wk 9- endocrine Flashcards

1
Q

Compare & contrast type I & II diabetes inc causes, pathogenesis, typical initial clinical presentation (prior to diagnosis/treatment)

A

type I:
-5-10% cases
-autoimmune disease, genetic predisposition, environmental factors
-develops in early childhood and presents in early teenage years
-can be normal or under weight

-lack of insulin despite high serum glucose so cells are starving
-energy deposits broken down (fat and muscle)
-renal effects including appearance of glucose in urine
-hyperglycemia, low blood volume, ketoacidosis might mean they present an acute medical emergency in a hyperglycemia coma

type II:
-lifestyle and environment, genetic factors
-insulin resistance (insensitive), b cell dysfunction (inappropriate response)
-they still make insulin but the respondence isn’t occurring as well.
-sensitize tissues to insulin by losing weight to reverse the disease

-has enough insulin to prevent ketoacidosis (prevents breakdown of fat stores)
-symptoms are non-specific, chronic

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2
Q

long term complications of diabetes mellitus

A
  • Hyperglycaemic
  • hyperosmolar state
  • Diabetic neuropathies
  • Microvascular disease
    – Diabetic retinopathy
    – Diabetic nephropathy
  • Macrovascular disease
    – Coronary artery disease
    – Cerebrovascular accidents
    – Peripheral vascular disease
  • Infection
    -atherosclerosis (can lead to peripheral, cardio and cerebral vascular disease)
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3
Q

Understand what is meant by ‘functional’ tumour & the possible implications for hormone levels

A

tumour cells are able to still make that hormone, an excess of the hormone

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4
Q

What is the most common cause of hyperthyroidism & the symptoms associated with the condition?

A

grave’s disease-immune system that makes an antibody that has a similar structure to TSH so it binds to the TSH receptor to stimulate the gland to make T3 and T4 which leads to increased levels of circulating T3/4

symptoms:
increased metabolic rate
weight loss
anxiety and irritability
fine tremor
proptosis (bulging eyes)

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5
Q

How does GH excess differ in pre/post puberty?

A
  • If adenoma presents in childhood before epiphyses close -gigantism
    – If adenoma presents after closure of epiphyses- acromegaly causes enlargement of body features
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6
Q

What is the result of GH deficiency in embryogenesis?

A

dwarfism

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7
Q

What is Cushing’s syndrome & how may it be caused?

A

condition caused by exposure to high levels of cortisol, what occurs in the body is; hyperglyceamia, immune suppression, loss of muscle/ fat / bone in periphery and redistribution of fat in the trunk and thinning of hair and skin

caused by excessive cortisol

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8
Q

how does MELANOMA differ from the common carcinomas of the skin?

A

-fewer mutations to get aggressive melanoma

-increased risk is associated with severe suburn at young age not a dose dependent exposure to UV

-people are genetically predisposed and some with increased risk bc of fari skin/blue or green eyes

-grow vertically rather than radially

-metastasized at time of diagnosis

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9
Q

how does basal cell carcinoma differ to the other skin carcinomas

A

-most common

-increases in incidence with age and UV exposure radiation

-grows slowly due to high rate of apoptosis and radially as a papule

-rarely metastasizes

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10
Q

how do squamous cell carcinomas differ to the other skin cancers

A

-common

-increases in incidence with age and UV exposure and radiation

-grows slower than melanoma but faster than BCC and radially

-usually diagnosed before it metastasizes

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11
Q

what is graves disease and what causes the condition?

A

Hyperthyroidism caused by an immune disorder in which B cells produce antibodies that mimic TSH.

Ordinarily TSH is released from the anterior pituitary in response to TRH from the hyperthalamus. TSH
induces growth of the thyroid gland and the synthesis and release of T3 and T4 which negatively
feedback to decrease the signals of TRH and TSH. The TSH mimicking antibodies are continually
produced but not subject to negative feedback regulation so TRH and TSH are low but T3/T4 and the antibody levels are high.

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12
Q

symptoms present with someone with graves disease

A

Increased metabolic rate, heat intolerance, weight loss, anxiety and agitation, fine tremor, proptosis

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13
Q

difference between well differentiated tumour versus a poorly-
differentiated tumour?

A

A well-differentiated tumour = functional tumour derived from endocrine cells cause hormone excess

non functional tumours cause a decrease in hormone production

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14
Q

how does GH excess differ in children v adults

A

children- growth plates have yet to fuse so we see gigantism

adult- acromegaly by growth of bones in skull, hands, feet and thickening of connective tissue leading to a coarsening of appearance

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15
Q

What is Cushing’s syndrome and how is it caused

A

caused by excess cortisol or prolonged use of corticosteroids, it includes increased fat
deposition in the trunk & face (moon face); the development of a buffalo hump, muscle atrophy & weakness,osteoporosis, thinning skin & the formation of striae (stretch marks); poor wound healing & increased risk of infections; hyperglycaemia & hypertension; mood changes & depression

caused by
-cortisol
-ACTH secreting tumour
-chronic stress
-inappropriate or excessive use of corticosteroids/glucocorticoids

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16
Q

what is osteoporosis and people at risk

A

Excessive loss of bone, particularly osteoblasts (bone building cells)

people at risk
-without peak bone mass (genetics, nutrition, physical activity while growing)
-females more at risk

17
Q

factors that increase rate of bone loss

A

ageing,
reduced physical activity, especially weight-bearing,
sarcopenia,
amenorrhea,
loss of oestrogenic activity after menopause, chronic use of NSAIDs and
glucocorticoids and
corticosteroids.

18
Q

how does type 1 differ?

A

type 1-
-autoimmune disease, born with normal beta cells but a trigger starts targetting their beta cells (no insulin production as a result)
-target tissues (liver, fat, skeletal muscle) cant take up blood glucose without insulin so are starving and use alternate food sources (weight loss and ketoacidosis occurs)
-blood glucose is severely high still (unable to use or store it)
-treatment can be an insulin production one

19
Q

how does type 2 diabetes differ?

A

-insulin insensitivity, the target tissues (liver, fat and skeletal muscle) take up enough blood glucose to sustain themselves (ketoacidosis doesnt occur or weight loss) but not enough to reduce the levels in the blood

-overweight, inactive are common risk factors

-weight loss can halt or reverse condition if it isn’t too far gone

20
Q

how does type 1 present and what are treatment options

A

acute emergency situation associated with severe 1. hyperglycaemia;
2. ketoacidosis and
3. volume depletion that can result
in altered consciousness and coma.

Type I patients will be advised how to best manage
their glucose levels using timed meals, short and
long-acting insulin injections

21
Q

how do type 2 patients present and what are treatment options

A

vague symptoms which often include
1. polyphagia, (excessive eating)
2. polydipsia & (thirst)
3. polyuria. (urination)

They may feel lethargic and are usually
overweight and sedentary. They may have some
signs of neuropathy including loss of sensation,
chronic pain or pins and needles.

Treatment initially is designed to increase insulin
sensitivity (weight loss, exercise and metformin)
but later insulin injections may be required if beta
cell burnout occurs

22
Q

what are other pathologies that are observed in diabetic patients?

A

Atherosclerosis and arteriosclerosis which predisposes the sufferer to ischaemic heart disease, cerebrovascular disease, peripheral vascular disease, neuropathy, nephropathy, retinopathy, glaucoma, cataracts and infections.

23
Q

which type of diabetes presents as an acute medical emergency with hyperglycaemia and ketoacidosis

A

type 1

24
Q

which type of diabetes presents in overweight poeple?

A

type 11

25
Q

which diabetes is an autoimmune disease

A

type 1

26
Q

what is not likely to occur in someone with grave’s disease

A

increased muscle mass. muscle is lost as metabolic rate increases and both fat and functional tissue is broken down

27
Q

list causes of squamous cell carcinoma of the skin

A
  1. UV exposure (dose development)
  2. immune suppression
  3. aging
  4. chemical carcinogen exposure
28
Q

give an example why melanomas differ from carcinomas

A

melanomas are not epothelial malignancies

it takes fewer mutations to create a melanoma

melanoma can occur at any age

they grow vertically rather than radially

diagnosed after they metastasize

29
Q

what skin cancer has the slowest growth rate

A

BCC- because of high rate of apoptosis
then SCC and then melanoma