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Year 3 - Metabolic Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is Addisons Disease?

A

Adrenal insufficiency leading to reduced cortisol and aldosterone (hypoadrenalism)

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2
Q

Key symptoms of Addisons Disease

A
  1. Lethargy and weakness
  2. Anorexia and salt cravings
  3. Hyperpigmentation in palmar creases
  4. Hyponatraemia and hyperkalaemia
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3
Q

Investigation to be done in Addisons disease

A

ACTH stimulation test (short synACTHen test)

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4
Q

How is the ACTH done?

A

Plasma cortisol measured before and 30 mins after administering synacthen 250ug IM

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5
Q

primary management of Addisons?

A

Hydrocortisone or fludrocortisone

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6
Q

Causes of Addisons crisis

A

Withdrawal from meds, sepsis, surgery, adrenal haemorrhage

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7
Q

What is Waterhouse friedrichsen syndrome?

A

Adrenal haemorrhage

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8
Q

Addisons crisis management?

A

Hydrocortisone IV
1L saline
Oral replacement

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9
Q

Hashimotos Thyroiditis what is it?

A

Autoimmune condition causing hypothyroidism and is more commmon in women

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10
Q

Associated symptoms to Hashimotos

A

Goitre
Bradycardia (bradycardia, reflex reduction, ataxia/amenorrhoea, dry hair/hair loss, yawn/tired, cold sensitivity, ascites, round puffy face, immobile, constipation

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11
Q

Antibodies for Hashimotos

A

Anti tpo and anti Tg

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12
Q

Secondary hypothyroidism causes?

A

Downs turners and coeliac disease

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13
Q

Investigations for hypothyroidism

A

Blood test and antibody test
- very high TSH, low T3/4 (primary)
- low TSH, LOW t3/4 (secondary)

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14
Q

MANAGEMENT OF HYPOTHYROIDISM

A
  1. Levothyroxine
  2. Avoid lithium and amiodarone
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15
Q

What is subacute de quervains

A

post viral infections, acute phase hyperthyroid and then hypothyroidism

Self-limiting

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16
Q

What is Graves’ disease?

A

most common form of hyperthyroidism.

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17
Q

what antibodies are seen with Graves’ disease

A

Anti TSH receptor antibodies that MIMIC TSH
And anti tpo in transient

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18
Q

Key symtpoms of graves

A

S: swearing
W: weight loss
E: exopthalmsu
A: anxiety/anorexia
T: pre-tibial myxoedema
I: irratable bowels
N: nervousness
G: goitre

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19
Q

what is the management for graves

A
  1. ATH drugs (propanolol for adrenergic symptoms) and carbimazole
    - propylthiouracil (not good because can cause severe hepatic impairment = death and agranulocytosis)
  2. Radioactive iodine - not if pregnant and usually requires years of supplements
  3. Beta blockers as mentioned for symptomatic management
  4. Surgery
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20
Q

What is toxic multinodular goitre

A

Multiple thyroid hormone releasing nodules

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21
Q

DKA key symptoms

A

Kussmaul breathing (deep hyperventilation)
Abdo pain
Headache
Acetone breath
Polydipsia and uria = dehydration

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22
Q

T1DM investigations

A
  1. Urine dip for ketons and glucose
  2. Fasting glucose >7.0
  3. Random glucose >11.1 (2 sep occasions if asymptomatic)
  4. C-peptide low
  5. Anti-GAD antibodies
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23
Q

What is C-peptide?

A

Predicted as a by product by the pancreas when insulin is produced it is in equal numbers to insulin produced

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24
Q

HbA1c parameters?

A

> /= - 48 (diabetic) asymptomatic needs repeating

42-47 pre diabetes

<41 normal

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25
Q

What is pre diabetic paramaeters

A

42-47 mmol/l
6.1-6.9 mmol/l

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26
Q

When shouldn’t HbA1c be used?

A

Children, gestational diabetes, iron deficiency anaemia, HIV, CKD

27
Q

WHAT IS THE FIRST LINE TREATMENT OF T2DM

A

Metformin

28
Q

How does metformin work?

A

Increases insulin sensitivity (moving GLUT-4)
Stops gluconeogenesis from liver

29
Q

What enzyme is activated by metformin

A

AMPK

30
Q

What is a key contraindication of metformin

A

Renal impairments <30 egfr

31
Q

What is a key side effect to be careful of with metformin

A

GI issues but mainly LACTIC ACIDOSIS

32
Q

WHAT CAN LACTIC ACIDOSIS CAUSE

A

Metabolic acidosis ( low pH, low HCO3-, low CO2)

33
Q

What diabetic medication is good to use in CVD

A

SGLT-2 (empagloflozins)

34
Q

What are sulfonyureas?

A

Gliclazides
- stimulates pancreatic beta cells to secrete insulin

35
Q

What are major negatives of sulfonylureas

A

Weight gain
Hypos
Hyponatraemia
Oedema

36
Q

What are major negatives of sulfonylureas

A

Weight gain
Hypos
Hyponatraemia
Oedema

37
Q

DPP-4 inhibitor moa?

A

Stops DPP-4 enzyme from breaking incretin. Incretin hormones are GLP-1 and increases insulin secretion and causes satiety

38
Q

Examples of DPP4 inhibitor

A

Sitagliptin

39
Q

Side effects of DPP4 inhibitors

A

Headache and GI problems but most importantly PANCREATITIS due to overuse

40
Q

When and why is saxagliptin good?

A

Can be used in renal impairment if at a titrated dose

41
Q

What is thiazolidinediones

A

Pioglitazone - activated PPAR gamma in adipose toes to promote fatty acid uptake and releases adiponectin which promotes insulin sensitivity

42
Q

Side effects on pioglitazone

A

Headache, GI problems, oedema

43
Q

What are SGLT-2

A

Empagliflozin - they block glucose reabsorption from proximal tubules and increase glucose secretion

44
Q

Main issue with SGLT-2 inhibitors

A

UTIs
Increased urination
Weight loss

45
Q

Main issue with SGLT-2 inhibitors

A

UTIs
Increased urination
Weight loss

46
Q

What are and give an example of a GLP-1 analogue

A

Exanatide

Incretin mimetic = inhibits glucagon secretion and increases insulin sensitivity

47
Q

Metformin guideline?

A

Metformin if >48.

If >58 metformin + DPP4/ulfonylurea/pioglitazone/sglt-2

If still not working

Same again + another

If triple therapy not effective then GLP-1 Analogue and if BMI >35

48
Q

When is insulin used in T2DM?

A

If metformin triple therapy not working and BMI <35
And if metfromin not tolerated therapy not working and hbA1c is still >58

49
Q

What is impaired fasting glucose

A

Fasting glucose of 6.1-6.9 mmol/l

They should be offered OGTT

50
Q

What is impaired glucose tolerance

A

Fasting glucose <7.0 AND OGTT 2-hour value of 7.8-11.1

51
Q

What causes IFG

A

Hepatic insulin resistance

52
Q

What causes impaired glucose tolerance

A

Due to muscle insulin resistance

53
Q

What are the 2 types of diabetes Insipidus

A
  1. Cranial = decreased ADH secretion = polyduria = polydipsia
  2. Nephrogenic = insensitivity to ADH
54
Q

What test is used to diagnose diabetes insipidus

A

Water deprivation test

55
Q

What is seen on water deprivation test

A

High plasma osmolaltiy and low urine osmolality

56
Q

What management is given to treat diabetes Insipidous

A

Nephrogenic diabetes = thiazides and low salt/protein

57
Q

What is respiratory alkalosis

A

Respiratory cause of Loss of acid and increase bicarbonate

Usually caused by hyperventilation or mechanical breathing

Blow off too much CO2

Lead to hypoxia (less CO2= less O2), Cerebral constriction (fatigues, confusion, seizure and comas)

58
Q

What is respiratory acidosis

A

Respiratory cause of loss of bicarb and increase acid

Hypoventilation and obstructive causes like asthma, GI syndrome, cystic fibrosis, severe pneumonia

59
Q

What is seen on a blood gas for resp acidosis

A

Ph low
CO2 high
Bicarb normal or slightly high due kidney retention

60
Q

What is see on a resp alkalosis blood gas

A

CO2 low
Ph high
Bicarb normal or lower (kidney compensating to remove bicarb)

61
Q

Role of aldosterone

A

Causes sodium retention and potassium excretion and water retention with it

62
Q

Role of cortisol

A

Blood volume monitor and water retainer.

Hypovolemia detected and cortisol released to retain water through secretion of ADH into renal collecting duct, independent of sodium

63
Q

What is metabolic acidosis and blood gas

A

Blood gas: ph low, Hco3 low, co2 low kussmaul breathing

Caused by lactic acidosis, DKA or toxin metabolites

Or diarrhoea and CKD

Loss of Hco3 and gain of h+

Can cause CNS Depression, hypocalcameia and arrhythmia due to elongated QRS complex

64
Q

What is metabolic alkalosis and blood gas

A

Loss of H+ and gain on HCO3-

Caused by vomiting, hyperaldosteronism and diuretics

Caused by more bicarb supplements, CKD, hypokalameia

Year 3 - Metabolic Medicine (2 decks)

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