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Med Year 3 > Obesity/Endocrinology > Flashcards

Obesity/Endocrinology Flashcards

1
Q

what is aldosterone

A

mineralocorticoid secreted by adrenal gland which stimulates absorption of sodium by kidneys and regulates water and salt balance

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2
Q

what is the physiology of the RAAS system

A

afferent arteriole: juxtaglomerular cells, sense BP

low BP = they secrete renin

liver secretes angiotensinogen and renin converts it to angiotensin 1

ACE converts it to angiotensin 2

AG 2 stimulates release of aldosterone from adrenal glands

aldosterone acts on sodium channels in collecting ducts, to increase membrane permeability = sodium reuptake increases in DCT

aldosterone also causes loss of potassium

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3
Q

what is the HPA axis

A

stress = HT release CRH
APG releases ACTH
ACTH causes release of cortisol from adrenal glands

this mobilises glucose for energy

if cortisol levels are too high = NF, receptors in hippocampus and HT recognise this and lower release of CRH and ACTH

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4
Q

what four regions of the adrenal gland produce what, and which conditions link to each zone?

A

zona glomerulosa = produces MCC (aldosterone) = conn’s syndrome

zona fasiculata = GCC eg cortisol = cushing’s syndrome

zona reticularis = androgen precursors eg DHEA and androstenedione = congenital adrenal hyperplasia

medulla = catecholamines eg adrenaline and NA (phaechromocytoma)

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5
Q

what is phaechromocytoma

A

neuroendocrine tumour of adrenal medulla

= HTN, anxiety, palpitations and weight loss

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6
Q

what is cushing’s?

A

syndrome = signs and symptoms that develop after prolonged abnormal elevation of cortisol

disease = pituitary adenoma secretes excessive ACTH

cushing’s disease causes the syndrome, but syndrome not always caused by CD

age onset is peak at 25-45

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7
Q

what are the features of cushing’s?

A

moon face, central obesity, abdominal striae, buffalo hump, muscle wasting

HTN, cardiac hypertrophy, hyperglycaemia, depression

osteoporosis, myopathy, easy bruising and poor skin healing

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8
Q

what electrolyte imbalances do you see in cushing’s?

A

hypokalameia and hypernatremia

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9
Q

what are the causes of cushing’s syndrome?

A
  • Exogenous steroids (patients on long term high dose steroid medications)
  • Cushing’s disease
  • Adrenal adenoma

(hormone secreting tumour on adrenal gland)

Paraneoplastic cushing’s

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10
Q

what is paraneoplastic syndrome?

A

o Excess ACTH released from a cancer NOT of the pituitary, which stimulates excessive cortisol release
o ACTH from somewhere other than pituitary = ectopic ACTH
o Small cell lung cancer is the most common cause of this

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11
Q

when are cortisol levels highest and lowest?

A

Plasma cortisol is highest in the morning and very low at night and while asleep

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12
Q

what are the investigations for cushing’s syndrome?

A

dexamethasone suppression test

DMT = like cortisol = lowers the amount of ACTH released by pituitary gland which in turn lowers the amount of cortisol released by adrenal gland

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13
Q

how do you do the tests and what do the results mean?

A

low dose (1mg) if normal = not CS

if abnormal (high cortisol even after DMT) = cushing’s syndrome

if abnormal, also do high dose test

high dose test low = cushing’s disease

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14
Q

what is the cause if the high dose DMT test shows up as high cortisol?

A

ACTH low = adrenal cushing’s

ACTH high = ectopic ACTH

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15
Q

what other tests can you do for cushing’s syndrome?

A

24h urinary free cortisol
salivary cortisol

FBC (raised white cells)
electrolytes
MRI brain for pituitary

CRH test
chest and abdo CT for small cell lung cancer and adrenal tumours

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16
Q

how do you treat cushings syndrome?

A

remove underlying cause (steroids)

surgical removal of tumours or both adrenal glands and put on replacement steroids

Ketoconazole (prevents ACTH secretion), mitotane (reduces cortisol production) and metopirone (fast acting, leads to reduction in cortisol levels in just 30 minutes)

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17
Q

what is adrenal insufficiency

A

adrenal glands do NOT produce enough cortisol or aldosterone

primary = addison's
secondary = inadequate ACTH stimulation on adrenals (loss or damage of pituitary, loss of blood flow or tumour removal)

tertiary = inadequate CRH release by hypothalamus (patients on long term steroids bc suppression of hypothalamus)

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18
Q

what is addison’s disease

A

specific condition where adrenal glands are DAMAGED

aka primary adrenal insufficiency, usually auto-immune cause

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19
Q

what happens with steroid withdrawal?

A

HT doesn’t activate fast enough so endogenous steroids not made fast enough = should be tapered off slowly

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20
Q

what are the signs and symptoms of adrenal insufficiency

A 
Fatigue 
Nausea 
Cramps 
Abdo pain 
Reduced libido

Bronze hyperpigmentation, particularly in skin creases, bc ACTH stimulates melanocytes to produce melanin

Postural hypotension

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21
Q

what is the investigation of choice for addison’s?

A

short synacthen test

In morning: give synacthen, which is synthetic ACTH. Blood cortisol is measured at baseline, 30 and 60 minutes after

Synacthen will stimulate healthy adrenals to produce cortisol – high

Failure to rise = addison’s

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22
Q

what other investigations can you do for addison’s?

A

U&E’s = hyponatremia and hyperkalaemia

adrenal autoantibodies
MRI/CT of adrenals and MRI of pituitary

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23
Q

how do you treat addison’s disease?

A

Hydrocortisone 10, 5mg 3x daily

OD longer-acting steroids such as prednisolone, dexamethasone given

Hydrocortisone = gcc to replace cortisol

Fludrocortisone = mineralocorticoid – replaced aldosterone

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24
Q

what is an addisonian crises

A

Acute presentation of severe addison’s, where the absence of steroid leads to life threatening situation

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25
Q

what are the signs and symptoms of addisonian crises

A

overall sick patient, hypotension, hyponatraemia
o Reduced consciousness
o Hypotension
o Hypoglycaemia, hyponatraemia, hyperkalaemia

also: abdo pain, fatigue, weight loss, aches and pains

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26
Q

what causes an addisonian crisis?

A

infection, trauma, withdrawal of steroids

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27
Q

how do you investigate/manage addisonian crises?

A

random serum cortisol and plasma ACTH but start treatment IMMEDIATELY:

high dose, stat hydrocortisone followed by 100mg iV every 6 hours

IV saline

correct hypoglycaemia

28
Q

what is conn’s syndrome?

A

primary hyperaldosteronism

29
Q

what is primary hyperadosteronism?

A

adrenal glands are directly responsible for producing too much aldosterone
o Serum renin will be low as it is suppressed by the high BP

Causes include:

Adrenal adenoma secreting aldosertone
Bilateral adrenal hyperplasia
Familial hyperaldosteronism
Adrenal carcinoma = rare

30
Q

what is secondary hyperaldosteronism?

A

Excessive renin stimulating adrenal glands to produce more aldosterone

Serum renin will be high

Several causes:

occur when BP in kidneys is disproportionately lower than the blood pressure in rest of the body

Renal artery stenosis
Renal artery obstruction
Heart failure

31
Q

what are the investigations you do for conn’s syndrome?

A

renin aldosterone ratio

high aldosterone and low renin = primary

both high = secondary

check BP, serum electrolytes (hypokalaemia), ABGs for alkalosis bc potassium and H+ exchanged for sodium and water

CT or MRI for tumour, renal doppler US and CT angio for stenosis

32
Q

how do you manage hyperaldosteronism?

A

aldosterone antagonists eg spironolactone

treat underlying cause

33
Q

what should you keep in mind that hyperaldosteronism can cause?

A

secondary HTN

34
Q

what is water-friderichsen syndrome?

A

adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection

35
Q

what is phaechromocytoma?

A

tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline

adrenaline tends to be secreted in bursts giving periods of worse symptoms followed by more settled periods

36
Q

how do you diagnose phaechromocytoma?

A

24 hour urinary collection of metanephrines

37
Q

symptoms of phaechromocytoma?

A

Anxiety
Sweating
Headache
Hypertension

Palpitations, tachycardia, and paroxysmal atrial fibrillation
 

38
Q

how do you manage phaechromocytoma?

A

surgery

alpha or beta blockers prior to surgery

39
Q

what is sheehan’s syndrome

A

complication of post-partum haemorrhage

necrosis of pituitary gland due to drop in circulating BV and then hypoperfusion

it ONLY affects the APG, so hormones from PPG are unaffected

40
Q

what hormones are released from which part of the pituitary gland?

A 
•	The anterior pituitary  releases: 
o	Thyroid-stimulating hormone (TSH) 
o	Adrenocorticotropic hormone (ACTH) 
o	Follicle-stimulating hormone (FSH) 
o	Luteinising hormone (LH) 
o	Growth hormone (GH) 
o	Prolactin

The posterior pituitary releases (not affected by Sheehan’s syndrome):
o Oxytocin
o Antidiuretic hormone (ADH)

41
Q

what are the signs and symptoms of sheehan’s?

A

reduced lactatin, amenorrhea, adrenal insufficiency and adrenal crisis (low cortisol), hypothyroidism

42
Q

how do you manage sheehan’s?

A

replacement as HRT, hydrocortisone, levothyroxine, growth hormone

43
Q

what is osmolaltiy

A

concentration of dissolved particles of chemicals and minerals such as sodium in serum

high osmolality = more particles in serum, low means particles are diluted

44
Q

where is ADH secreted from

A

ADH produced in hypothalamus, but released by PPG

45
Q

what happens when plasma osmolality increases?

A

(may happen bc of increased sodium levels or body water decreases)

the receptors in the HT cause thirst to increase water intake

also signal PPG = release of vasopressin (ADH)

ADH acts on collecting ducts of kidney to increase the number of aquaporin channels allowing water to be absorbed in the blood

46
Q

what is diabetes insipidus

A

rare condition with lack of ADH

47
Q

what causes DI?

A

cranial: (too little production from HT) = idiopathic, brain tumours, head injuries, brain infection

kidney becomes insensitive to ADH and does not make aquaporin channels and reabsorb water from collecting ducts = nephrogenic DI

caused by drugs eg lithium, electrolyte disturbance, intrinsic kidney disease

48
Q

how does DI present?

A

polyuria, polydipsia, dehydration, postural hypotension

hypernatremia

49
Q

how do you investigate for DI?

A

low urine osmolality
high serum osmolality

water deprivation/desmopressin stimulation test

50
Q

what is the water deprivation test

A

fluid deprivation for 8 hours then urine osmolality measured and synthetic ADH administered

8 hours later, measure urine osmolality again

in cranial: patient lacks ADH but kidneys still capable of responding to ADH
o Hence urine osmolality remains low bc continues to be diluted by excessive water secretion in the kidneys
o Then when synthetic ADH = UO is high

• In nephrogenic = patient unable to respond so UO will be low all the time

Primary polydipsia (drinks too much water = too much urine) = UO will be high even before ADH given = no DI

51
Q

how do you manage DI

A

underlying cause
conservatively

desmopressin to replace ADH

52
Q

what is SIADH

A

many stimuli can override osmolality control and cause release of inappropriately high amounts of ADH = reabsorption of water from CD of kidneys

  • Causes urine = high sodium content or osmolality
  • Serum sodium levels drop as water is retained
53
Q

how do you diagnose SIADH

A

diagnosis of exclusion
euvolemia, high UO and low SO
hyponatremia on u&E’s
negative short synacthen to rule out adrenal insufficiency

54
Q

what causes SIADH

A

lung disease = cancer, pneumonia

brain lesions = tumour, head injury and bleed, stroke

drugs = carbamezapine, SSRU;s

55
Q

what are some non-specific symptoms of SIADH

A

headache, fatigue, muscle aches and cramps, confusion

56
Q

how do you manage SIADH

A

fluid restriction
acute = hypertonic saline
aim for change in sodium of less than 10mmol/per 24h to prevent central pointine myelinolysis

or vaptans (ADH receptor antagonists) which acts on V1 and V2 receptors causing vasoconstriction and water diuresis

57
Q

what is hyponatremia

A

low sodium levels

causes = excessive loss due to drugs (PPI’s, SSRIs, ACEI) or insufficient intake

symptoms include CONFUSION, headache, nausea, dizziness

may be either dehydrated or fluid overloaded so signs related to that

58
Q

how do you investigate SIADH

A

hydration status
urinary sodium and somolality
if urine sodium is high = SIADH, it should be low bc body is conserving it

59
Q

how do you manage SIADH

A

mild: fluid restriction less than 800ml
loop diuretics
may need hypertonic saline

60
Q

what is hypernatremia?

A

unusual, high sodium levels only seen in association with severe dehydration

replace water deficit with iV sodium chloride 0.9%

61
Q

what is hyperkalaemia?

A

> 5.5 serum potassium
caused by drugs like spironolactone, ARBs, ACE-I

main symptoms include fatigue, muscle weakness and confusion

Complications:
Can cause a cardiac arrhythmia and bradycardia, which is fatal

62
Q

how do you treat hyperkalameia

A

calcium gluconate or B2 agonist nebulised

or insulin with dextrose

these increase potassium shift form plasma into cells

can also give sodium bicarbonate to reverse acidosis, given in hyperkalaemia bc most patients also have acidosis

63
Q

what is obesity

A

classified according to BMI

o	Healthy weight – 18.5-24.9 kg/m^2
o	Overweight: 25-29.9
o	Obesity 1: 30-34.9
o	Obesity 2: 35-39.9
o	Obesity 3: 40 kg/m2 or more
64
Q

how would you manage obesity?

A

consider:
o 1. General advice on healthy weight and lifestyle
o 2. Diet and physical activity
o 3. Diet and physical activity, consider drugs
o 4. Diet and physical activity; consider drugs; consider surgery

65
Q

how do you assess patients with obesity?

A

social
measurements eg BMI and waist circumference
RF, presenting symptoms, lipid profile, hba1c, LFTs and TFTs

comorbidities

66
Q

what drugs could you give for obesity?

A

o Orlistat: pancreatic lipase inhibitor, leading to malabsorption of fat by in intestine
o Lorcaserin: a selective 5-HT2c serotonin receptor agonist, decreasing food intake by increasing satiety
o Phentermine/topiramate = first combination drug approved for weight loss

67
Q

when is bariatric surgery considered?

A

if BMI is >40 or >35 and siginificant comorbidites

have tried all other measures
patient commits to need for long term follow up and is fit for surgery

Med Year 3 (25 decks)

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