilation
· Malabsorption
37
Q

What are some effects of hypocalcaemia?

A 
· Cardiovascular:
	• Long QT intervals
	• Hypotension
	• Heart failure
· Neuromuscular
	• Cramps / spasms
	• Tetany
	• Bronchospasms
· Neurological:
	• Irritability
	• Seizures /Convulsions
	• Hyperreflexia
	• Positive chvostek sign
	• Positive trousseau sign
	• Parathesias
· Abdominal
	• Intestinal cramps
	• laryngospasm
38
Q

What are some causes of hyperphosphataemia?

A

· Increase absorption of phosphate
○ Excess use of some laxatives and enemas
○ Excess Vit D
· Shift of phosphates from cells into blood
○ High levels of cell destruction –metastatic tumour cell lysis during chemotherapy
· Inadequate excretion of phosphate
○ Renal failure
○ Hypoparathyroidism

39
Q

What are the clinical manifestations of hyperphosphataemia?

A 
· Neuromuscular:
	• Muscle cramping / Muscle twitching
	• Tetany
	• Hyperreflexia
	• Hypotension
· Neurological:
	• Confusion
	• Paraesthesia
	• Seizures
	• Coma
· Other:
	• Soft tissue calcification – Aching, stiff joints
	• Alkalosis
	• Itching skin
	• Cardiac dysrhythmias
40
Q

What are some causes of hypophosphataemia?

A 
· Inadequate absorption of phosphate
	• Chronic diarrhoea
	• Vomiting
	• Malabsorption
	• Misuse of phosphate-binding antacids
	• Chronic alcoholism
	• Vit D deficiency
· Shift of phosphate from blood into cells
	• Respiratory Alkalosis
	• Insulin administration
	• Adrenalin administration
· Excessive phosphate excretion
	• Increased diuresis
	• Hyperparathyroidism
· Other:
	• Severe burns
	• Severe sepsis
41
Q

Magnesium:
What is its role in the body?
Where is it stored?
Where is it sourced from?

A 
Role:
· Nerve and muscle function
· Neurotransmission
· Bone structure
· Constituent of several enzymes

Stored:
· 50% is stored in the bone and muscle
· 1/3 is bound to protieins

Dietary source:
· Green vegetables
· Cereal 
· Nuts 
· Dairy products
42
Q

What are some causes of Hypermagnesaemia?

A 
· Increased absorption of Mg:
	• Excessive use of Mg-containing antacids
	• Excessive infusion of Mg
· Decreased excretion of Mg:
	• Renal failure
	• Metabolic acidosis
43
Q

What are the clinical manifestations of hypermagnesaemia?

A 
· Neuromuscular:
	• Decrease in deep tendon reflexes - Hyporeflexia
	• Muscular weakness
	• Paraesthesia
	• Paralytic ileus
· Other:    
	• Platelet aggregation
	• Hypotension
	• Dysrhythmia
	• Respiratory depression
	• Drowsiness and lethargy
	• Flushed skin and sweating
	• Cardiac arrest

PBL Notes (14 decks)

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