Obesity Flashcards
1
Q
What clinical features are suggestive of Cushing’s syndrome?
A
- Recent rapid weight gain
- Truncal obesity
- Fullness of face (moonface)
- Increased blood pressure
- Glycosuria (associated with insulin resistance)
2
Q
What signs would be seen on examination that would suggest Cushing’s syndrome?
A
- Truncal obesity
- Gynaecomastia
- Striae
- Normal body hair distribution
3
Q
How should we assess obesity in adults?
A
- Take waist and BMI measurements and determine weight
Assess: - Presenting symptoms
- Underlying causes of being overweight or obese
- Eating behaviours
- Comorbidities (T2DM, hypertension, cardiovascular disease, osteoarthritis, dyslipidaemia, sleep apnoea)
- Risk factors assessed uding lipid profile (BP, HbA1c)
- Patient’s lifestyle (diet and activity)
- Psychosocial distress
- Environmental, social, and family factors, including family history
- Patient’s willingness and motivation to change lifestyle
- Potential of weight loss to improve health
- Psychological problems
- Medical problems and medication
- Role of family and care works in supporting individuals with learning disabilities to make lifestyle changers
4
Q
What should be done to help a patient reach a healthy weight?
A
- Offer support depending on the patient’s needs, and be responsive to changes over time
- Praise successes
- Educate patients:
- On the risks of carrying excess weight
- Realistic targets for weight loss
- The distinction between losing weight and maintaining weight loss
- Advise that the change from losing weight to maintenance typically happens after 6-9 months of treatment
- Realistic targets for outcomes other than weight loss, such as physical activity and healthier eating
- Diagnosis and treatment options
- Healthy eating in general
- Medication and side-effects
- Surgical treatments
- Self-care
- Voluntary organisations and support groups and how to contact them
5
Q
What is the classifications of overweight versus obesity?
A
Different weight classes are defined based on a patient’s BMI:
- 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 or more
6
Q
When do adults need to be referred to tier 3 care?
A
- Underlying causes of being overweight/obese need to be assessed
- Patient has complex disease tates/needs that cannot be adequately managed in tier 2 (eg learning disabilities)
- Conventional drug treatment has been unsuccessful
- Drug treatment is being considered for a person with a BMI of more than 50kg/m2
- Specialist interventions (such a very-low-calorie diet) may be needed
- Surgery is being considered
7
Q
Which group of patients should be considered for bariatric surgery?
A
ALL of the following criteria:
- BMI of 40+, or between 35-40 and other significant disease (T2DM, hypertension) that could be improved if they lost weight
- All appropriate non-surgical measures have been tried but the patient has not achieved or maintained adequate, clinically beneficial weight loss
- Patient has been receiving or will receive intensive management in a tier 3 service
- Patient is generally fit for anaesthesia and surgery
- Patient commits to the need for long-term follow-up
8
Q
What is the dexamethasone suppression test?
A
Dexamethasone is an exogenous steroid that causes suppression of the pituitary through negative feedback
- Used to assess the integrity of the hypothalamo-pituitary-adrenal axis
- Dexamethasone binds to glucocorticoid receptors in the pituitary and therefore inhibits ACTH secretion by the pituitary gland
- When testing the adrean function in patients with Cushing’s syndrome, dexamethasone may be administered in low (1-2mg) and/or high (8mg) doses
- Low dose dexamethasone suppresses cortisol production in normal subjects
- High dose dexamethasone suppresses steroid production in pituitary dependant Cushings syndrome - or Cushing’s disease
- It will not reduce steroid production in patients with primary adrenal tumours or in those with ectopic ACTH production
9
Q
What are the types of results seen in the dexamethasone suppression test?
A
Normal subject:
- Reduction in cortisol levels following low-dose dexamethasone
Cushing’s disease:
- No reduction in cortisol output after low-dose dexamethasone, but inhibition of cortisol output following high-dose dexamethasone
Adrenal tumour or ectopic ACTH:
- No reduction in steroid production after low or high dose dexamethasone
In patients with high resting cortisol and ACTH levels, but ACTH not being suppressed by dexamethasone, ectopic ACTH should be considered
10
Q
Which three arteries supple the adrenal gland?
A
- Superior suprarenal artery arising from the inferior phrenic artery
- Middle suprarenal artery arising directly from the abdominal aorta
- Inferior suprarenal artery arising from the renal artery
The adrenal glands have a very rich blood supply and this accounts for the frequent metastasis of malignancies – such as lung cancer, to the adrenal gland
11
Q
How is venous blood drained from the adrenal glands?
A
- Venous blood is drained via the suprarenal veins
- Right suprarenal vein drains into inferior vena cava
- Left suprarenal vein drains into the left renal vein
The adrenal glands have a very rich blood supply and this accounts for the frequent metastasis of malignancies – such as lung cancer, to the adrenal gland
12
Q
What are the four causes of Cushing’s?
A
- Iatrogenic
- Pituitary ACTH
- Ectopic ACTH
- Primary adrenal (ACTH independent)
13
Q
What is Cushing’s disease?
A
- Cortisol excess
- Caused by Pituitary ACTH producing adenoma
- 70% of adult Cushing’s
- Female:male 3:1 up to 10:1
- Age 25-45
- Incidence 1/100,000 per annum
14
Q
What are the clinical features seen in Cushing’s?
A
- Central obesity (fat redistribution)
- Protein wasting (osteoporosis/ myopathy)
- Plethora
- Acne
- Striae (red, purple)
- Hypertension (diastolic >105)
- Oedema
- Hirsutism
- Bruising
- Hypokalaemia
15
Q
What are clinical features that may be seen in Cushing’s that are not discriminating?
A
- Generalised obesity
- Oligomenorrhoea
- Headaches
- Abnormal GTT
16
Q
Why might it be difficult to diagnose Cushing’s?
A
- One symptom may predominate
- Severity of disease (mild disease-less florid clinical features)
- Fluctuating cortisol secretion, cyclical Cushing’s
- Male gender (? Confounding effects of testicular androgens)
17
Q
What investigations should be done for hypercortisolaemia?
A
- Plasma cortisol (am vs pm vs midnight sleeping)
- Salivary cortisol
- Urine collection (urinary free cortisol)
- Dynamic tests#0 O/N Dexamethasone suppression test
- Low dose, 2 day dexamethasone suppression test
18
Q
What is the clinical significance of urinary cortisol?
A
- 24 hour collection: complete collection - loss of collection depends on timing
- Overnight collection
- Good distinction between normal and Cushing’s
- Sensitive
- Need repetition
- Repeated normal test unlikely in Cushing’s
- ‘Raised’ UFC obesity, PCOS, depression
19
Q
What is the clinical significance of plasma cortisol?
A
- 9am cortisol, significant overlap with normals
- 8-9pm cortisol 10-15% overlap
- Midnight sleeping cortisol 50nM/l separates normals from Cushing’s
- Acclimatise patients to inpatient stay, inpatient cost, timing of sample, stress-free sample
20
Q
What is the clinical significance of salivary cortisol?
A
- Sample collection
- RIA, ELISA, Platform, LC/MS
- Late night salivary cortisol highest sensitivity for diagnosis of Cushing’s
- Correlates with free serum cortisol
- CBG raised with oestrogens (eg OCP)
- CBG suppressed in illness (eg medical inpatients)
- ELISA cross-reacts with cortisone and prednisolone
21
Q
What is the Dexamethasone suppression test?
A
Low dose + high dose tests
OVernight 1mg test:
- 1mg dex at 11pm, serum cortisol measured at 8am
- Timing, compliance, metabolsim (drugs)
- Threshold (<50 nM/l)
- 13% obese, 23% hospitalised flase positive
- Low dose, 2 day test:
- 0.5mg dex every 6 hours for 2 days
- Serum cortisol at 9am on day 0 and 9am day 2
0 Cortisol <50 nM.l - > 95% sensitivity and specificity
- Useful as a confirmatory test
22
Q
How do we determine if Cushing’s is ACTH dependent?
A
- Measure ACTH when confriemd hypercortisolaemia
- If ACTH is easily detectable (normal range or raised) then ACTH dependent
- Low ACTH compatible with primary adrenal causes (nodular adrenocortical hyperplasia)
23
Q
What is ACTH dependent Cushing’s?
A
- Usually pituitary adenoma, can be ectopic (lungs)
- Aggressive ectopics usually obvious (CXR, systemic features)
- Small ectopics can mimic pituitary adenoma
- Pituitary can have adenomata incidentally
- Use dynamic tests, imaging and venous sampling
- Time and patience required!
24
Q
What is the high dose dexamethasone suppression?
A
- Pre ACTH assay means to differentiate adrenal from pituiarry ACTH dependent
- 2mg dexamethasone ever 6 hours
- Measure cortisol at 9am on days 0, 1, and 2
25
What is the CRH test?
- Overnight admission
- At 9am, insert cannula
- Obtain 3-4 basal samples
- IV CRH (human) 100ug
- Serial samples after
- Measure ACTH and cortisol
- Define increment (>25% increase)
26
How do we interpret the combined dexamethasone suppression tests and the CRH tests?
- High dose dexamethasone CRH
- If either is positive, suggests pituitary
- If both are negative, suggests ectopic
27
What is an adrenal crisis?
- Sick patient, hypotension, hyponatraemia
- Random serum cortisol and plasma ACTH
- TREAT, high dose, replacement hydrocortisone
(100mg IV every 6 hours)
- IV saline
(2-3l first hour, then 3-4l per day)
Morning plasma cortisol would be <140nM/l
28
How do we diagnosed a chronic deficiency in cortisol?
High dose short synacthen test
- Convenient, catches are pituitary disease of recent onset
- Peak cortisol >55onM/l
CRH test:
- Expensive, variable responses, rarely used
ITT
- Significant risk (CV disease, epilepsy), not for use in patients with high probability of adrenal insufficiency
29
How do we treat chronic steroid deficiency?
- Replacement of the missing steroids
- Primary adrenal disease: cortisol and aldosterone
- Pituitary disease: cortisol
- Hydrocortisone = cortisol
- Once a day, twice a day, or three times daily
Hydrocortisone 10mg, 5mg, 5mg
- Waking, lunch, late pm
- Longer acting steroids can be once a day
- Prednisolone 2.5-7.5mg
- Dexamethasone 0.35-0.75mg
- Single dose at night or on waking
30
How do we monitor chronic steroid deficienct?
Clinical indicies
- Underreplacement: weight loss, hyponatraemia, pigmentation
- Overreplacement: Cushing's syndrome, changes in bone turnover and osteoporosis
- Biochemical tests
- Measure cortisol after Hydrocortisone dosing
31
How do we ensure adequacy of glucocorticoid cover?
```
NB hepatic enzyme inducers:
- Phenytoin
- Rifampicin
- Barbiturates
Require increased doses!
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- Intercurrent illness, patient education
- Steroid card and medic alert bracelet
- Injection kit of hydrocortisone or dexamethasone
32
How do we adjust steroid doses around surgery and major stress?
- Estimated cortisol production increases to 200ug/day
- Therefore hydrocortisone 100mg IV/IM every 6 hours
- Half daily dosage each day post-op
- Back to routine replacement by day 5-6
33
How are our water levels regulated?
- Plasma osmolality increases (usually due to increased sodium levels) or body water decreases
- Receptors in the hypothalamus cause “thirst” to increase water intake
- Receptors also result in a signal to the posterior pituitary prompting the release of vasopressin (also known as ADH – anti diuretic hormone)
- ADH acts on the collecting ducts of the kidney to increase the number of aquaporin channels allowing water to be absorbed in the blood
34
What is Diabetes insipidus?
Either:
- Too little vasopressin is produced by pituitary (cranial)
- Or kidney becomes insensitive to vasopression (ADH) and does not reabsorb water from collecting ducts
- Large quantities of dilute urine gets produced, and patients must compensate by drinking large quantities of water (nephrogenic)
- If patients are unable to drink water they will become hypernatraemic and deydrated
Diagnosis:
- Water restriction test
Treatment: desmopression replaces ADH if it is not produced (oral, IM or nasal spray)
If nephrogenic - Reduce salt and protein in diet, thiazide diuretics and NSAID to reduce amount of urine produced by kidneys
35
What is Syndrome of Inappropriate ADH secretion (SIADH)?
- Stimuli override osmolality control
- Causes release of inappropriately HIGH amounts of ADH/vasopressin
- Causes reabsorption of water from collecting ducts
- This means urine is very little in volume
- Patient becomes hyponatraemic as water is retained
Diagnosis: check paired serum osmolality and urine osmolality
- Find serum osmolality to be low (too much water for relative amount of sodium)
- Urine osmolality is high
Causes:
- Lung diseases: cancer, pneumonia
- Brain lesions: tumour, head injury and bleed, stroke
- Drugs: eg carbamzepine, SSRIs
- Miscellaneous causes
Treatment:
- Treat underlying cause
- Fluid restriction
- Contact endocrinology
36
What are the clinical signs of hyponatraemia?
Symptoms:
- Headache
- Nausea
- Dizziness
Signs: CHECK HYDRATION STATUS
Dehydration/hypovolaemic:
- Cool peripheries, long cap refill
- Tachycardia
- Weak, thready pulse
- Postural hypotension
- Confusion
- Dry mucous membranes
- Reduced skin turgor
Fluid overloaded/hypervolaemia:
- Tachycardia
- Bounding pulse
- Raised JVP
- Pulmonary oedema or pleural effusions
- Ascites
- Peripheral oedema
