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Memorize for 2nd Year Exams > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Describe three hormonal responses to exercise

A
  1. Glucagon releases sugar from stored glycogen and stimulated gluconeogenesis
  2. Cortisol enhances the metabolic utility of glucose
  3. Adrenaline helps to pump leaked K back into the cell via the Na/K pump as there is a tendency for K concentration to increase in the blood during exercise
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2
Q

How do steroid hormones leave the cell?

A

Simple diffusion

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3
Q

Describe the steps in insulin secretion

A
  1. Beta cell imports glucose by facilitated diffusion by GLUT2
  2. Glucose is transformed to glucose-6-phosphate by glucokinase
  3. This yields ATP, which binds to the Kir6.2 subunit of the KATP channel
  4. This causes the channel to close, which depolarises the membrane
  5. This causes voltage gated Ca channels to open and so insulin is released
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4
Q

How are ATP, ADP and Mg related to the KATP?

A

ATP binds to the Kir6.2 subunit to close the channel

ADP+Mg binds to the SUR1 subunit to open the channel

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5
Q

Give at least one example of each of the following insulins:

  • Rapid acting analogue
  • Short acting
  • Intermediate acting
  • Long acting analogue
  • Rapid acting analogue-intermediate mixture
  • Short acting-intermediate mixture
A
  • Rapid acting analogue: Humalog, NovoRapid
  • Short acting: Humulin S, ActRapid
  • Intermediate acting: Humilin I, insulatard
  • Long acting analogue: Lantus, Levemir
  • Rapid acting analogue-intermediate mixture: Humalog Mix25
  • Short acting-intermediate mixture: Humulin M3
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6
Q

What are target blood sugars pre meal and 1-2 hours after beginning a meal?

A

Pre meal: 4-7

1-2h after beginning: <10

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7
Q

How many units of insulin should you start a patient on?

A

0.3 units per kg body weight for the whole day

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8
Q

How many units of insulin should you add per CHO?

A

1 unit per 10g CHO

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9
Q

What should a diabetic patient’s blood sugar be before going to bed?

A

8

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10
Q

When should you not use Metformin?

A

Renal impairment with eGFR <40 or creatinine >150

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11
Q

When should you stop Metformin?

A

Pre-operatively or in severe illness - risk of lactic acidosis

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12
Q

Aside from effects in insulin + glucose, what else does Metformin do?

A

Decreases triclycerides

Decreases BP

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13
Q

TZDs

  • Side effect
  • Contraindication
  • Prevent micro or macrovascular complications?
A
  • 3-4 kg weight gain due to increased fat mass and fluid retention
  • heart failure - because of fluid retention
  • prevent macrovascular complications
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14
Q

Do SUs prevent micro or macrovascular complications?

A

Microvascular

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15
Q

Main side effect of Acarbose?

A

Diarrhoea and flatulence

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16
Q

What should an annual review of diabetes include?

A 
Weight
Blood pressure
Bloods: HbA1c, renal function, lipids
Retinal screening 
Foot risk assessment 
Record severe hypoglycaemia episodes of admission with DKA
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17
Q

Give some examples of autonomic neuropathy

A 
Resting tachycardia 
Urinary infrequency
Erectile dysfunction 
Hypoglycaemic unawareness 
Delayed gastric emptying 
Dry foot
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18
Q

What is proximal neuropathy in diabetes?

A

Dermatomal distribution of a single neuron e.g. pain in the thighs, buttocks or legs, leading to profound muscle wasting

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19
Q

What is focal neuropathy in diabetes?

A

Sudden weakness in one nerve or a group of nerves causing muscle weakness or pain e.g. carpal tunnel, ulnar neuropathy, foot drop

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20
Q

What are normal urinary creatinine albumin ratios in men and women?

A

Men <2.5 mg/mmol creatinine

Female <3.5 mg/mmol creatinine

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21
Q

Treatment of Charcot’s foot?

A

Cast

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22
Q

What are the following in DKA:

  • Creatinine
  • Sodium
  • Amylase
  • WCC
  • BP
A

Creatinine if often raised
Sodium is often reduced
Amylase is frequently raised - doesn’t necessarily mean pancreatitis
WCC is often raised - doesn’t necessarily mean infection
BP is reduced

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23
Q

What is the insulin regimen for DKA?

A

Fixed rate intravenous insulin infusion
Also give IV 0.9% NaCl
If hypotensive give bolus of 500 mls normal saline
Even if hypotension is resolved, patient still needs large volumes of fluid

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24
Q

What is potassium like in DKA and how should you treat it?

A

Likely will need to replace it - add KCl to bags of fluid
Initially patient is hyperkalaemic - because insulin is required to drive K into the cells
Titrate potassium to hourly VBG
K >5.5 - don’t replace
K 3.5-5.5 - replace by using 40 mmol infused solution
K <3.5 - seek senior help

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25
Q

What other investigations should you do in DKA?

A

Often infection with no fever, so do MSU, blood cultures, CXR
Start broad spec antibiotics early if infection is suspected

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26
Q

Give two causes of hyperkalaemia in DKA

A

The patient is in acidosis, so there is increased H+ - this is then driven into the cell at the expensive of K+
Insulin is required for uptake of K into cells

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27
Q

What is the classic triad in HHS?

A

Hypovolaemia
Hyperglycaemia
Hyperosmolar

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28
Q

Name two precipitants of HHS

A

Glucocorticoids
Thiazide diuretics
Also MI, bowel infarct

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29
Q

Give two precipitants of LA

A

Metformin

Septicaemia

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30
Q

What is lactate?

A

End product of anaerobic metabolism of glucose

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31
Q

What are the two types of LA?

A

Type A - associated with hypoxia

Type B - associated with liver disease

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32
Q

Lab findings of LA?

A

Raised anion gap

Decreased bicarbonate

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33
Q

Age of onset of MODY

A

Before 25

Also strong FHx

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34
Q

What are the clinical differences between the two types of MODY?

A

Glucokinase type - onset at birth, stable hyperglycaemia

Transcription factors type - onset in teenage years, progressive hyperglycaemia

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35
Q

What is LADA also called?

What does the presentation mimic?

A

Aka slowly progressive type I
“Typical” type II diabetes, but tend to not be overweight
Also autoantibody positive

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36
Q

Name an enzyme that insulin inhibits

A

Glycogen phosphorylase - i.e. inhibits degradation of glycogen to glucose

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37
Q

Describe the synthesis of insulin

A

Formed from preproinsulin - cleaved to proinsulin in the ER
Proinsulin contains A and B subunits, linked by C
C peptide is cleaved off of proinsulin at the Golgi apparatus
A and B are now bound by disulphide bonds
This structure is insulin

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38
Q

The insulin receptor is what type of receptor?

A

Tyrosine kinase receptor

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39
Q

What does the insulin receptor consist of?

A

Two alpha subunits
Two beta subunits
Two tyrosine kinase - enzyme which is active when phosphorylated

40
Q

Describe activation of the insulin receptor

A

Two insulins bind to the alpha subunits
This causes tyrosine kinase to phosphorylate the target protein (called IRS-1)
IRS-1 then exerts the intracellular effects of insulin

41
Q

Give seven functions of thyroid hormone

A
  1. Increases basal metabolic rate
  2. Increases thermogenesis
  3. Increases insulin-independent glucose uptake into cells
  4. Increases fatty acid oxidation in tissues
  5. Increases protein synthesis
  6. GHrH production + secretion requires thyroid hormones
  7. Permissive sympathomimetric action - increases responsiveness to adrenaline and sympathetic NS
42
Q

What are the types of deiondinase enzymes and what are their uses?

A

Important in de/activation of thyroid hormone
D1 - commonly found in liver and kidney
D2 - found in the tissues - main one concerned in interplay between T3 and T4
D3 - found in foetal tissue + placenta + brain

43
Q

How do carbimazole and propylthiouracil work?

A

Inhibit attachment of iodine to thyroglobulin

44
Q

Treatment of hypothyroidism?

A

Must gradually restore metabolic rate, or patient will get arrhytmias
Younger - thyroxine 50-100 ug daily
Older - thyroxine 25-50 ug daily

45
Q

What is DeQuervains thyroiditis?

A

Aka subacute thyroiditis
Vital trigger, usually self limiting after a few months
Initially have hyperthyroidism, then hypothyroidism, then back to normal

46
Q

What does differentiated thyroid cancer refer to?

Why is the word “differentiated” important?

A

Papillary and follicular
Differentiated - two reasons
- Looks like normal thyroid cells
- Vast majority take up iodine and secrete thyroglobulin

47
Q

What is Medullary thyroid cancer associated with?

A

MEN2

48
Q

What is seen on histology of medullary thyroid cancer?

A

Amyloid deposition

49
Q

What is the most serious type of thyroid cancer?

A

Anaplastic - causes rapid growth, involvement of neck structures and death

50
Q

How is cytology of thyroid cancer graded?

What are follicular lesions graded at?

A 
Thy 1 - insufficient/uninterpretable
Thy 2 - benign 
Th 3 - atypia, probably benign/equivocal
Thy 4 - atypia suspicious of malignancy 
Thy 5 - malignant
Follicular lesions are Thy 3
51
Q

What does AMES stand for?

A

Age
Metastases
Extent of primary tumour
Size of primary tumour

52
Q

What is Tayside lymph node removal policy in papillary thyroid cancer?

A

Central compartment clearance and lateral node sampling

53
Q

When and how is whole body iodine scanning done?

A 
After surgery 
Monday - rhTSH IM injection 
Tuesday - rhTSH IM injection
TSH should be greater than 20 for best results
Wednesday - give the capsule 
Friday - scan
54
Q

How should you treat a patient after thyroid remnant ablation?

A

Suppress TSH with thyroxine - improved prognosis if suppressed TSH in the long term

55
Q

What can be used as a tumour marker post thyroid ablation?

What can throw this reading of?

A

Thyroglobulin

Antibodies to thyroglobulin can throw it off - scan these patients every 6 months

56
Q

Important risk of thyroid remnant ablation?

A

Small but significant increased risk of leukaemia

57
Q

What does a primary follicle contain and what is the purpose of the contents?

A

Contains an oocyte surrounded by granulosa cells and theca cells
Theca cells produce androgens, which are converted to estrogens by the granulosa cells via the enzyme aromatase

58
Q

What happens to the corpus luteum after ovulation?

A

It is left behind in the ovary and starts to secrete progesterone

59
Q

Give to functions of progesterone

A

Causes the endometrium to thicken

Inhibits FSH and LH

60
Q

What is the role of androgens and diabetes in PCOS?

A

Hyperinsulinaemia causes an increase in androgens in the body
The rise in insulin drives thecal cells of the follicle to produce more androgens
The granulosa cells convert this to excess estrogen
High levels of estrogen and androgens cause a disordered release of LH and FSH

61
Q

What is the role of estradiol in the negative feedback loop?

A

Low concentrations of estradiol inhibit the release of FSH

High estradiol has a positive feedback on the pituitary to stimulate LH release

62
Q

Where are Leydig cells found?
Where are Sertori cells found?
What else is found here?

A

Leydig - interstitium of the seminiferous tubules
Sertori - seminiferous tubules
Also in the seminiferous tubules are spermtogonia - male germ cells with the ability to become sperm

63
Q

What is the role of Leydig cells?

A

LH targets Leydig cells and causes them to secrete testosterone

64
Q

What is the role of Sertoli cells?

A

Tertosterone produced by Leydig cells stimulates Sertoli cells to maintain libido, maintain muscle + bone growth, maintain male secondary sexual characteristic
FSH stimulates Sertoli cells to release androgen binding protein

65
Q

What all do Sertoli cells need for stimulation?

A

Presence of testosterone

Stimulation from FSH

66
Q

What is the role of ABP in the male reproductive system?

A

ABP binds to androgen in the seminiferous tubule to promote sperm growth aka spermatogenesis and spermiogenesis

67
Q

Which two things are required for sperm production?

A

ABP and testosterone

68
Q

What role do Sertoli cells have in the negative feedback loop?

A

Release inhibin - inhibits the secretion of FSH in order to regulate sperm production

69
Q

What is the difference between the size of the gametes in spermatogenesis compared to oogenesis?

A

Sperm are smaller than spermatocytes

Ova are larger than oocytes

70
Q

What is the difference in onset between spermatogenesis and oogenesis?

A

Spermatogenesis begins at puberty

Oogenesis begins in the foetus (pre-natal)

71
Q

How long does spermatogenesis take?

A

65-75 days in the human male

72
Q

In spermatogenesis, where do meiosis and mitosis occur?

A

Meiosis inside the cell

Mitosis outside

73
Q

At birth, what does each follicle contain?

A

A dormant primary oocyte - a diploid cell that is resting in prophase of meiosis I

74
Q

What happens to the follicles after puberty?

A

Every 28 days, FSH from the pituitary stimulates one of the dormant follicles to develop
The primary oocyte then completes meiosis I and starts meiosis II

75
Q

What is the role of LH in oogenesis?

A

It halts the egg at metaphase II, to allow cytoplasmic maturation
When fertilized, completion of meiosis occurs

76
Q

Which hormones are responsible for the fertile and infertile cervical mucus?

A

Estrogen - fertile cervical mucus

Progesterone - infertile (thick) cervical mucus

77
Q

Describe the clinical features of Rubella syndrome

A 
Rash at birth 
Low birth weight 
Small head size 
Heart abnormalities
Visual problems 
Bulging fontanelle
78
Q

How can you confirm ovulation?

A

Midluteal (D21) serum progesterone - >30 nmol/l in two samples

79
Q

What are hormone profiles like in WHO ovulatory disorder II?

A

Normal gonadotrophs/excess LH
Normal estradiol
Low progesterone
Raised testosterone (in PCOS)

80
Q

When in the cycle is clomid given?

A

Day 2-6 (i.e. for 5 days)

NB - cumulative conception rate plateus at 12 months on this drug

81
Q

Treatment of hyperprolactinaemia?

A

Dopamine agonist - Cabergoline, Bromocriptine

82
Q

In which ovulatory disorders in estradiol low?

A

WHO type I

WHO type III

83
Q

Treatment of premature ovarian failure?

A

Hormone replacement with estrogen

Egg or embryo donation

84
Q

Dysmenorrhoea (before menstruation) + dyspareunia + menorrhagia + painful defaecation + chronic pelvic pain = ?

A

Endometriosis

85
Q

How would you investigate tubal disease in women?

A

If no known risk factors - hysterosalpingogram

Laparoscopy if known or suspected tubular pathology from suspicious history

86
Q

List some causes of functional hypothalamic amenorrhoea

A 
Weight change
Stress
Exercise
Anabolic steroids 
Iatrogenic - surgery, radiotherapy
Recreational drugs
Head trauma 
Infiltrative disorders e.g. sarcoidosis
87
Q

What is the gold standard test for pituitary function?

A

Insulin stress test
You give someone insulin to make them go hypo - stimulated the hypothalamus
Normal response is for cortisol and GH to rise significantly

88
Q

What happens in the water depravation test?

A

Give patient no water for 8 hours to try and stimulate ADH production
Can’t measure ADH directly, so measure the concentration of the urine

89
Q

What is the most common cause of Cushing’s syndrome?

A

Exogenous steroid use

90
Q

What is Cushing’s disease?

A

Bilateral adrenal hyperplasia from ACTH-secreting pituitary adenoma

91
Q

What are some clinical features of ACTH-dependent Cushing’s?

A 
Skin pigmentation 
Hypokalaemic metabolic acidosis 
Weight loss
Hyperglycaemia
Classic features of Cushings are often absent
92
Q

When is an overnight dexamethasone suppression test positive?

A

if > 50

93
Q

Describe the meaning of the results in a high dose dexamethasone suppression test

A

If ACTH still high then problem is adrenal of SCLC

If ACTH is suppressed by 50% or more then pituitary adenoma

94
Q

What other physiology should you consider in Cushings, aside from cortisol?

A

Zona reticularis is also controlled by ACTH - if Cushing’s is caused by high ACTH, then ZR will be affected
This produces large amounts of testosterone in the body

95
Q

Give two common causes of hypokalaemia

A

Hyperaldosteronism

Bartter’s syndrome

96
Q

What is barter’s syndrome?

A

Defect in Loop of Henle

Bloods show hypokalaemia

Memorize for 2nd Year Exams (13 decks)

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