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Medicine year 2 semester 2 > Case 25- physiology > Flashcards

Case 25- physiology Flashcards

1
Q

Hypercalcaemia

A

1) Mild hypercalcaemia may asymptomatic
2) Moderate to severe hypercalcaemia- symptoms of neuromuscular suppression
3) Other symptoms include: kidney stones, dehydration, weight loss, nausea, vomiting and fatigue
4) Main causes: Primary Hyperparathyroidism, Malignant Disease

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2
Q

Primary Hyperparathyroidism

A

1) Ca+2 homeostatic loss due to excessive PTH secretion
2) Excess PTH secreted from benign parathyroid tumour (adenoma) or hyperplastic parathyroid tissue
3) Primary hyperparathyroidism causes hypophosphataemia and excessive bone resorption

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3
Q

Hypercalcaemia results from the combined effects of

A

PTH-induced bone resorption
Intestinal Ca2+ absorption
Renal tubular Ca2+ reabsorption
Stimulates conversion to active form of Vit D

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4
Q

Primary Hyperparathyroidism (2)

A

1) Pathophysiology related to- PTH excess, Excessive production of 1,25 DHCC
2) Deposition of Ca+2 in the heart, lungs and soft tissue

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5
Q

Malignant disease of Hypercalcaemia

A

1) Common cause of severe hypercalcaemia
2) Malignant cells (metastases) in bone cause destruction of the bone and release Ca2+- Direct tumour invasion, Local Osteolytic Hypercalcemia (LOH) caused by secretion of osteoclast activating factors
3) Metastases not in bone synthesise and secrete parathyroid hormone-related peptide (PTH-rP). Structurally similar to PTH, particularly amino terminus
4) Endogenous levels of PTH are low, in response to hypercalcaemia

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6
Q

Vitamin D dependent hypercalcaemia

A

Overdose on pharmacological preparations

Granulomatous disease i.e. TB, leprosy

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7
Q

Hyperthyroidism

A

Increased bone turnover (osteoclast activity), usually asymptomatic

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8
Q

Acromegaly

A

Stimulation of 1α-hydroxylase in kidney by elevated levels of growth hormone
Immobilization (due to accelerated bone resorption; More seen in people with Paget’s disease of bone).Causes enlarged bones
Excessive milk ingestion or Ca2+-containing antacids - rare

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9
Q

Causes of Hypocalcaemia

A

Hypoparathyroidism
Pseudohypoparathyroidism
Vitamin D deficiency and dependency
Renal disease

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10
Q

Hypoparathyroidism

A

1) Inadequate response of the PTH - vitamin D axis to hypocalcaemic stimuli
2) Deficient PTH can occur- in autoimmune disorders. After the accidental removal. Damage to several parathyroid glands during thyroidectomy
3) Twitching - Tetany
4) Hyperphosphatemia

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11
Q

Renal disease- Hypercalcaemia

A

Acquired proximalrenal tubular acidosis. Heavy metals – cadmium. Distal renal tubular acidosis

Cause:
Abnormal renal loss of calcium
Decreased conversion of vitamin D to active 1,25DHCC
Decreased formation of 1,25DHCC- direct cell damage, suppression of 1α hydroxylase (Hyperphosphatemia)

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12
Q

Secondary hyperparathyroidism- main causes

A

Advanced chronic kidney disease (most common)

Malabsorption of vitamin D in the GI tract

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13
Q

Secondary hyperparathyroidism

A

1) Hyperphosphatemia- can enhance CaPO4 deposition in skin (pruritis) and in blood vessels of CKD patients
2) Risk factor of CDVS morbidity
3) May accelerate metabolic bone disease
4) Sensitivity of the parathyroid to calcium may be diminished- pronounced glandular hyperplasia, elevation of the calcium set point

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14
Q

Causes of vitamin D deficiency

A

1) Inadequate exposure to sunlight (elderly, some communities)
2) Inadequate intake of vitamin D (elderly/ housebound/ hospitalized
3) Reduced absorption of vitamin D (GI problem)

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15
Q

Abnormal metabolism of vitamin D

A

Type I vitamin D–dependent rickets,
CKD, Hepatic dysfunction,
Anticonvulsants, GC hormones

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16
Q

Resistance to the effects of vitamin D

A

Type II vitamin D dependent rickets

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17
Q

Pseudohypoparathyroidism

A

Target organ resistance to PTH (not by hormone deficiency). Complex genetic transmission disorders
Type Ia - failure of normal renal phosphaturic response)
Type Ib, Type II (less common)

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18
Q

Other causes pf Pseudohypoparathyroidism

A

1) Acute pancreatitis- lipolytic products released from the inflamed pancreas chelate calcium
2) Hypoproteinemia
3) Septic shock (Suppress PTH release)
4) Anticonvulsants (phenytoin,phenobarbital)
5) Rifampin (altered vitamin D metabolism)
6) Magnesium depletion

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19
Q

Calcitonin pathophysiology

A

1) Tumours of the parafollicular cells of the thyroid produce calcitonin – hypercalcitonaemia
2) Often heriditary
3) Although calcitonin levels are high, serum Ca2+ and bone architecture are normal
4) Low serum calcium concentrations rarely occur in patients with medullary carcinoma of the thyroid

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20
Q

Different ratios in the Sociology of ageing

A

1) dependency ratio: ratio of economically active to economically inactive or dependent people in a population
2) neontic ratio: ratio of children (0-14) to adults of ‘working’ age (15-59)
3) gerontic ratio: ratio of ‘retired’ (60+) people to adults of ‘working’ age (15-59)

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20
Q

Different ratios in the Sociology of ageing

A

1) dependency ratio: ratio of economically active to economically inactive or dependent people in a population
2) neontic ratio: ratio of children (0-14) to adults of ‘working’ age (15-59)
3) gerontic ratio: ratio of ‘retired’ (60+) people to adults of ‘working’ age (15-59)

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21
Q

Ageing- male sexual dysfunction

A

1) Both testosterone levels and sperm production decrease progressively in men over 50 years of age
2) Additionally the prostate gland typically enlarges
Erectile dysfunction= the persistent inability to initiate or sustain penile erection sufficient for satisfactory sexual activity
Age is a big factor in the prevalence of erectile dysfunction

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22
Q

Why do we age- Programmed theory

A

Ageing is genetically determined with organisms having an ‘internal clock’ related to ageing and the length of life

23
Q

Why do we age- Stochastic theories

A

Ageing is caused by random damage to vital molecules. The damage eventually accumulates to a sufficient level which results in the physiological decline associated with ageing

24
Q

Why we age- Evolutionary theories

A

1) There is evolutionary pressure towards populations with an ‘optimal average age’
2) Energy is required to make and maintain a complex organism
3) Anatagonistic pleiotropy theory- alleles which increase early life fitness are selected for, even if those alleles undermine later fitness. A more refined version of this theory is the disposable soma theory

25
Q

Disposable soma theory

A

It is beneficial to maintain stability of the germ-line for reproductive success, and reduced regulation of the somatic cells may save energy that can be used instead to promote faster growth and reproduction

26
Q

Ageing- genetics and environment

A

1) Genes contribute around 20-30% to ageing/lifespan
2) There is no genewhich specificially programmes ageing
3) There are genes that affect longevity i.e. progeria
4) Environmental factors play a big part i.e. smoking and calorie intake

27
Q

Three sociological perspectives of ageing

A

1) Functionalist perspective: focus on the role of older people in society
2) Conflict perspective: focus on how older people, as a group, differ from other social groups
3) Symbolic interactionism: focus on how the identities of older people are created through their interactions

28
Q

The nine biological hallmarks of ageing

A

1) Genomic instability
2) telomere attrition
3) epigenetic alterations
4) loss of proteostasis
5) deregulated nutrient sensing
6) mitochondrial dysfunction
7) cellular senescence
8) stem cell exhaustion
9) altered intercellular communication.

29
Q

Ageing- genomic instability

A

Accumulation of genetic mutation= Point, Gene disruption (virus DNA), Translocation, Chromosomal gains/losses
These are all cuntered by DNA repair mechanisms
Genomic instability may affect Nuclear DNA, Mitochondrial DNA and Nuclear architecture
May effect essential genes and cause apoptosis or dysfunctional cells

30
Q

Ageing- Telomere attrition

A

1) Telomeres offer another cell division control mechanism
2) Telomeres (repetitive DNA sequences) found at the end of chromosomes
3) Many cells can only make a limited number of divisions – Heyflick Limit.
4) Cultured human fibroblasts divide 40-50 times then stop - this is replicative Cell Senescence.

31
Q

Telomere attrition part 2

A

Replicative DNA polymerases can repair terminal ends of DNA

Telomerase
Specialised DNA polymerase
Most adult somatic cells don’t express telomerase
Telomerase activated in immortal cancer cells
Can telomerase be activated in somatic cells without causing oncogenesis

32
Q

Ageing- Epigenetic alterations

A

1) Modifications to DNA during life
2) DNA methylation, Histone modification, Chromatic remodelling causes impaired DNA repair and chromosome instability which leads to ageing

33
Q

Ageing- Loss of Proteostasis

A

1) Proteostasis – maintaining stability and functions of proteins. Correct folding/repair folding. Correct degradation (proteasome)
2) Prevents accumulation damaged proteins
3) Protein missfolding/accumulation linked to age-related neurodegeneration

34
Q

Ageing- Deregulated Nutrient sensing

A

1) Alterations in specific metabolic and signalling pathways

2) Calorie restricted diet increases lifespan

35
Q

Some examples of Deregulated nutrient sensing

A

Insulin and Insulin growth factor 1 (IGF-1) signalling (IIS) – glucose sensing
Sirtuins - senses low energy states through high NAD+ levels
AMP activated protein kinase (AMPK) – senses low energy states through high AMP levels

Mammalian target of rapamycin (mTOR)

36
Q

Ageing- Mitochondrial dysfunction

A

1) Mitochondrial free radical hypothesis of ageing
2) The free radicals damage proteins, Mutate DNA and damage RN this causes Gene mutations, Impaired cell function, Protein deposition and Cell death
3) This links to loss of proteostasis and genomic instability

37
Q

Mitochondrial dysfunction

A

1) There is evidence that increased free oxygen radicals prolongs lifespan in yeast and nematodes
Genetic modification in animal models to increase levels of free oxygen radicals does not increase rate of ageing
2) So what might be going on- increased free oxygen radicals activate compensatory protective mechanisms. As you age increased damage to cells increases free radicals until the tipping point is reached
3) Mitochondrial dysfunction may be caused by other factors- decreased mitochodriogenesis, build up of mutations in mitochondrial DNA

37
Q

Mitochondrial dysfunction

A

1) There is evidence that increased free oxygen radicals prolongs lifespan in yeast and nematodes
Genetic modification in animal models to increase levels of free oxygen radicals does not increase rate of ageing
2) So what might be going on- increased free oxygen radicals activate compensatory protective mechanisms. As you age increased damage to cells increases free radicals until the tipping point is reached
3) Mitochondrial dysfunction may be caused by other factors- decreased mitochodriogenesis, build up of mutations in mitochondrial DNA

38
Q

How mitochondrial dysfunction can result in ageing

A

1) Mitochondrial dysfunction increases free oxygen radical production causing decreased energy production, increased cell death and increased inflammation
2) Mitochondrial dysfunction may be due to a mtDNA mutation, oxidation mitochondrial proteins and Reduced mitochondriogenesis as a result of Nuclear DNA damage

39
Q

Ageing- Cellular senescence

A

1) Arrest of the cell cycle plus phenotypic changes to cells
2) Linked to telomere attrition and Heyflick number
3) But also other mechanisms- DNA damage, disruption to the cell cycle (oncogenic and mitogenic)

40
Q

Normal- Cellular Senescence

A

Sporadic damage -> Cellular senescence -> Remove damaged cells -> Anti-cancer and Anti-ageing

41
Q

Ageing- Cellular senescence

A

Increased damage/Reduced repair/Reduced Clearance/Reduced cell renewal -> Cellular Senescence -> Remove damaged cells -> Reduced function tissue/Increased inflammation/Stem cell exhaustion -> Ageing

42
Q

Stem cell Exhaustion/Attrition

A

1) Accumulation of damage and Telomere attrition (low level telomerase activity in adult stem cells)
2) Loss of cell cycle control i.e. p53 -> Cancer
3) Decreased cell cycle activity of stem cells (Increased expression of cell cycle inhibitor p16)
4) Decreased number of stem cells. Redcuction in Haematopoietic stem cells can cause Immunosenescence and loss of Mesenchymal stem cells can cause Osteoporosis and reduced fracture repair

43
Q

Ageing- altered intracellular communication

A

1) Endocrine, neuroendocrine and neuronal

2) May be linked to an increased inflammatory environment

44
Q

Effects of altered intracellular communication

A

1) Accumulation of pro-inflammatory tissue damage
2) Immunosenesccence- failure to clear pathogens and senescent cells
3) Cellular senescence- production of pro-inflammatory cytokines
4) This all leads to systemic inflammation

45
Q

Ageing- effects of systemic inflammation

A

Neurohormonal signalling is dysregulated (renin-angiotensin, agrenergic, insulin IGF-1)
Inhibits stem cell production- stem cell exhaustion
NF-KB- Hypothalamus reduced GnRH causes bone fragility, muscle weakness and reduced neurogenesis

46
Q

Assessing Gait

A

Observe the patient entering the room - speed, stride, balance

Ask the patient to:

1) Walk across the room, turn, and come back.
2) Walk heel-to-toe in a straight line, may be difficult for older patients
3) Walk on their toes in a straight line, then to walk on their heels in a straight line
4) Hop in place on each foot
5) Do a shallow knee bend
6) Rise from a chair, walk forwards across the room, turn and come back

Assess cerebellar function: Romberg’s test, finger-nose pointing, dysdiadochokinesia, heel-to-shin testing

47
Q

Change with age: strength

A

1) Strength peaks in the mid-20s and declines after 5th decade
2) All sensory functions slowly diminish
3) Gait speed slows modestly after the 7th decade
4) Age-related decreases in strength and balance may contribute to the increased incidence of falls in older people
5) Generally disease has a greater impact than age-related changes

48
Q

Changes with age: Posture

A

1) Unless disease impacts on posture older people walk upright with no forward lean
2) Older people walk with ~ 5° greater ‘toe out‘ with a possible reduction in internal rotation of hip
3) Gait velocity falls due to shorter steps by about 15% per decade from the age of 70

49
Q

Change with age: Limb movement

A

1) Cadence (rhythm) does not necessarily change with age
2) Double stance (the time when both feet are on the ground) increases with age from 20% to 26%. This reduces momentum and the time for the swing leg to advance causing a short step length
3) Elderly people with a fear of falling increase their double stance time

50
Q

Frailty

A

A medical syndrome with multiple causes and contributors, characterised by diminished strength, endurance, and physiological function
This increases a patients vulnerability for increased dependency, illness and death

It is often just physiological changes across systems that builds up and contributes to this effect

51
Q

Examples of frailty syndrome

A 
Falls
Immobility
Delirium
Incontinence
Suspectibilty to medication side effects
52
Q

How frailty contributes to morbidity and mortality

A

Increased risk of falling, delirium and other ‘acute fraility syndromes’
Falling more dangerous as trauma is less well recognised in the elderly, and they may be on anticoagulants
Increased care home admission

53
Q

Frailty intervention

A 
Strength and balance training
Home hazard assessment
Vision assessment
Medication review and withdrawal
Gait assessment

Medicine year 2 semester 2 (47 decks)

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