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Medicine year 3 ANNA > Obesity > Flashcards

Obesity Flashcards

1
Q

What are the signs of cushing’s syndrome?

A
  • Moon face
  • Frontal balding (female)
  • Pigmentation
  • Skin infections
  • Hypertension
  • Osteoporosis
  • Pathological fractures – particularly vertebrae and ribs
  • ‘buffalo hump’ – a dorsal fat pad
  • Kyphosis – hunch back
  • Striae – stretch marks – can be purple or red- occur on the abdomen.
  • Oedema
  • Proximal myopathy
  • Glycosuria
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2
Q

What are the symptoms of Cushing’s syndrome?

A

Symptoms:

  • Weight gain
  • Change of appearance
  • Depression
  • Insomnia
  • Amenorrhoea / oligomenorrhoea
  • Poor libido
  • Thin skin / easy bruising
  • Hair growth
  • Acne
  • Slow growth in children
  • Back pain
  • Polyuria
  • Dyspepsia
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3
Q

What are the effects of high cortisol?

A
  • Blood glucose
    • Increase in glucose in blood
    • Due to increase gluconeogenesis
    • Resultant increase of insulin
    • = responsible for the central adiposity in Cushing’s
  • Increased breakdown of skin, bone and muscle
    • Due to ↑proteolyisis
    • ↑ lipolysis
    • ↓ bone formation
  • Increased blood pressure due to:
    • ↑ Sensitivity of peripheral blood vessels to catecholamines
    • Cross reaction with mineralocorticoid (aldosterone) receptors
  • Decreased immune / inflammatory response
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4
Q

How does the cortisol negative feedback system (HPA axis) work?

A
  1. Hypothalamus releases Corticotropin-releasing hormone (CRH)
  2. CRH stimulated anterior pituitary to release ACTH
  3. ACTH stimulates adrenal cortex to release cortisol
  4. Cortisol levels increase
  5. Cortisol acts on both the hypothalamus and the pituitary to inhibit CRH and ACTH
  6. Cortisol levels decrease
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5
Q

What are some man-made glucocorticoids?

A
  • Hydrocortisone (synthetic cortisol)
  • Prednisolone
  • Dexamethasone (see suppression test)
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6
Q

Mineralocorticoids: give an example of:

  1. Endogenous
  2. Synthetic / man-made
  3. Antagonist
A
  1. Aldosterone
  2. Fludrocortisone
  3. Spironolactone
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7
Q

What are the 3 endogenous causes of Cushing’s syndrome?

A
  1. Pituitary adenoma (benign)
    1. ↑ACTH production → adrenal glands secrete more cortisol
  2. Ectopic source e.g. small cell lung Ca
    1. Ectopic ↑ACTH production → adrenal glands secrete more cortisol
  3. Adrenal tumours
    1. adrenal adenoma (benign)
    2. adrenal carcinoma (malignant)
      1. excess cortisol secreted by tumours
      2. inhibits ACTH
      3. decreased production of cortisol by cortex (but blood levels still high due to tumours)
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8
Q

Why is it important not to suddenly stop exogenous steroids even if Cushing’s has developed?

A
  • ↑ cortisol (from meds) → ↓ACTH → ↓endogenous cortisol production → shrinking of adrenal cortex
  • If you remove the medication, the adrenal cortex will not be able to compensate
  • This will send the patient into adrenal (addisonian) crisis
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9
Q

How do you diagnose Cushing’s syndrome?

A
  1. Measure free cortisol
    1. 24 hour urine sample (↑in CS)
    2. Blood/saliva late at night (↑in CS)
  2. If high, low dose overnight dexamethasone suppression test (1-2mg)
    • dexamethasone (exogenous cortisol) → ↓ACTH → ↓cortisol levels (<5g/dL)
    • if there is incomplete suppression (cortisol remains high, >5g/dL) then the test is positive and there must be some endogenous cortisol production.
  3. Measure ACTH
    1. Low → adrenal tumour (secreting cortisol so inhibiting ACTH production)
    2. High: either
      1. Pituitary adenoma
      2. Ectopic source e.g. small cell lung ca
  4. High dose overnight dexamethasone suppression test
    • If cortisol is completely unaffected, it must be an ectopic tumour (as lots of cortisol will have some effect on a pituitary adenoma)
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10
Q

Which imaging would you do with each endogenous cause of excess cortisol?

A
  1. Pituitary - MRI head
  2. Ectopic - CT abdo, chest, pelvis (looking for Ca)
  3. Adrenal - Adrenal CT
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11
Q

What hormones are produced by the anterior / posterior pituitary?

A

AaaaaayO! (posterior only produces ADH and Oxytocin)

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12
Q

What are the main disorders of ADH secretion?

A
  1. Diabetes insipidus
  2. SIADH
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13
Q

What is diabetes insipidus?

A

2 Types:

  1. Cranial
    • too little vasopressin is produced by the pituitary
  2. Nephrogenic
    • kidney becomes insensitive to vasopressin
    • → does not make aquaporin channels to reabsorb water from the collecting ducts

Symptoms are

  • polyuria (large quantities of dilute urine)
  • polydipsia (increased thirst)

Can lead to

  • Hypernatraemia (concentrated blood due to water loss ie. dehydration)

Hypokalaemia and Hypercalcaemia can cause –> nephrogenic DI

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14
Q

What are the tests for diabetes insipidus?

A
  1. Urine osmolality
    • low in DI, ie. dilute urine
    • if >700 mOsm/kg then this excludes DI
  2. Blood osmolality
    • high in DI, ie. concentrated blood
  3. Water deprivation test
    • In normal pt, or primary polydipsia (increased thirst and drinking) this should result in ADH release and therefore reduced UO of more concentrated urine
    • In DI, the UO remains high and the urine is still dilute
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15
Q

How do you distinguish between cranial and nephrogenic DI?

A

Vassopressin (ADH)

  • Cranial DI will have a resultant increase in urine osmolality (ie kidneys will respond and urine will become more concentrated)
  • Nephrogenic DI will have no response as they are insensitive to vasopressin.
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16
Q

What does a paired serum osmolality and urine osmolality look like in SIADH?

A
  • Serum / blood osmolarity is low (blood is dilute)
  • Urine osmolarity is high (urine is concentrated)
17
Q

What is SIADH?

A

Syndome of Inappropriate ADH secretion

  • Causes increased levels of ADH
  • Which causes water retention, diluting the blood
    • decrease in Na+ concentration
    • increase in plasma volume
      • causes inhibition of RAAS
      • less aldosterone means Na+ loss
  • Thus, Na concentration is decreased as it is lost in the urine (which is very concentrated)
18
Q

What are the symptoms of hyponutraemia?

A
  • Headache
  • Nausea
  • Vomiting
  • Muscle cramps
  • Weakness
  • Cerebral oedema
    • confusion
    • mood swings
    • hallucinations
    • seizures
    • coma
    • death
19
Q

What is the treatment for hyponutraemia?

A
  • correction must be done slowly to avoid precipitating central pontine myelinolysis
  • fluid restriction
  • demeclocycline (an antibiotic): reduces the responsiveness of the collecting tubule cells to ADH
  • ADH (vasopressin) receptor antagonists - vaptans
  • very severe - hypertonic IV fluids
20
Q

When is hyponutraemia acute onset or severe enough to consider admission?

A

If there are symptoms or if serum sodium concentration is less than 125 mmol/L

21
Q

What are some causes of SIADH?

A
  1. Lung diseases – cancer, pneumonia
  2. Brain lesions – tumour, head injury and bleed, stroke
  3. Drugs – e.g. carbamazipine, selective serotonin reuptake inhibitors (SSRIs)
22
Q

Dilute solution has a high or low osmolality?

A

Low

23
Q

Concentrated solution has a high or low osmolality?

A

High

24
Q

What is the mechanism of action of aldosterone?

A

Aldosterone acts to increase BP by retaining Na+, and thus water (water follows Na+)

25
Q

What are the types of hypoadrenalism?

A
  1. Primary hypoadrenalism
    • ie Addison’s disease
  2. Secondary hypoadrenalism
    • Hypothalamic-pituitary disease leading to inadequate ACTH production, most often panhypopituitarism
    • Long-term steroid therapy, leading to hypothalamic pituitary suppression (may be somewhat reversible)
26
Q
  1. How do you assess hypoadrenalism?
  2. How do you distinguish between primary hypoadrenalism (Addison’s) and secondary hypoadrenalism?
A
  1. Perform the ACTH stimulation test. Little response will be given by the adrenal glands to secrete cortisol.
  2. take an ACTH level:
    1. In Addison’s / primary hypoadrenalism the level is likely to be very high (pituitary is saying “come on adrenal glands! Secrete already!”)
    2. In secondary disease the level is likely to be low (there is a problem with ACTH secretion)
27
Q

What is the ACTH stimulation test?

aka short synacthen test

A
  • the patient is given a dose of synthetic ACTH (tetracosactide) in an attempt to stimulate cortisol production.
  • take cortisol blood levels at 0 and 30 minutes.
  • The cortisol should rise sharply.
  • Addison’s should be ruled out if the cortisol rises to above 550nmol/L (it shouldn’t rise in Addison’s as there is adrenal insufficiency)
28
Q

What is pituitary apoplexy?

What can it be caused by?

A

Sudden enlargement of a pituitary tumour (usually non-functioning macroadenoma) secondary to haemorrhage or infarction.

  • Most common type is Sheehan’s syndrome (post-partum haemorrhage causes reduced perfusion of pituitary)
  • Can also be caused be a haemorrhage
  • Can be caused by a tumour
29
Q

What are the signs and symptoms of pituitary apoplexy / sheehan’s (post-partum)?

What investigations need doing?

Treatment?

A
  • Sudden onset headache (similar to SAH)
  • Neck stiffness
  • Rapidly worsening visual field defect / double vision (compression of optic nerve) classically bitemporal hemianopia
  • Extraoccular nerve palsy
    • Primary pituitary insufficiency
      • → adrenal insufficiency (hypotension and hyponatraemia)
  • Investigations:
    • MRI head
    • Bloods (electrolytes, hormones, glucose)
  • Treatments:
    • Replace hormones :
      • URGENT hydrocortisone
      • levothyroxine
    • Surgical:
      • transsphenoidal surgical decompression
      • +/- pituitary removal
    • Careful fluid balance
30
Q

What kind of VF defect will a pituitary lesion cause?

A

Bitemporal hemianopia

31
Q

What is the definition of SIADH on data interpretation?

A
  1. True plasma hypo-osmolality (100 mOsm/kg H2O)
  2. Inappropriate urinary response to hypo-osmolality (urine osmolality >100 mOsm/kg H2O)
  3. Euvolemia; no edema, ascites, or signs of hypovolemia
  4. Elevated urine sodium (>30 mEq/L) during normal sodium and water intake
  5. No other causes of euvolemic hyponatremia
  6. No recent use of Diuretics

Supplemental criteria

  1. No significant increase in serum sodium after volume expansion, but improvement with fluid restriction..
  2. Unable to excrete >80% of a water load (20 cc/kg) in 4 hours and/or failure to achieve urine osmolality <1mOsm/kg H2O
32
Q

What are the BMI classifications of weight?

A
  • healthy weight: 18.5–24.9 kg/m2
  • overweight: 25–29.9 kg/m2
  • obesity I: 30–34.9 kg/m2
  • obesity II: 35–39.9 kg/m2
  • obesity III: 40 kg/m2 +
33
Q

For whom do the BMI thresholds decrease (23 kg/m2 to indicate increased risk and 27.5 kg/m2 to indicate high risk)?

Why?

A
  • Black African,
  • African-Caribbean
  • Asian (South Asian and Chinese)
  • to trigger action to reduce the risk of conditions such as type 2 diabetes
34
Q

How is waist circumference classified for men and women?

A

For men

  • less than 94 cm is low,
  • 94–102 cm is high and
  • more than 102 cm is very high.

For women

  • less than 80 cm is low,
  • 80–88 cm is high and
  • more than 88 cm is very high
35
Q

What co-morbidities are more likely with obesity?

A
  • type 2 diabetes
  • hypertension
  • cardiovascular disease
  • osteoarthritis
  • dyslipidaemia
  • sleep apnoea
36
Q

What management should be offered to overweight/obese patients?

A

NB

  • If co-morbidities are present, level 3 or above is always necessary (drug +/- surgery)
  • If patient’s BMI is above 35 the same applies
  • If the patient’s BMI is 40+ then surgery is considered
37
Q

When is bariatric surgery considered for obese patients?

A
  • They have a BMI of 40 or more
  • or between 35 - 40 and other significant disease (for example, type 2 diabetes or high blood pressure)
  • All appropriate non-surgical measures have been tried but the person has not achieved or maintained adequate, clinically beneficial weight loss.
  • The person has been receiving or will receive intensive management in a tier 3 service
  • The person is generally fit for anaesthesia and surgery
  • The person commits to the need for long-term follow-up.
38
Q

What is the difference between Cushing’s Syndrome and Cushing’s Disease?

A

Cushing’s disease is caused by the presence of an ACTH secreting adenoma, and is more common in females though is rarer over-all

39
Q

When might Cushing’s-like signs also be present?

A
  • Pregnancy
  • Depression and other psychiatric conditions
  • Alcohol dependence
  • Glucocorticoid resistance
  • Morbid obesity
  • Poorly controlled diabetes mellitus

Medicine year 3 ANNA (30 decks)

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