Endocrinology Flashcards

1
Q

Which hormones are released by anterior pit

A
FLAT GP
FSH
LH
ACTH
TSH
GH
Prolactin
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2
Q

Which hormones are released by post pit

A

Oxytocin

ADH

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3
Q

Describe the thyroid axis

A

Hypothalamus releases TRH
Ant pit releases TSH
Thyroid releases T4-> T3

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4
Q

Symptoms of hypothyroidism

A
  1. Weight gain
  2. Fatigue/weakness
  3. Cold
  4. Depression
  5. Hair loss
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5
Q

Causes of hypothyroidism

A
  1. Autoimmune (hashimotos, atrophic)
  2. Treatment of hyper (iodine, surgery)
  3. Natural course of thyroiditis and graves
  4. Drug (amiodorone, lithium, phenytoin)
  5. Central - hypopituitarism

WORLDWIDE = iodine deficiency

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6
Q

Diagnosis of hypothyroidism

A
  1. TSH high
  2. T4 and T3 low
    MAY SEE
    TPO antibodies raised
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7
Q

Treatment of hypothyroidism

A

100-150mcg Levothyroxine or 25 for elderly/IHD
Rare SE
interacts with warfarin

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8
Q

Symptoms of hyperthyroidism

A
Weight loss/inc appetite
Heat intolerance/sweating
Fatigue/cant seep
tremor
Palpitations/nervousness
Irregular periods
Eye problems
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9
Q

Causes of hyperthyroidism

A
  1. Graves disease
  2. TNG
  3. Thyroiditis (autoimmune or viral)
  4. Drug induced (amiodarone)
  5. Iodine induced Jod basedow
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10
Q

Diagnosis of hyperthyroidism

A
  1. Low TSH
  2. High T4/3
    MAY SEE
    anti TSH antibodies (TRab)
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11
Q

Treatment of hyperthyroidism

A
GRAVES
- long course carbimazole 20mg 1 daily
- radioiodine
TNG
- radioiodine 
- surgery
-long term carbimazole
BRIDGE = beta blocker for 1st month
propanolol = mild
nadolol = severe
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12
Q

Graves disease natural history, presentation and assd conditions

A

strong genetic asscn
Spontaneous remission 1-2 yrs common. then long term remission, R+R, hypo (TRab)
Can present with dermopathy, smooth diffuse goitre, eye signs assd with smoking
ASSD with addisons, pernicious anaemia and vitiligo

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13
Q

RF for hyperthyroidism to elicit in history

A
  1. FH of autoimmunity
  2. Female
  3. Smoking
    if post partum thyroiditis suspected ask about t1 diabetes
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14
Q

Describe hypothalamic- adrenal axis (EDIT)

A

hypothalamus releases ARH
Ant pit releases ACTH
Adrenal glands release cortisol and androgens

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15
Q

Functions of cortisol

A
  1. Stress response- alert
  2. Inc blood glucose
  3. Inc metabolism
  4. Suppress immune response
  5. Suppress bone formation
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16
Q

Causes of primary adrenal insufficiency

A
  1. Autoimmune = Addison’s disease
  2. Infective = TB, HIV
  3. Congenital = CAH
  4. Neoplastic = adrenal, mets from RCC, lung
  5. Non malignant infiltration = sarcoidosis, amyloidosis, haemochromatosis
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17
Q

Symptoms of primary adrenal insufficiency

A
Low aldosterone:
- fatigue, weakness
- orthostatic hypo
Abdo signs:
- weight loss
- N/V
- abdo pain

XS ACTH = hyperpigmentation

TANNED TIRED TEARFUL TUMMY

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18
Q

Causes of Cushing syndrome

A
  1. Cushing disease = acth secreting pituitary adenoma
  2. Exogenous steroids= long term tx
  3. Ectopic source = paraneoplastic syndrome eg SCLC ACTH secreting
  4. Cancer- Adreno-cortical carcinoma
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19
Q

Growth hormone axis

A

Hypothalamus releases GHRH
ant pit releases GH
Liver releases insulin like growth factor 1 IGF1
IGF1 acts everywhere - bone density, muscle mass, cell turnover and organ growth

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20
Q

What is function of somatostatin

A

Growth hormone inhibiting hormone

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21
Q

What is ghrelin

A

Hormone released by digestive organs onto Ant pit to stimulate GH release

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22
Q

Describe PTH axis

A
  1. Low calcium, low magneisum and high P04 cause PTH release from 4 glands on thyroid
  2. Inc in number and activity of osteoclasts -> Ca release
  3. Kidneys reabsorb calcium
  4. Kidneys activate vit D -> inc calcium absorption from food in gut
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23
Q

Describe PTH axis

A
  1. Low calcium, low magneisum and high P04 cause PTH release from 4 glands on thyroid
  2. Inc in number and activity of osteoclasts -> Ca release
  3. Kidneys reabsorb calcium
  4. Kidneys activate vit D -> inc calcium absorption from food in SI
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24
Q

Describe RAAS

A
  • low circ volume detected
  • renin released from kidney
  • acts on angiotensin 1 (liver)-> 2
  • angiotensin 2-> angitoensinogen by ACE
  • angiotensinogen causes vasoconstriction and aldosterone release (adrenal)
  • aldosterone = water and Na reaborsption DT and H,K secretion?
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25
Q

Carbimazole indication, SE and alternative

A

Used to control Graves, TNG
Works by blocking TPO from organifying the iodine
RISK = agranulocytosis = low neutrophils = check fbc in pxs on this drug when ill
SE- rash, GI
Teratogenicity
Alternative in preg esp 1st trimester: propylthiouracil
SE: hepatotoxicity and fulminant hepatitis

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26
Q

How does thyroid cancer present, diagnosis, treatment

A

Asymptomatic, palpable nodule in 30-40 year old women
risk - previous head /neck radiation
Diagnose: USS and FNAC
Tx: thyroidectomy, radioiodine ablation, TSH suppressing dose of levothyroxine
rare but good prognosis for most types

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27
Q

Role of steroids in thyroid problems

A

If treating px with thyroid eye disease with radioactive iodine need to give prophylactic steroids
Can give prednisolone in severe thyroiditis symptom management

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28
Q

What is T1 diabetes

A

Autoimmune or idiopathic destruction of beta cells that result in complete loss of insulin
So there is no uptake of glucose from blood, no glyconeogenesis, no inhibition of glycogenolysis

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29
Q

Diagnosis of diabetes

A

HbA1c > 48
Fasting bgc > 7
Random bgc or OGTT > 11

If T1 symptomatic = 1 test is enough
if T2 need 2 tests

30
Q

Diagnosis of pre-diabetes

A

HBA1c > 38
Fasting > 5.5
Random > 7.8

31
Q

Treatment of T1 diabetes

A

Insulin injection or subcut infusion
Never stop, inc when ill (hyperglycaemic)
Take a mixture of long and short acting

Monitor 3 monthly with Hba1c or fructosamine if blood disorder

32
Q

What is DKA

A
  1. Hyperglycaemic or known diabetic
  2. Ketonaemia >3 bloods or urine >2
  3. Metabolic acidosis VBG > 7.3 pH or Hc03 <15

Cause
- forgot to take insulin/infection

33
Q

Presentation of DKA

A
ACUTE < 24 HOURS
T1 DIABETIC
Usual t1 symptoms + 
N+V
Abdo pain 
Reduced conciousness,low bp, excessive tiredness, headache
Hyperventilation
Hot dry skin
Hypothermic
34
Q

Presentation of DKA

A
ACUTE < 24 HOURS
T1 DIABETIC
Usual t1 symptoms + 
N+V
Abdo pain 
Reduced conciousness,low bp, excessive tiredness, headache
Hyperventilation
Hot dry skin
Hypothermic
35
Q

Treatment of DKA

A
  1. 500ml of 0.9% NaCL
  2. FRII 0.1unit/kg/hour of insulin
  3. Potassium if <5.5 because insulin lowers K risk of hypokalaemia
  4. VTE prophylaxis
  5. Glucose if bgc <14
36
Q

What is T2 diabetes

A

Beta cell of pancreas dysfunction = reduced sensitivity to and production of insulin

37
Q

Presentation of T2 diabetic

A

Asymptomatic

Chronic fatigue, may have blurred vision

38
Q

RF for T2 diabetes

A

Non modifiable:

  • age
  • ethnicity
  • FH
  • PCOS
  • exisitng CVD

Modifiable:

  • activity, weight status (BMI 25-30 over, 30+ obese)
  • hypertension
  • hyperlipidaemia
39
Q

Management of T2 diabetes other than OHA

A
Conservative: 
activity = reduce cv risk, directly use glucose, inc glycogen stores, directly inc sensitivity to insulin 
change diet 
stop smoking = cvd
alcohol = risk hypo

DRUGS

  • BP
  • Lipid
  • Antiplatelet asprin, clopidogrel CV risk
40
Q

What is HHS

A
  1. Hyperosmolar ( >320 mosmol/kg)
  2. Marked Hyperglycaemic (>30)
  3. Hypovolemic
  4. non ketotic

Causes - old diabetic who is ill or poorly controlled
Present - confused, dehydrated over a few days

41
Q

Treat HHS

A

SLOW fluid replacement, naturally lowers glucose
if not -> insulin
Watch for hypernatraemia with saline replacement
Watch for hypokalaemia
VTE and ulcer protection

42
Q

OHA for T2 diabetes

A
  1. Metformin
  2. SU eg gliclazide
  3. Pioglitazone
  4. Incretin based - gliptins, exenatide
  5. Acarbose
  6. SGLT2 inhibitors
43
Q

How does metformin work, benefits and SE

A

Increases insulin sensitivity by
- inc glucose uptake into muscle
- reduce gluconeogensis
- decrease gut absorption of glucose
Benefit: cannot cause hypo or weight gain
BUT risk of lactic acidosis so check LFT and U+E before.
SE- GI, impaired B12 absorption

44
Q

How do SU’s work, examples, side effects.

Name a similar drug

A

Change electrochemical gradient accross B cells via K = MORE INSULIN secreted
EG gliclazide, tolbutamide (s), glibenclamide (l)
SE- hypo, weight gain
CI- pregnancy/breastfeeding
SIMILAR- REPAGLINIDE
but shorter half life, less risk of hypo

45
Q

What is pioglitazone an example of, how does it work and what are its SE

A

Thiazolidinediones
Increases lipid metabolism -> secondary glucose uptake
SE- weight gain, peripheral oedema, inc risk bladder cancer, reduce bone density

46
Q

How do gliptins work, examples, SE

A
Gliptins = inhibit DPP4 = inhibit incretin(GLP1) breakdown 
= inc glucose mediated insulin release
SE- pancreatitis 
CANT cause hypo
Eg
Linagliptin, Alogliptin, Saxagliptin
47
Q

What kind of drug is exanatide, how does it work for diabetes and SE

A

Exanatide is a GLP1 analogue (mimetic) = glucose mediated insulin release increases
also : impaired glucagon secretion, slow gastric emptying
Benefit = only one good for obese px except acarbose
SE- subcut injection, N+V, pancreatitis

48
Q

How do SGLT2 inhibitors work for diabetes, examples, SE

A

Reduce renal resorption of glucose
Gliflozins
SE- DKA, peripheral vasc disease
Eg dapagliflozin, clanagliflozin

49
Q

Risk factors/associations of primary adrenal insufficiency

A
  1. Hypothyroidism
  2. Female
  3. Hypercoaguable state
50
Q

Symptoms of Cushing’s syndrome

A
  1. Central adiposity, buffalo hump
  2. Purple striae
  3. Think skin, bruising
  4. Facial plethora
  5. Diabetes symptoms
  6. Prem osteoporosis
51
Q

How to investigate cushing syndrome

A

PMH: steroid use, cancers
DEXAMETHASONE suppression test
Low dose = fails to suppress axis, cortisol still high
High dose = lowers cortisol in cushings disease. Ectopic or endogenous = stay high.

MRI pituitary for disease

52
Q

How is cushings syndrome treated

A

DISEASE: trans-sphenoidal hypophysectomy, radiotherapy

SYNDROME: metyrapone, ketoconazole, etomidate ICU, mitotane (ACC)

53
Q

How is primary adrenal insufficiency diagnosed

A

Low sodium, high potassium
SHORT SYNACTHEN TEST
primary = low or no cortisol response

54
Q

How is secondary adrenal insufficiency diagnosed

A

high suspicion -> treat
Early morning cortisol
May do a synacthen if stable later

55
Q

How is adrenal insufficiency treated

A
  1. Replace aldosterone if primary = fludrocortisone

2. Replace cortisol = hydrocortisone

56
Q

What is an adrenal crisis and how is it prevented

A
Emergency situation where a patient has insufficient cortisol response to stress
They will be 
- hypotensive, tachycardic
- hypoglycaemic
- hyponatraemic -> confused
hyperkalaemic

PREVENT = sick day rules, pxs on cortisol should take more when ill

57
Q

Causes of secondary adrenal insufficiency

A
  1. Exogenous steroid use
  2. Ectopic ACTH secretion
  3. Hypopituitarism
58
Q

What are the causes of primary hyperaldosteronism/Conn’s syndrome?

A
  1. Aldosterone secreting adenoma of adrenals

2. Idiopathic (familial)

59
Q

How does Conn’s present

A
  1. Hypertensive (always consider)
    - headaches
    - retinopathy
    - weakness/tired
  2. Hypokalaemic (can be normal, but they can end up swapping H,K for Na)
    risk of met acidosis

could also present with hypertensive complications eg stroke

60
Q

Diagnosis of conn’s

A
  1. Plasma aldosterone: renin ratio= increased

2. Fludrocortisone suppression test = would expect aldosterone to drop but it doesn’t

61
Q

How is conn’s treated

A
  1. Excise adenoma

2. Spironolactone (gynae SE), triamterene for K preservation + amiloride diuretic for fluid overload

62
Q

What is phaeochromocytoma

A

Excess catecholamines (ad,nad, dop) due to adrenal medullary tumour

63
Q

Symptoms of phaeochromocytoma

A

random

  • sweating
  • palpitation
  • headache

-tremor
-pallor
- weakness
hypertension

64
Q

How is phaeochromocytoma diagnosed + tx

A

No consensus for diagnostic test

Tx- alpha and beta blockers, excise tumour

65
Q

Causes of secondary hyperaldosteronism

A
  • Benign JMA growth = inc renin

- RAS = false activation

66
Q

Causes of primary hyperparathyroidism and blood results

A
  1. benign PT adenoma
  2. Hyperplasia
  3. Cancerous tumour

PTH high
Calcium high
Phosphate low
vit d high

67
Q

Causes of secondary hyperparathyroidism and blood results

A
  1. renal disease
  2. vit d deficiency
  3. malabsorption eg pancreatitis

PTH high
calcium low
Phosphate high
low vit d (renal fail)

68
Q

Causes of tertiary hyperparathyroidism and blood results

A
Continued secondary, px given tx but axis doesnt respond
PTH high 
calcium high
phosphate high
vit d low
69
Q

Symptoms of hypercalcaemia

A

Stones
Bones
Abdo moans
Pyschic groans(confusion)

70
Q

Symptoms of hypocalcaemia

A
CATs go numb
convulsions
arrhythmias
tetany 
numb hands, feet, around mouth
= chvosteks sign 
= trosseau sign