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Y3 Charis > Endo - general > Flashcards

Endo - general Flashcards

1
Q

Drugs that can cause DI

A
  • Lithium
  • Gentamicin
  • Rifampin
  • Colchicine
  • Cisplatin
  • Demeclocycline
  • Orlistat
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2
Q

Drugs that can cause T2DM

A
  • Thiazide diuretics
  • Corticosteroids
  • Atypical anti-psychotics
  • Antiretroviral protease inhibitors
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3
Q

Complications of DKA

A
  • Cerebral oedema (mannitol infusion, mechanical ventilation)
  • Pulmonary oedema
  • ARDS
    treatment related reduction in colloid volume –> water accumulation in the lungs –> decreased lung compliance + hypoxaemia
    monitor blood O2 levels, lower fluid intake, replace colloid
  • Iatrogenic hypoglycaemia
  • Iatrogenic hypokalaemia
  • Arterial/venous thromboembolism
  • prophylatic heparin
  • gastric stasis
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4
Q

Plasma osmolarity equation

A

2 (Na+K) + glucose + urea

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5
Q

Anion gap equation

A

Generally used formula, K is excluded on the grounds that its value is small enough to be disregarded

Na - (Cl + HCO3)
Formula used when the value of the K is expected to vary significantly as in renal patients (+ is the one that is on bb)

(Na + K) - (Cl+ HCO3)

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6
Q

Describe the plasma osmolarity in DKA + HONK

A

Increased in both DKA + HONK (both are hyperosmolar states)
Much higher in HHS/HONK
o >290 mOsm/kg + ketonaemia/ketonuria - DKA
o >320 mOsm/kg + no significant ketonaemia/ketonuria - HHS/HONK

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7
Q

Actions of insulin

A
  • Glucose uptake
  • Increase in glycogen synthesis
  • Decreased gluconeogenesis and glycogenolysis
  • Increase fat synthesis
  • Decreased lipolysis
  • Increased amino acid uptake
  • Decreased proteolysis
  • Increased potassium uptake
  • Increased phosphate uptake
  • Decreased renal sodium excretion
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8
Q

Factors that

  • Increase Ca
  • Derease Ca

and where are they produced

A

Increase

  • Calcitriol (skin + UV light)
  • PTH (parathyroid glands)

Decrease
- Calcitonin (parafollicular cells of thyroid gland)

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9
Q

How does vitamin D get converted to active Vitamin D (calcitriol)?

A

Diet + UV light form vitamin D (skin)

25 hydroxylase turns vitamin D to 25-hydroxyvitaminD3 (liver)

1a-hydroxylase turns 25-hydroxyvitamin D3 into 1,25-dihydroxyvitaminD3 (calcitriol, activated vitamin D) (kidney)

PTH increases renal production of 1,25-dihydroxyvitaminD3

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10
Q

Function of PTH on kidneys, bone, small intestines

+ resultant effect

A

Kidneys
1a hydroxylase stimulation
Increase calcium absorption
Increase phosphate excretion

Bone
Increased bone resorption

Intestines
Increased calcium absorption
Increased phosphate absorption

Resultant effect

  • Increased Calcium
  • Decreased phosphate

Calcitriol raises blood calcium levels more than PTH

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11
Q

Function of calcitriol/Vitamin D on kidneys, bone, small intestines

+ resultant effect

A

Kidneys
Increase calcium absorption
Decreased phosphate reabsorption

Bone
Increased bone resorption

Intestines
Increased calcium absorption
Increased phosphate absorption

Resultant effect

  • Increased Calcium
  • Decreased phosphate

Calcitriol raises blood calcium levels more than PTH

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12
Q

Which 2 substances provide negative feedback to the parathyroid gland?

A

High Calcium

High Calcitriol

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13
Q

Which substance should be used to monitor vitamin D levels?

A

25-hydroxyvitamin D
- Major circulating form of vitamin D used to determine vitamin D status
NOT 1,25-dihydroxycholecalciferol

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14
Q

Causes of secondary hyperPTH

A 
- Vitamin D deficiency
   Poor sunlight
   Poor dietary intake
   Malabsorption
- CKD
- Liver disease
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15
Q

Endo causes of proximal myopathy

A
  • Cushing’s
  • Osteomalacia (2ndary hyperparathyroidism)
  • Thyrotoxicosis (hyperthyroidism enhances metabolism of 25-hydroxyvitamin D)
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16
Q

What is MEN 1?

A

Pituitary tumours
Pancreatic tumours
Parathyroid gland hyperplasia

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17
Q

What is MEN2A?

A

Medullary thyroid cancer
Phaechromocytoms
Parathyroid gland hyperplasia

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18
Q

What is paget’s disease?

A
  • Disease of bone remodelling
  • Excessive bone resorption followed by excessive bone growth
  • Results in abnormal “mosaic pattern” of lamellar bone (new bone that is being build is woven and not lamellar)
  • The marrow spaces are filled by an excess of fibrous tissue with a marked increase in blood vessels
  • This leads to skeletal deformities and potential fractures
  • Most often it involves the skull, lumbar vertebrae, pelvis, femur
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19
Q

Which are the three main phases of Paget’s disease?

A
  • Lytic phase - osteoclasts - demineralisation + bone resorption
  • Mixed phase - lytic phase + blastic phase (rapid disorganized proliferation of new bone tissue by osteoblasts)
  • Sclerotic phase - bone formation exceeds bone resorption - structurally disorganised bone (weaker than normal healthy bone, woven bone not lamellar)
  • Burned out state - osteoblastic activity slows down + there is a dormant state in the disease
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20
Q

Definition of osteoporosis

A

reduced bone density resulting in bone fragility and increased fractured risk

T-score < -2.5

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21
Q

What is the difference between the T score and the Z score in a DEXA scan?

What does a T-score of < -2.5 mean?

A

o T score = the number of S.D. the bone mineral density measurement is above or below the YOUNG NORMAL mean bone mineral density
Used to define osteoporosis

o Z score = the number of S.D. the measurement is above or below the AGE-MATCHED mean bone mineral density.
Used to identify patients who may need a work-up for secondary causes of osteoporosis

T-score of < -2.5 = means 2.5 SD or more below the young adult reference mean i.e. less than -2.5 SD therefore -3.5, -4.5 etc

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22
Q

List some RF for osteoporosis

A

Primary - post menopausal, old age >50 years

Secondary
Drugs - steroids, thyroxin
Endo - Cushing’s, primary hyperparathyroidism, hyperthyroidism, hypogonadism
Cancer - myeloma, metastatic carcinoma
MSK - RA, ankylosing spondylitis, SLE
GI - coeliac disease, IBD

  • Post-menopause
  • Primary hypogonadism/Secondary amenorrhea – low oestrogen can lead to decreased bone mineral density
  • Late menarche/early menopause
  • Corticosteroid use (antagonise vitamin D and therefore decrease calcium absorption from the gut)
  • Glucocorticoid excess e.g. Cushing’s syndrome
  • Vitamin D deficiency
  • Low calcium intake
  • Prolonged immobilisation/Physical inactivity
  • Low BMI
  • Smoking, Alcohol
  • FHx
  • F>M
  • > 50 women
  • > 65 men
  • Afro-carribeans have a higher bone mass than Caucasians
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23
Q

Function of excess PTH

A
  • Stimulates osteoclasts to break down bone

* Makes kidneys hold on to calcium + get rid of phosphate - hypercalcemia, hypophosphatemia

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24
Q

What causes primary hyperparathyroidism?

A

Parathyroid adenoma
Parathyroid hyperplasia
Parathyroid carcinoma

Parathyroid gland makes PTH independently of the calcium level

RF – MEN1, MEN2A, HTN

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25
Q

What causes tertiary hyperparathyroidism?

A
  • Individuals who have had secondary hyperparathyroidism for many years develop primary hyperparathyroidism
  • Chronic stimulation of the parathyroid gland by low Ca results in autonomous PTH secretion even after the cause of hypocalcaemia has been corrected
  • Makes PTH independently of calcium levels –> hypercalcaemia
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26
Q

Causes of vitamin D deficiency

A

• Poor sunlight
• Poor dietary intake
• Malabsorption
• Old age
o Decreased ability of skin to produce vitamin D
• Obesity – body fat stores vitamin D
• CKD
• Granulomatous diseases (e.g. sarcoidosis, TB) – enhanced destruction of Vitamin D
• Hyperthyroidism – enhances metabolism of 25-hydroxyvitamin D
• Medication use – glucocorticoids, antiepileptic medication, rifampicin, St John’s wort

vitamin D deficiency = secondary hyperparathyroidism = osteomalacia

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27
Q

Definition of DI

A

Inadequate secretion or insensitivity of the renal collecting ducts to ADH leading to hypotonic polyuria

(Craniopharangyomas are much more likely to cause cranial DI than actual pituitary tumours e.g. prolactinomas)

28
Q

Type of acid-base derangement in Cushing’s syndrome

A

hypokalaemic metabolic alkalosis

29
Q

Definition of DKA

A

Glucagon driven breakdown of fatty acids to ketones

In the setting of insulin deficiency, stress hormones like glucagon, cortisol, catecholamines increase glucose and stimulate ketogenesis

30
Q

Na status in patients with DKA

A

Pseudohyponatraemia due to increased glucose in the blood

Distiniguished from true hyponatraemia in the following way
Pseudohyponatraemia - N/High plasma osmolarity
High –> hyperglycaemia
N –> hyperlipidaemia, hyperproteinaemia
True hyponatraemia - Low plasma osmolarity

31
Q

What is myxoedema maddness?

A

Psychosis with delusions and hallucinations or dementia

Occurs in severe hypothyroidism
May be seen in the elderly after starting levothyroxine treatment

32
Q

What is Plummer’s disease?

A

One type of hyperthyroidism

Toxic multinodular goitre on producing TSH on one side of the thyroid gland
This causes the other side to atrophy

33
Q

Give some examples of conditions that cause thyrotoxicosis without hyperthyroidism

Technetium scan uptake

Mx

A

Autoimmune thyroiditis
Postpartum thyroiditis
Subacute/de Quervains thyroiditis
Amiodarone-indiced thyroiditis

Low uptake

Mx

  • B blockers
  • Thinoamides (propylthiouracil, carbimazole) wont work - problem is not that thyroid is overactive but that it has been damaged + released the hormones prematurely
34
Q

Pathophysiology of Grave’s disease

A

Antibodies/Plasma IgG to thyroid TSH receptor stimulates thyroid hyperplasia and thyroid hormone hypersecretion, causing exaggerated thyroid hormone action and autonomic overactivity.
Type V hypersensitivity

35
Q

List the 5 types of thyroid cancer

Which is the most common
Which has the worst prognosis

A

Papillary thyroid carcinoma 30-50 y/o
Follicular thyroid carcinoma 40-60 y/o (particulalry metastasises to the lungs)
Medullary thyroid carcinoma
Primary thyroid lymphoma (almost always non-Hogkin;d lymphoma)
Anaplastic carcinoma 60-70 y/o

Papillary thyroid carcinoma - most common
Anaplastic carcinoma - worst prognosis (mean survival is 6m)

36
Q

Hashimotos thyroiditis

What is it 
Epidemiology
Presentation
Biopsy 
Associated with
A

What is it - chronic autoimmune thyroiditis, causes hypothyroidism
T-lymphocyte infiltration of the gland + reactive ab against TSH receptor + less commonly TG
T cell mediated destruction of the thyroid gland
Type IV hypersensitivity

Epidemiology - middle age and elderly

Presentation - symptoms of hypothyroidism, firm non-tender goitre
Moves on swallowing

Biopsy
Lymphocytic infiltrate
Destruction of follicles
Variable fibrosis

Associated with - personal/FHx of other autoimmune conditions

37
Q

Commonest cause of goitre in developed countries
Commonest cause of goitre worldwide

+ other causes

A

developed countries – Graves (hyperthyroidism)
worldwide – iodine deficiency (hypothyroidism)

other causes
iatrogenic - post surgery, radioiodine, amiodarone
congenital dysgenesis
de Quervain’s thyroditis

38
Q

Causes of nephrogenic DI

A
  • Hypercalcaemia
  • Hypokalaemia
  • Lithium
  • Inherited (AVPV2 gene)
  • Idiopathic
39
Q

MEN

Inheritance pattern
Defect on which genes + on which chromosomes for MEN1, MEN2A, MEN2B?

A

AD

MEN1
MEN1 gene on Chr 11
Tumour suppressor gene

MEN 2A, MEN 2B
RET gene on Chr 10
Proto-onco gene

40
Q

What do carcinoid tumours release?

A

Humoural factors

o	Amines (SEROTONIN, histamine)
o	Polypeptides (bradykinin - vasodilator)
o	Prostaglandins (vasodilators)
41
Q

Where are carcinoid tumours commonly found?

A

Anus + rectum

42
Q

Why in carcinoid syndrome are there no symptoms unless the tumours metastasise to the liver?

A

 Because hormones released in the portal circulation are metabolised in the liver, therefore liver dysfunction decreases the liver’s ability to metabolize the hormones which get released from neuroendocrine cells allowing them to build up and cause symptoms

 Hepatic metastases result in the secretion of tumour products into the hepatic vein

 This is the most common site for a neuroendocrine tumour to metastasize

43
Q

Carcinoid syndrome RF

A

• Genetic MEN1 syndrome (neuroendocrine tumours are associated with MEN-1)

44
Q

Adrenal histology and what hormones are being produced where

A

Adrenal cortex
Zona glomerulosa - mineralocorticoids e.g. aldosterone
Zona fasciculata - glucocorticoids e.g. glucose
Zona reticularis - sex steroids

Adrenal medulla - catecholamines

45
Q

Definition and causes of primary hyperalodteronism

A

Autonomous aldosterone overproduction from the adrenal gland with subsequent suppression of plasma renin activity

Conn’s syndrome/ adrenal adenonma (70%) - young females
Bilateral adrenal cortex hyperplasia (30%)- old males
Familial hyperaldosteronism
aldosterone producing adrenal carcinoma

46
Q

DDx for a presentation of HTN + Hypokalaemia

A
  • Conn’s syndrome/bilateral adrenal hyperplasia - high aldosterone, low renin
  • RAS - all pt will have HTN + hypokalaemia
  • Cushing’s disease may also present with HTN + hypokalaemia - low aldosterone, low renin
47
Q

Causes of Cushing’s syndrome

A

Exogenous causes
• Exogenous cortisone (e.g. prednisolone) – MOST COMMON CAUSE

Endogenous causes
• Cushing’s disease –> ACTH secreting pituitary tumours
• Ectopic ACTH secreting tumours (small cell lung cancer, bronchial carcinoids)

• Autonomous adrenal cortisol overproduction (adenomas (benign), carcinomas (malignant), bilateral adrenal hyperplasia)

48
Q

What is a phaeochromocytoma?

A

Tumour arising from catecholamine-producing chromaffin cells of the adrenal MEDULLA

10% are extra-adrenal (paragangliomas)
10% are bilateral
10% are malignant

consider phaeos in patients with
Young onset
Resistant intractable HTN

49
Q

Which familial sydroomes are assosciated with phaeochromocytoma?

A
  • MEN 2A, 2B
  • NF1
  • Von Hippel-Lindau
50
Q

Commonest cause of adrenal insufficiency in the UK vs woldwide

A

UK - autoimmune addison’s
Worldwide - TB addison’s

but generally most common causes are iatrogenic
primary causes are rare

51
Q

With which syndrome is Addison’s disease related?

A

AIPES
Autoimmune polyendocrine syndrome

Type 1 - AR caused by mutations in the AIRE gene

Type 1
• Addison’s disease
• Chronic mucocutaneous candidiasis
• Hypoparathyroidism

Type 2
•	Addison’s disease
•	T1DM 
•	Hypothyroidism 
•	Hypogonadism
52
Q

Pathophysiology of PCOS

A
  • Hyperinsulinemia –> excess insulin binds to theca cells –> causes them to grow and divide -> too many LH receptors
  • Increased LH production from anterior pituitary –> stimulates theca cells to produce androgens (androstenedione)
  • Granulosa cells overloaded cant convert enough androgen to oestradiol –> build up of androgens in the blood –> symptoms
  • Because the LH levels are really high, there’s no LH surge to trigger the dominant follicle to break away from the ovary so it may remain there appearing as a cyst or it might degenerate with the other follicles –> ovulation doesn’t occur

• Insulin resistance –> hyperinsulinemia:
o Increased androgen production
o Decreased production of SHBG in the liver (free testosterone may be raised even if total testosterone is normal)

53
Q

Top 2 dx if you suspect SIADH

A

SIADH is not a dx

  • Chest XR (lung caner)
  • Head CT (brain tumour)

(you don’t really start with brain MRI, CT is usually first line)

54
Q

Why is prolactin increased in hypothyroidism?

A

Because excess TRH released to stimulate the pituitary gland to stimulate the thyroid also has a role in stimulating prolactin release

55
Q

Endocrine tests in multinodular goitre

A

Normal

56
Q

BP targets for diabetic

with vascular damage (e.g. diabetic retinopathy)
without vascular damage

A

with vascular damage (e.g. diabetic retinopathy) - <130/80 mmHg
without vascular damage - <140/90 mmHg

57
Q

Hyponatraemia + hyperkalaemia unresponsive to IV rehydration dx

A

Addison’s disease

low serum cortisol, high ACTH

58
Q

What is Pemberton’s sign?

A

Elevation of arms above the head –> facial venous congestion + plethora due to thoracic inlet obstruction by retrosternal mass (e.g. goitre)

59
Q

Type of hypersensitivity

Graves
Hashimotos

A

Graves - Type V hypersensitivity
Antibody mediated stimulation of the TSH receptor

Hashimotos - Type IV hypersensitivity
T cell mediated destruction of the thyroid gland

60
Q

T scores in osteoporosis vs ostopenia

A

Osteoporosis less than minus 2.5 (i.e. -3.5, -4.5)

Osteopenia between minus 1 and minus 2.5

61
Q

Hypopituitarism, list the order with which the hormones will be affected

A

LH/FSH
GH
TSH
corticotrophin

62
Q

Cushin’s disease

which of the following is likely to be decreased/inhibited?

protein catabolism
free water clearance
circulating neutrophils
uric acid production
circulating lymphocytes
A

circulating lymphocytes (suppression of the immune system + t cell responses)

63
Q

commonest cause of adrenal insufficiency

A

autoimmune (UK)*
TB (worldwide)

*immune reaction against 21-hydroxylase - destruction of the adrenal cortex

64
Q

Most common cause of Cushing’s syndrome

A

Pituitary adenoma that secretes cortisol

65
Q

How does Cushing’s syndrome / high levels of cortisol / steroids lead to increased risk of infections?

A

Decrease in circulating lymphocytes

Suppression of the innate immune + T cell responses resulting in lymphopenia

66
Q

C peptide interpretation

A

C-peptide indicates ENDOGENOUS insulin production
low in T1DM
high in T2DM

If C-peptide is ABSENT but there are symptoms of hypoglycaemia then it means EXOGENOUS insulin production

67
Q

T2DM BP monitoring - how often?
>150/90mmHg
>140/80mmHg
>130/80mmHg with renal/ophthalmic/cerebrovascular pathology

A

T2DM BP monitoring
>150/90mmHg – every month
>140/80mmHg – every 2 months
>130/80mmHg with renal/ophthalmic/cerebrovascular pathology – every 2 months

Y3 Charis (35 decks)

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