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Medicine Podiatric > wk 5- endocrinolgoical > Flashcards

wk 5- endocrinolgoical Flashcards

1
Q

what is diabetes mellitus

A

Impaired glucose uptake into the cell resulting in hypergycaemia

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2
Q

microvascular complications of DM

A
  1. Retinopathy (retinal capillary microaneurysms, neovascularization and macular oedema)
  2. Nephrophathy (Thickening of the glomerular basement membrane, mesangial expansion and glomerular sclerosis)
  3. Neuropathy (nerve ischemia or damage, predisposes patients to ulceration and joint degeneration)
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3
Q

macrovascular complications of DM

A
  1. CAD
  2. Stroke
  3. PAD
  4. Immune dysfunction- predisposes to infection due to effect of hyperglycemia on neutrophil and t cell function (fungal infection of the foot and bacterial infection of the tissue/bone more common)- tinea, cellulitis, osteomyelitis.
    and nutrients, o2 arent available for healing
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4
Q

diagnosing DM

A

BG: >7mmol/L fasting
or
>11mmol/L random + symptoms

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5
Q

T1DM is what

A

autoimmune disorder. autoantigens activate a T cell mediated immune response that leads to destruction of pancreatic beta cells, which is responsible for insulin production.
Genetic component.

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6
Q

symptoms of T1DM

A

increased urination(polyuria),
increased thirst (polydipsia)- body’s attempt to remove excess glucose,
dehydration,
weight loss,
nausea,
vomiting,
weakness,
fatigue,
immunocompromised,
poor wound healing

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7
Q

T1DM emergency

A

diabetic ketoacidosis

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8
Q

management of T1DM

A
  1. Dietary modification
  2. Physical activity
  3. Insulin
    -Basal bolus regimen: long acting insulin once daily, very short acting insulin given with each meal

-Mixed insulin regimen: intermedite and short acting insulin twice daily

-Insulin pump

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9
Q

T2DM is what

A

insulin resistance due to insensitivity of receptor cells.
resistence of the liver to effects of insulin result in persistent unregulated hepatic glucose production and resistance of peripheral tissues to the effects of insuling results in reduced uptake of glucose into cells
Obesity and weight gain cause this type, a link to genetic susceptibility.

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10
Q

symptoms of T2DM

A

increased urination(polyuria),
increased thirst (polydipsia)- body’s attempt to remove excess glucose,
dehydration,
weight gain,
nausea,
vomiting,
weakness,
fatigue,
immunocompromised,
poor wound healing

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11
Q

T2DM emergency

A

hyperosmolar hyperglycaemia state (hypergymaeia with dehydration)

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12
Q

T2DM mangement

A
  1. education
  2. Lifestyle modifications
  3. oral hypoglycemic agents (single or combined)
    - Metformin (reduced hepatic gluconeogenesis)
    - Sulphonylureas (increase insulin secretion)
    - DPP-4 inhibitors (increase insulin secretion)
  4. Insulin (single or combined with metformin)
    - Regimes
    - Pump
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13
Q

how often do diabetes need to be checked

A

every 3-6months
-BP
-weight
-HBA1C

every day
-BG

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14
Q

what are pre diabetes diagnosing levels

A
  1. Impaired fasting glucose
    Fasting glucose measurement >6.0mmol/L but <7.0mmol/L
  2. Impaired glucose tolerance
    Random or post-prandial glucose measurement >7.7mmol/L but <11.1mmol/L
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15
Q

obesity is defined as

A

BMI>30

caused by long standing imbalance between energy intake and energy expenditure,
things that also play a role

  1. genetics (BMR, hormones)
  2. medications
  3. sleep
  4. enviornment
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16
Q

overweight is defined as

A

BMI 25-30

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17
Q

management of obesity

A
  1. physical acivity and diet (lifestyle)- mediteranian and 30mins
  2. medications
    orlistat inhibits pancreatic lipase = reducing absorption of fat
    phentermine is appetite suppressant (tolerance)
  3. surgery
    gastric band or sleeve
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18
Q

what is metabolic syndrome

A

At least 3 of the following conditions:
-Excessive abdominal fat (>102cm M and 88cm F)

-hypertension (.130/85MMhG)

-abdnormal fasting glucose (>5.5mmol/L) or insulin resistance

-dislipidaemia or hyperlipidemia

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19
Q

pathophysiology of metabolic syndrome

A

depends on
1. amount and
2. distribution of body fat (central obesity apple shape increases risk of metabolic syndrome)

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20
Q

loss of 5-10% bw can do what?

A

improve diabetes, dyslipdemia, and hypertension

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21
Q

complications of metabolic syndrome

A

Fatty liver disease
Gout
Obstructive sleep apnoea
PCOS
Infertility in men

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22
Q

how much bw loss can reverse metabolic syndrome

23
Q

what is hypothyroidism

A

Deficiency of thyroid hormone

  1. Primary (thyroid gland disease, most common)

-Hashimoto’s thyroiditis: chronic autoimmune inflammation of thyroid gland
- Post therapeutic hypothyroidism: caused by medical, surgical or radio iodine destruction of the thyroid gland for hyperthyroidism

  1. secondary (disease of hypothalamus or pituitary gland)

-tumours

24
Q

symptoms and clincal signs of hypothyriodism

A

tiredness,
weight gain,
cold intolerance,
goltre,
dry coarse skin,
muscle weakness/stiffness,
anameia
braycardia
oedema
dyslipidemia

25
treatment of hypothyroidism
levothyroxine or L-thyroxine
26
diagnosis of hypothyroidism
measurement of serum TSH then T4 measured. HYPO in primary - TSH elevated and T4 low in secondary- TSH elevated and T4 normal HYPER TSH is low and T4 elevated
27
what is hyperthyroidism
Overactivity of thyroid hormone 1. graves disease most common, autoimmune antibody against TSH receptor specific symptoms: - goitre -protuding eyes -infiltrative dermopathy 2. thyroditis, acute inflammation of thyroid gland 3. toxic multinodular goitre 4. solitary toxic thyroid nodules
28
symptoms and clinical signs of hyperthyroidism
weight loss, increased appetite, tremor, heat intolerance, stiffness, muscle weakness, breathlessness, goitre, onycholysis, sweating tremor, hyperkinesis, tachycardia, warm, protuding eyes
29
management for hyperthyroidism
1. carbimazole 2. surgery- goitre 3. beta blocker for tremor, palpitations and sweating
30
osteoporosis
Metabolic disease of bone caused by an imbalance between bone resorption (osteoclasts) and formation (osteoblasts) Primary- increased osteoclast activity and lack of calcium and vitamin D Secondary- conditions/diseases causing an increase in osteoclast acitvity or restricting parathyroid action to promote calcium/Vitamin D
31
diagnosis of osteoporosis
DEXA scan to find BMD through a T score Normal: higher than -1 Osteopenia: -1 - -2.5 Osteoporosis: -2.5+ or imaging
32
clinical features of osteoporosis (regional bone loss) on radiograph
- decrease in bone mineral density -changes in trabecular pattern -cortical thinning
33
treatment of osteoporosis
1. manage risk factors 2. weight bear 3. antiresportive medications - bisphosphonates - denosumab - raloxifene
34
what is osteomalacia
Normal bone quantity but not mineralised (weakened bone) due to inadequate intake of vitamin D (lactose intolerance, lack of sun, malabsorption, advanced renal disease) looser zone fractures
35
what is rickets
infant/young children version of osteomalacia (vitamin D deficiency) can be calcipenic: low serum calcium levels due to insufficient intake or metabolism of vitamin D/calcium which can be caused by 1. lack of sun 2. renal disease 3. rapid bone resorption phosphopenic: low serum levels of phosporus due to renal phosphate wasting
36
radiographic features of rickets
Widened growths plates. decrease in Bone mineral density Cortical thinning Scoliosis may be present. bowing deformities greenstick fractures
37
symptoms of rickets
Muscle weakness Enlarged wrists and ankles. Long bones exhibit curvatures. Waddling gait. Pain may be present. Growth may be hindered
38
what is renal osteodystrophy
combination of renal insufficiency and secondary hyperparathyroidism with resultant widespread calcifications renal insufficiency = increased phosphorous levels = parathyroid hormone stimulated to reduce levels of phosphorous (secondary hyperparathryoidism) high levels of parathyroid hormone = increase osteoclastic acivitiy = bone resorption = increased serum calcium and phosphorous which is depositited into soft tissues
39
renal osteodystrophy radiogrphic features
-loosers zones -brown tumor -osteosclerosis -widen growth plate -varus deformity of femurs -soft tissue calcification -osteopenia
40
what is pagets disease
Tumour like process, continuous destruction of bone and replacement by a soft, poorly mineralised matrix (abnormal bone remodelling), most patients are asymptomatic, tibia is common
41
pagets disease radiographic features/ clincial signs
Localised pain and tenderness Increased focal temperature Increased bone size coarsened trabecular pattern Bowing deformities Kyphosis of spine Decreased ROM
42
what is hypopituitarism and symptoms
Deficiency of pituitary function, onset often insidious Symptoms: Decreased sex hormones (infertility, amenorrhea, impotence, atrophy) Decreased thyroid stimulating hormone (hypothyroidism) Decreased ACTH (fatigue, hypothermia, infection)
43
what is giantism
Excessive growth hormone from anterior pituitary gland prior to growth plate closure (children), causes larger build
44
what is acromegaly
Excessive growth hormone in adults, causes large/enlarged extremeities
45
what is galactorhoea
Excessive prolactin secretion due to pituitary adenoma
46
what is hyperparathryoidism
Parathyroids produce parathyroid hormone which 1. Increase calcium and decrease phosphate resportion by kidney 2. Increases vitamin D production 3. Increases osteoclast activity adenomas cause majority and hyperplasia secondary hyperparathyrodism with hypertrophy from renal failure
47
clinical features of hyperparathyroidism and diagnosis
stones (renal stones) bones (osteoporosis/penia) abdonimal groans (pain/pancreaitis) psychic moans (behavioural disturbance and thirst) diagnosis increased serum calcium decreased serum phosphate
48
cushings syndrome is
Increased cortisol in the body due to Adrenal adenoma pituitary adenoma Iatrogenic Ectopic ACTH production
49
symptoms of cushings syndrome
Weight gain Muscle weakness Back pain polyuria/polydipsia Thin skin Hypertension Pathological fractures Striae Proximal myopathy Bruising
50
diagnosis of cushing syndrome
24 hour urine free cortisol excretion/imaging
51
hyperaldosteronism what is it
excess production of aldosterone due to 1. adenoma 2. hyperplasia results in * Increase retention Na → high serum sodium * Increase loss K → low serum potassium * Fluid retention * Hypertension
52
what is addisons disease
Hypofunctioning of adrenal cortex Cortisol and aldosterone deficiency Autoimmune typically, can be due to destruction of gland
53
symptoms and clinical features of addisons
May be asymptomatic until: metabolic stress, surgery or severe infection Clinical features: * Weakness & fatigue * Cold intolerance * Orthostatic hypotension * Pigmentation (esp. skin folds and mucous membranes, Addison’s “tan”) * Abnormal CHO, fat and protein metabolism-weight loss, hypoglycaemia * Inability to concentrate urine – dehydration
54

Medicine Podiatric (13 decks)

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