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BRS High Yield errors > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Front

A

Back

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2
Q

Treatment of Adrenal Failure (eg. 21 hydroxylase deficiency) + the amount

A

Aldosterone: Fludrocortisone, 50-100 mcg daily

Cortisol: Prednisolone 3mg daily or Hydrocortisone 10/5/2.5 daily

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3
Q

Range for …

A
  • Impaired fasting

6 - 7 mmol/L

  • Impaired glucose tolerance
    7. 8 - 11 mmol/L
  • Prediabetes

42-48 mmol/L

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4
Q

Explain the function of theca cells and granulosa cells in ovulation.

A
  • During the follicular phase, the follics (surrounding the egg) are made of theca cells and granulosa cells.
  • Theca cells bind LH + Granulosa cells bind FSH
  • Theca cells secrete Androdestedione which is converted to Oestrogen by Granulosa cells.
  • High Oestrogen acts as NEGATIVE FEEDBACK and switches off the pituitary.
  • Dominant follicle grows LH receptors on Granulosa cells
  • Only dominant follicle grows and secrete oestrogen → THIS BECOMES POSITIVE FEEDBACK
  • Rupture causes ovulation
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5
Q

Calcium average intake

A

700 mg

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6
Q

Cushing’s Syndrome: Most common screening test? Most common Diagnostic test?

A

Screening: Urine 24h

Diagnostic: Overnight dexamethasone suppression test.

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7
Q

PCOS: Pathology

A

High LH levels, low FSH levels

  • While the exact cause of PCOS is unknown, patients have elevated luteinizing hormone (LH) levels that often lead to theca cell hyperplasia.
  • An LH:FSH ratio > 2 is typical.
  • Theca cells produce excess androgens which aromatase converts to estrogens in fat cells. Abnormally high estrogen levels stimulate endometrial hyperplasia, a precursor to endometrial carcinoma.
  • Hirsuitism is caused by elevated androgens.
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8
Q

PCOS: 3 hormonal changes

A
  • There is often a high total and free testosterone level. The free androgen index is often high. This index is calculated by 100 times total testosterone divided by sex hormone-binding globulin.
  • FSH levels are normal in PCOS, whilst LH tends to rise, and hence there is a raised LH:FSH ratio
  • Prolactin levels are often raised
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9
Q

Why take caution when reading basal GH + thyroid + FSH/LH + cortisol?

A

Thyroid: Half life ~ 6.5 DAYS

FSH/LH: Can circulate in some woman

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10
Q

Which receptors are targeted in Graves? Which antibody type targets the receptor?

A

TSH receptor: IgG activates them

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11
Q

Name the eye popping and leg oedema effects in Graves.

A

Pretibial Myxoedema

Exophthalmos

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12
Q

Criteria for thyroid storm

A

CHAD Jaundice

Cardiac Failure
Hyperpyrexia >41
Arrhytmia
Delirium

Jaundice

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13
Q

Side effect of PTU/Carbemazole

A

Agranulocytosis/Rashes (more common)

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14
Q

Length of time for hyperthyroid/hypothyroid states in Viral thyroiditis

A

1 month/3 month

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15
Q

Which iodine isotope used in radioiodine

A

131 (99-Tc used in scans)

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16
Q

Method of Desmopressin administration

A

Nasal

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17
Q

Draw the cholesterol to aldosterone/cortisol etc pathway

A

3-hydroxsteroid dehydrogenase converts cholesterol → progesterone

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18
Q

3 treatments for secondary hyperparathyroidism

A

No renal failure:

  1. Ergocalciferol (25 hydroxy vitamin D2)
  2. Cholecalciferol (25 hydroxy vitamin D3)

Renal failure:

  1. Alfacalcidol (1 α hydroxycholecalciferol)
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19
Q

Most common cause of Addison’s in developing world

A

TB

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20
Q

Explain production of calcitriol.

A

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21
Q

How does PTH increase and decrease phosphate levels? What do FGF23 do?

A

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22
Q

2 signs of hypocalcemia

A

Trosseau’s Sign: Carpopedal spasm

Chvostek’s Sign: Facial paraesthesia (gentle twictch of facial muscle when tapping on the face of hypocalcemia)

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23
Q

What are the causes of infertility in women (in order of proportion of which are most common?)

A

Ovarian: CiA

Tubal: TIEd Tubes

Uterine: FACE

Cervical: CIa

Pelvic: EA sports…to the game

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24
Q

Explain tertiary hyperparathyroidism?

A

Context of chronic renal failure; prolonged calcitriol deficiency turns the parathyroid glands into OVERDRIVE.

→ Elevated PTH levels

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25
Q

What happens to calcium levels in tertiary parathyroidism? How do you differentiate from secondary hyperparathyroidism?

A

Tertiary: Calcium decreases then increases as PTH increases substantially

Secondary: Calcium remains low (can progress to tertiary if result of kidney injury that becomes CKI)

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26
Q

What’s the definition of infertility

A

(regular intercourse = every 2-3 days)

  1. Primary: no live births
  2. Secondary: Live birth more than 12 months previously
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27
Q

What % of couples experience infertility at 12 + 24 months?

A

14% → 7%

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28
Q

What are the causes of infertility in men?

A

Missed: vascular/toxins/immunological

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29
Q

Which drug treats hyperprolactinaemia?

A

Cabergoline - Dopamine Agonist

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30
Q

What’s the rough structure of an appointment for an individual with male infertility?

A

MRI THE PITUITARY

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31
Q

Terms for no sperm and reduced sperm?

A

No sperm: Azoospermia

Reduced sperm: Oligospermia

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32
Q

What should you always check before determining female infertility?

A

Pregnancy or breastfeeding.

> Women who breastfeed their children have a longer period of amenorrea and infertility following delivery than women who do not breastfeed. The length of postpartum amenorrhea varies greatly and depends on several factors, including maternal age and parity and the duration and frequency of breastfeeding.The effect of lactation on ovulation and fertility - PubMed

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33
Q

What are the general cut-offs for the menstrual cycle, primary amenorrhea, secondary amenorrhoea and oligomenorrhea?

A

Oligo-menorrhea also <21 days (21

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34
Q

Most common endocrine/infertility disorder in women?

A

PCOS

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35
Q

What’s Turner’s Syndrome?

A

45XO

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36
Q

What’s the rough structure of an appointment for an individual with female infertility?

A

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37
Q

What are the primary risks of testosterone replacement?

A

Increased haematocrit, prostate specific antigen levels increase

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38
Q

What’s the treatment for male factor infertility?

A

Initially, hCG injections, after 6 month add FSH injections

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39
Q

What’s the mechanism of the two main ovulation induction medications for PCOS?

A

Letrozole: Aromatase Inhibitors

Clomiphene: Receptor modulation (oestrogen)

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40
Q

Explain the long/short regimes for GnRH agonists in IVF?

A

Short term

  • As you give FSH supplements, give a GnRH antagonist quickly to rapidly supress LH (day6)

Long term

  • As you give FSH supplements, give a GnRH agonist ages ago, so that it becomes an antagonist by the time normally LH would cause ovulations.
  • This is desensitisation.
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41
Q

Reason for giving LH after just trying to supress it

A

Supress it to stop ovulation and allow it to fully mature inside the ovary.

Giving it to convert from diploid → haploid once it’s ready.

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42
Q

What are the main ‘emergency’ contraceptives?

A

43
Q

5 main risks with HRT

A
  1. VTE (higher risk in oral, combined)
  2. Increased risk of breast cancer (higher risk in continous combined)
  3. Increased risk of ovarian cancer
  4. Increased risk of endometrial cancer: Provide progesterone as well!
  5. CVD/stroke (higher risk in oral, combined)
44
Q

What 3 blood levels increase as a result of taking HRT (not oestrogen)?

A

Increased triglycerides, CRP + SHBG

45
Q

Which condition causes genetic absence of a vas deferens?

A

Cystic Fibrosis

46
Q

What cardiological complication do individuals with Turner’s Syndrome commonly develop?

A

Aortic Co-arctation

47
Q

From which cells is Ghrelin secreted?

A

P/D1 cells

48
Q

From which cells is leptin secreted?

A

Adipose tissues

49
Q

How do we check Vitamin D?

A

25 HYDROXYVITAMIN D: More stable

50
Q

What are some associated comorbidities of obesity?

A
  • Depression
  • Sleep Apnoea
  • Stroke
  • Myocardial Infarction
  • BMI
  • Arthritis
  • Hypertension
  • Diabetes
  • PVD
  • Bowel Cancer
  • Gout
51
Q

Which bacteria is orlistat based off?

A

Streptomyces Toxytricini

52
Q

What does the bacteria above do?

A

Inhibit gastric and pancreatic lipase

Inhibits absorption by about 30%

53
Q

For which patients do we consider bariatric surgery?

A
  1. BMI 40 or more
  2. BMI 35-40 + other co-morbidities
  3. BMI 30-34.9 + newly diagnosed T2DM
54
Q

For which obese patients do we use first line bariatric surgery?

A

BMI 50 or more

55
Q

What are some requirements for bariatric surgery?

A

Generally fit for anaesthesia and surgery, commit to need for long-term follow up

56
Q

What are 3 specific types of bariatric surgeries?

A

Gastric bypass: connect Small intestines to first part of stomach.

Gastric band: place a Band around the stomach with sensor under skin.

Sleeve gastrectomy: cut half the stomach away.

57
Q

What’s the most effective form of gastric bariatric surgery?

A

Gastric bypass

58
Q

Place the following into order of most effectiveness: Gastric Band, Vertical Gastric Banding, Gastric Bypass

A
  1. Gastric Bypass
  2. Vertical Gastric Banding
  3. Gastric Banding
59
Q

What’s LADA?

A

The majority of patients with autoimmune-related diabetes present younger in life. There are however a small group of patients who develop such problems later in life. These patients are often misdiagnosed as having T2DM

60
Q

What’s MODY?

A

MONOGENIC!

A group of inherited genetic disorders affecting the production of insulin. Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis

61
Q

Diabetes may present following pancreatic damage - true or false?

A

True

62
Q

How do we measure insulin levels?

A

Measure C-Peptide

63
Q

What are the stages of Type 1 Diabetes development?

A
  1. Genetic Predisposition
  2. Potential Precipitating Event
  3. Immunological activation
  4. Immunological response
  5. Normal blood sugar
  6. Abnormal blood sugar
  7. Clinical Diagnosis
  8. Antibodies made ✅
64
Q

All people with Type 1 Diabetes have 0 insulin - true or false?

A

False

65
Q

Which HLA genes pose a significant risk to Type 1 Diabetes?

A

HLA-DR3 + HLA-DR4

“If you buy 4 DiaMonds and only pay for 3, you get 1 for free:” DR4 and DR3 are associated with Diabetes Mellitus type 1.

66
Q

Which GWAS has the greatest association with Type 1 Diabetes?

A

HLA (human leukocyte antigen)

67
Q

Name the most common environmental factor for Type 1 Diabetes and some other factors.

A
  1. Enteroviral infections
  2. Cow’s milk exposure/Seasonal exposures/Changes in microbiota
68
Q

Which antibodies are detectable in Type 1 Diabetes patients?

A

Insulin antibodies

  • Insulinoma-associated-2-autoantibodies
  • Zinc-transporter 8
69
Q

Which neurotransmitter enzyme is widespread in Type 1 Diabetes?

A

Glutamic acid decarboxylase (GADA)

70
Q

What 2 things are a T1 Diabetes diagnosis based off?

A

Clinical features + Presence of ketones

71
Q

What are the 4 T’s of Diabetes

A

Toilet, Thirst, Tired, Thinner

72
Q

What do muscle cells, liver + fat cells do in the absence of insulins?
Name the products of the fat cells’ response.

A

Muscle: Proteinolysis → amino acids

Liver: Hepatic glucose output increases → glucose

Fat cells: Lipolysis → Glycerine + Non-esterified fatty acids

73
Q

What are the 3 keto acids we make?

A

Acetone, 3-hydroxybutyrate + Acetoacetate

74
Q

What molecule enters our liver to be converted to keto acids?

A

NEFAs

75
Q

What are the 4 aims of treatment for T1DM?

A

Split into glucose/insulin/other effect/complication

76
Q

How do we describe T1DM management?

A

‘self-managed’

77
Q

How many peaks do we have prandially?

A

2

78
Q

What are the 2 types of insulin replacement?

A

Short or quick acting with meals

Long acting or basal in the background

79
Q

What part of the abdominal wall does pump therapy inject insulin into?

A

Subcutaneous fat

80
Q

What should ALL people with T1DM be offered?

A

Structured Education Programme e.g. DAFNE

81
Q

During Islet Cell Transplantation, where do we insert the Islet Cells?

A

Hepatic Portal Vein

82
Q

When Pancreas Transplantation, what other structure is associated with better survival if transplated as well?

A

Kidneys

83
Q

What type of haemoglobin provides info on the last 3 months?

A

Glycated Haemoglobin (linear reaction)

84
Q

What are some problems with using HbA1C?

A

85
Q

HbA1C is measured how often?

A

Every 3-4 months

86
Q

What blood level of glucose qualifies as severe hypoglycaemia?

A

>3.6 mmol/L

87
Q

HbA1C is a good marker of hypoglycaemia - true or false?

A

False

88
Q

What type of medication is prescribed to the following?

A
  • T1DM patient who is hypoglycaemic but alert

Sweets, Coca Cola or longer lasting sandwich

  • T1DM patient who is hypoglycaemic and confused but can swallow foods

Buccal glucose, glucogel, complex carbs

  • T1DM who is unconscious
    • IV, Glucose - what percentage?

20%

  • T1DM who is unconscious and has limited IV access

IM/Subcutaneous 1mg Glucagon

89
Q

What 2 things are a T2 Diabetes diagnosis based off?

A

Random glucose + Clinical features

90
Q

What inflammatory cells are produced in T2DM?

A

Adipokines

91
Q

Name a monogenic diabetes.

A

MODY

92
Q

What do adipokines do?

A

Drive organs to decrease insulin sensitivity

93
Q

What’s the target HbA1C to reduce risk of microvascular complications?

A

53mmol/mol

94
Q

Which microvascular complication is associated with the highest risk of development?

A

Retinopathy > Nephro > Neuro > Microalbumin

95
Q

What’s the mechanism behind complications of diabetes?

A

96
Q

What 2 things are required to reduce risk of complications?

A

BP (< 130/80) + HbA1C

97
Q

What medication could be started for a type II diabetic under diabetic nephropathy?

A

SGLT2 Inhibitor

98
Q

Which vessels are blocked in Diabetic Neuropathy?

A

Vasa Nervorum

99
Q

Which complication of diabetes is a risk factor of diabetic neuropathy?

A

Retinopathy diabetic

100
Q

Mechanism of diabetic nephropathy

A

101
Q

BP Cut-off when managing Cardiovascular risk?

A

140/80

Presence of microvascular complications: 130/80

102
Q

Low Density Lipids + cholesterol for managing CVR in DM?

A

Lipids less than 2

Cholesterol less than 4

103
Q

Explain the graph below.

A
  • Graph
  • Answer

Decrease glucose disposal and increased hepatic glucose output contributes to
increased fasting plasma glucose (FPG) in diabetes mellitus.

* The diminished ability to store or oxidise glucose in muscle due to impaired  insulin activity reduces metabolic clearance rate of glucose.

* Excessive amount of glucose is converted to lactate (Anaerobic respiration).  Lactate is returned to the liver (**Cori cycling**) → Glucose → Early increase in FPG.

* A result of Cori-cycling from the previous night’s meal.  Inappropriate **glucagon secretion** induces continued glucose production by stimulating *glycogenolysis and gluconeogenesis.*

Inadequate insulin action causes a flux of substrates – glycerol, free-fatty acids to the liver for increase gluconeogenesis.

104
Q

U&Es for Conn’s

A

Normal sodium typically + low potassium

BRS High Yield errors (4 decks)

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