endo important Flashcards

1
Q

insulin actions

A

fasting state- regulates glucose release by the liver

postprandial state- promotes glucose uptake by fat and muscle

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2
Q

hormones which act in opposition to insulin (are counterregulatory)

A

glucagon, adrenaline, GH and cortisol- they all increase glucose production by the liver and reduce its utilisation in fat and muscle for a given level of insulin

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3
Q

cells which produce insulin

A

beta cells in the pancreatic islets

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4
Q

cells which produce glucagon

A

alpha cells

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5
Q

sign of severe insulin resistance

A

acanthosis nigricans- blackish pigmentation at the nape of the neck and in the axillae

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6
Q

diagnostic criteria for diabetes mellitus

A

1- random blood glucose measurement >11mmol/L
2- fasting plasma glucose>7mmol/L
3- HbA1c>48mmol/L (6.5%)
4- OGTT: fasting>7mmol/L, 2 hours after glucose >11mmol/L

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7
Q

Type 2 DM management- someone who can tolerate metformin

A

1 - upon diagnosis, if lifestyle measures still do not get HbA1c <48mmol/L then ofer metformin

2- if HbA1c >58mmol/L then add second drug- sulfonylurea/glitpin/pioglitazone/SGLT-2 inhibitor

3- If HbA1c still rises to or remains above 58mmol/L, then triple therapy should be offered metformin +: 
- glitpin &amp; sulfonylurea
- pioglitazone &amp; sulfonylurea 
- sulfonylurea &amp; SGLT-2 inhibitor
- pioglitazone &amp; SGLT-2 inhibitor 
OR insulin therapy
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8
Q

Type 2 DM management- someone who cant tolerate metformin

A

1- upon diagnosis if lifestyle measures do not get HbA1c <48mmol/L, consider a sulfonylurea/glitpin/pioglitazone

2- if the HbA1c rises to above 58mmol/L, then one of the following combinations should be used:

  • gliptin + pioglitazone
  • gliptin + sulfonylurea
  • pioglitazone + sulfonylurea

3- If HbA1c rises to/remains above 58mmol/L then consider insulin therapy

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9
Q

Hypertension management in T2DM

A
  • ACE inhibitors are first line
    Same targets as patients without T2DM (140/90 in clinic, 135/85 at home)
  • Patients with a 10 year cardiovascular risk >10% should be offered a statin (first line atorvastatin)
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10
Q

T1DM management

A
  • target HbA1c<48mmol/L. HbA1c should be monitored every 3-6 months
  • blood glucose should be self-monitored at least 4 times a day, including before each meal and before bed
  • blood glucose targets 5-7mmol/l on waking and 4-7mmol/l before meals and at other times of day
  • treatment of choice= mixed basal-bolus insulin regimen. Twice daily insulin detemir, and offer rapid-acting insulin analogues injjected before meals
  • consider adding metformin if BMI>25
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11
Q

hormones produced in the anterior pituitary

A
  • GH
  • ACTH
  • Prolactin
  • thyroid stimulating hormone
  • LH
  • FSH
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12
Q

treatment hypercalcaemia

A
  • Bisphosphonates- prevent bones releasing calcium
  • calcimimetic agents e.g. cinacelcet reduce production of PTH
  • calcitonin IV/subcut- given to control very high levels of calcium
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13
Q
  • adrenal cortex hormones

- adrenal medulla hormones

A
  • cortex: glucorticoids, mineralcorticoids (aldosterone), sex hormones (androgens)
  • medulla: adrenaline (increases heart rate and converts glucose to liver), noradrenaline (vasoconstriction, increases blood pressure)
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14
Q

Phaechromocytoma

symptoms

A

PHEochromocytoma;
Palpitations
Headache
Episodic sweating

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15
Q

posterior pituitary hormones

A

vasopressin and oxytocin

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16
Q

Grave’s treatment

A
  • Propanolol to block adrenergic effects
  • carbimazole to manage normal thyroid function
  • Thyroxine is added when patient is euthyroid
17
Q

major complication of carbimazole therapy

A

agranulocytosis- low level of white cells, most commonly neutrophils

18
Q

Hashimoto’s thyroiditis

A
  • Antibodies against thyroid peroxidase (TPO) and/or thyroglobulin
  • Type IV hypersensitivity reaction
19
Q

medication which can Cushing’s

A

Steroids

20
Q

tests most commonly used to diagnose cushing’s

A

overnight dexamethasone

24h urinary free cortisol

21
Q

diagnostic test for acromegaly

A

serum IGF-1

22
Q

symptoms of Conns ( hyperaldosteronism)

A

general hyperaldosteronism:
Headaches + facial flushing (high BP)
- Constipation, weakness + heart rhythm changes (due to hypokalemia)
Consider Primary hyperaldosteronism if hypertension, hypokalaemia or
alkalosis in someone not on diuretics

23
Q

treatment for hyperaldosteronism

A
  • spironolactone

- treatment of underlying cause: if conns/carcinoma remove the adrenal tumour, treat heart failure/cirrhosis

24
Q

test for adrenal insufficiency

A

ACTH (synacthen) test: give synthetic ACTH and measure cortisol and aldosterone produced:

  • if cortisol is low and plasma ACTH is high, then is primary adrenal insufficiency
  • If cortisol and plasma ACTH are both low, then is secondary/tertiary adrenal insufficiency
25
Q

hypocalcaemia signs/symptoms:

A
  • Chvostek’s sign- tap facial nerve in front of mastoid bone to trigger facial twitching on one side of the mouth, nose and cheek
  • Trosseau’s sign: keep bp cuff elevated above patient’s systolic for 1-4 mins. positive sign if hands and fingers go into spasm in palmar flexion
  • anxious/irritable/irrational
  • Muscle spasms
  • Tetany
  • QT PROLONGATION ON ECG
26
Q

hyperkalaemia ECG

A
  • tall, tented T waves
  • wide QRS
  • depressed ST segment
  • prolonged PR
27
Q

Addisons disease mnemonic

A

tanned, tired, tearful, thin, throwing up