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UKMLA > Endocrinology passtest > Flashcards

Endocrinology passtest Flashcards

1
Q

What will a deficiency in ApoB-100 molecules cause and why?

A

Cholesterol build up because when there is a normal amount of ApoB-100 molecule it binds to LDL so the cholesterol doesn’t accumulate.

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2
Q

What is the cause of familial hypercholesterolaemia?

A

LDL receptor deficiency

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3
Q

What is the 1st line treatment of symptomatic graves?

A

Propranolol

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4
Q

What is long term treatment of Graves?

A

Carbimazole

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5
Q

How does carbimazole work?

A

Inhibits thyroid production

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6
Q

What is a risk to be aware of with carbimazole?

A

Agranulocytosis

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7
Q

Can carbimazole be used anytime during pregnancy?

A

Not safe in1st trimester but safe in 2nd and 3rd

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8
Q

What is a risk of propylthiouracil?

A

Hepatotoxicity

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9
Q

What is the mechanism of action of propylthiouracil?

A

inhibiting the enzyme thyroid peroxidase, which usually converts iodide to an iodine molecule and incorporates the iodine molecule into amino acid tyrosine.

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10
Q

What is chvostek’s sign?

A

Ipsilateral facial twitching when facial nerve is stimulated by touching just in front of the ear.

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11
Q

What does chvostek’s sign indicate?

A

Low calcium level

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12
Q

What is trousseau sign?

A

Involuntary hand and wrist contraction?

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13
Q

What does trousseau sign indicate?

A

Low calcium

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14
Q

What happens to calcium and phosphate levels in a total thyroidectomy causing acquired hypoparathyroidism?

A

It can cause high phosphate and low calcium

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15
Q

What are the calcium and phosphate levels in chronic renal failure?

A

Low calcium and high phosphate

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16
Q

What are the calcium and phosphate levels in vitamin D deficiency?

A

Low calcium and low phosphate

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17
Q

When does glucose peak in insulin dependent diabetics?

A

Peak plasma glucose between 1 and 2 hours

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18
Q

What is the the expected fasting glucose for a insulin dependent diabetic?

A

Over 7 mmol

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19
Q

How is metabolic syndrome defined?

A

3 or more of the following:
1. Increased waist circumference
2. BMI over 30
3. Increased triglycerides
4. Decreased HDL
5. Hypertension
6. Increased fasting glucose

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20
Q

What is the differences between primary and secondary hyperparathyroidism?

A

Primary can be caused by a parathyroid adenoma
Where as secondary is caused by vitamin D deficiency or chronic renal failure

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21
Q

What is the pathophysiology of the mineral levels in primary hyperparathyroidism?

A

PTH acts on kidneys to increase calcium reabsorption from bones so calcium increases meanwhile more phosphate is excreted.

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22
Q

What else other than PO4- and Calcium is usually elevated in primary hyperparathyroidism? and why?

A

ALP because PTH increases bone turnover by stimulating osteoclasts. Moreover PTH causes osteoblasts to increase production of RANKL which causes osteoclastic formation and activation which leads to the bone degradation and calcium releases

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23
Q

What are the sodium and potassium levels in Addison’s?

A

Low sodium and high potassium

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24
Q

How does Conn’s syndrome present?

A

High BP and Metabolic alkalosis

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25
Q

What is the most common form of thyroid cancer?

A

Papillary

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26
Q

Are neuropathic ulcers painful?

A

Usually no

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27
Q

Who do neuropathic ulcer usually present in?

A

Diabetics

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28
Q

Where do neuropathic ulcers usually present?

A

Heel and metatarsal head - basically pressure bearing areas

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29
Q

What is the mechanism that causes familial hypocalcuric hypercalcaemia?

A

Mutation in the calcium sensing receptor gene which then impacts calcium homeostasis - therefore increased calcium in serum and decreased calcium excretion

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30
Q

What is orlistat?

A

Encourages weight loss by inhibiting pancreatic lipases - so lipase doesn’t break down the triglycerides into free fatty acids for absorption

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31
Q

What is a side effect of orlistat?

A

Steatorrhea

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32
Q

What’s the pathophysiology of DKA?

A

There is a lack of insulin, therefore glucose builds up as the glucose can’t be shovelled into the cells. Therefore because there isn’t any glucose in the cells for cells to utilise they begin to break down the fatty acids to create ketones for energy. Therefore ketoacidosis occurs

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33
Q

What is the glucose measurement in DKA?

A

Same as Over 11

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34
Q

What is the ketone measure in DKA?

A

3 or ore

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35
Q

What is the pH in DKA?

A

7.3 or under

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36
Q

What type of breathing may be seen in DKA?

A

Kussmauls - deep rapid laboured breathing

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37
Q

In what scenarios may euglycemic DKA present

A

When glycogen stores are exhausted for example in:
1. malnutrition
2. Severe vomiting
3. Alcohol use
4. SGLT2 inhibitors - flozin’s

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38
Q

What is initial treatment of DKA?

A

Fluid recuss
K+ replacement
Fixed rate insulin infusion

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39
Q

What is the rate of fixed rate insulin used in DKA treatment?

A

0.1units/kg/hr

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40
Q

What tumours are found in MEN1

A

PPP:
- Pituitary adenoma
- Parathyroid
- Pancreas - look out for a new onset of diabetes

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41
Q

What is C peptide a measurement of?

A

How much natural insulin a person makes by beta cells

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42
Q

What is giardia?

A

a tiny parasite (germ) that causes diarrhea. Giardia can spread easily from one person to another or through water, food, surfaces, or objects.

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43
Q

What is the treatment for giardia?

A

Tinidazole - it’s an a tiny parasite (germ) that causes diarrhea. Giardia can spread easily from one person to another or through water, food, surfaces, or objects.

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44
Q

In a thyroid function, why may thyroid levels be normal but TSH still super high in a non compliant pt ?

A

They just started taking their tablets a few days just before blood test

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45
Q

Which thyroid cancer is spread through bloodstream?

A

Follicular

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46
Q

Which thyroid cancers are spread through lymph?

A

Papillary and medullary

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47
Q

Which thyroid cancer is spread through local invasion?

A

Anaplastic

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48
Q

What is the classic grave’s symptoms triad?

A

Pre-tibial myxoedema
Thyroid ophthalmology
Thyroid acropachy (clubbing of fingers and toes) - like they can get super chubby

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49
Q

What is the primary investigation for acromegaly?

A

IGF1 - it’s used instead of GH as it has a longer half life

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50
Q

What tumours are seen in MEN2?

A

Parathyroid
Medullary thyroid
Phaeochromocytoma

Remember MEN 2B is associated with marfans

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51
Q

What is pathophysiology of Addison’s?

A

Automimmune dystruction of adrenal glands so loss of gluco, mineral and corticosteroids

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52
Q

What symptoms present in Addison’s?

A

Hypotension
Nausea
Abdo pain
In women loss of pubic hair and libido

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53
Q

What is secondary adrenal insufficiency?

A

There is a decrease in ACRH from pituitary

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54
Q

What is tertiary adrenal insufficiency and what is most common cause?

A

Decreased in CRH from hypothalamus
Usually caused by overuse of external glucocroticosteroids

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55
Q

What are the mineral levels in a addinsonian crisis? and what other feature may be seen on skin?

A

Low Sodium
High potassium
Low glucose
Hyperpigmented creases

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56
Q

Why does hyperpigmentation happen in Addinson’s?

A

caused by the stimulant effect of excess adrenocorticotrophic hormone (ACTH) on the melanocytes to produce melanin. The hyperpigmentation is caused by high levels of circulating ACTH that bind to the melanocortin 1 receptor on the surface of dermal melanocytes.

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57
Q

What actually is short synachten?

A

Artificial ACTH

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58
Q

What is the short synachten test?

A

Addison’s - primary adrenal insufficiency. Basically tests how well your adrenal glands can produce cortisol when stimulated by ACTH

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59
Q

How is short synacthen test done?

A

250MG given. Cortisol is then measured immediatley before, after 30 mins and after 60 mins. Baseline should be over 180-190. After the synachten given in a normal person the cortisol levels should rise to over 500-550.

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60
Q

How is Addison’s treated?

A

Glucocorticoid replacement with hydrocortisone (15-30mg) and mineral corticoid is replaced with fludrocortisone

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61
Q

What is Addisonian crisis management?

A

IV hydorocrtisone (100mg) and fluids

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62
Q

What is first line management for type 2 diabetes? If that doesn’t work then what?

A

Lifestyle changes
Then metformin if Hba1c is still above 48. Then insulin if metformin doesn’t work

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63
Q

What is mechanism of metformin?

A

Metformin decreases blood glucose levels by decreasing hepatic glucose production (also called gluconeogenesis), decreasing the intestinal absorption of glucose, and increasing insulin sensitivity by increasing peripheral glucose uptake and utilization

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64
Q

What antibodies are present in Hashimoto’s thyroiditis?

A

Autoantibodies to thyroid peroxidase and thyroglobulin

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65
Q

What’s the difference between kleinfelter’s and reifenstein syndrome?

A

Kleinfelters: tall and infertile
Reifenstein: Breast development, Erectile dysfunction, normal height - type of partial androgen insufficiency

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66
Q

What is the main symptoms that 17-a hydroxylase deficiency causes?

A

Hypertension due to an enzyme defect in the mineral corticoid pathway causing it to be overactive

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67
Q

What other condition is acromegaly associated with?

A

Diabetes and insulin resistance

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68
Q

What percentage of diabetes is type 1?

A

10%

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69
Q

Can hypothyroidism cause anaemia?

A

Yes

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70
Q

Why does a high amount of aldosterone = a low potassium?

A

Because aldosterone acts on collecting ducts to promote excretion of potassium and reabsorption of sodium

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71
Q

What hormone is high in Conn’s?

A

Primary hyperaldosteronism

72
Q

What is inheritance pattern for MEN?

A

Autosomal dominant

73
Q

Who is affected by X liked recessive?

A

Females can only be the carriers but can pass the condition on to 50% of their sons

74
Q

What can distinguish between primary hyperparathyroidism and squamous cell lung cancer?

A

Parathyroid RELATED hormone is released in SCLC not PTH so PTH won’t be raised but calcium will still be high and phosphate will be low.

75
Q

In patients from 40-45 with menopausal symptoms what hormones can be used to test for menopause?

A

FSH will be high as there is a drop in progesterone production therefore oestrogen acts uninhibited and raises FSH. If FSH is greater than 30 then diagnose menopause.

76
Q

When should a serum FSH be measured to diagnose menopause?

A

Day 3 menstrual cycle

77
Q

Who is at risk population for De Quervain’s thyroiditis?

A

Females after a viral URTI.

78
Q

What is the thyroid status in de quervain’s thyroiditis?

A

inflammation of the thyroid characterised by a triphasic course of transient thyrotoxicosis, followed by hypothyroidism, followed by a return to euthyroidism

79
Q

What is treatment of phaechromocytoma?

A

Laparoscopic adrenalectomy and manage hypertension with a-adrenoreceptor antagonists

80
Q

Which a-adrenoreceptor antagonist can be used to manage hypertension?

A

Phenoxybenzamine

81
Q

What are some side effects of phenoxybenzamine?

A

Reflex tachycardia
Dizzy
Droswy
Nausea/ vomit
Congestion
Fatigue

82
Q

Which hormone inhibits release of growth hormone?

A

Somatostatin

83
Q

What is somatomedin C? and where is it produced?

A

Produced in liver from GH and promotes growth in cartilage and bone

84
Q

When does GH conc peak?

A

During sleep - secreted in a pulsatile manner

85
Q

What does GH do to insulin?

A

Anti-insulin effects - it promotes gluconeogenesis

86
Q

Does IGF1 have proinsulin or anti-insulin effects?

A

Pro-insulin effects

87
Q

What molecules does lipoprotein lipase hydrolyse ?

A

Chylomicrons & VDL. Therefore a reduction in lipoprotein lipase results in a build of chylomicrons and VDLS

88
Q

What receptors are decreased in familial hypercholesterolaemia?

A

Decreased LDL receptors so increase in LDL.

89
Q

What hormone stimulates contraction of uterus muscles during labour?

A

Oxytocin - production of oxytocin then further enhances release of prostaglandins.

90
Q

What is seen on histopathology in papillary thyroid cancer?

A

Opthalmic nuceli and psamomma bodies, orphan annie cells

91
Q

What are psamomma bodies?

A

round, microscopic calcifications found in certain cancers,

92
Q

What is the incretin effect?

A

Oral intake of glucose leads to a higher insulin secretion that if it’s parenteral glucose infusion.

93
Q

What’s the physiology behind incretin effect?

A

When glucose is consumed orally, the body releases incretin hormones, such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate the pancreas to produce insulin. This results in a higher insulin response than if the glucose were administered intravenously.

94
Q

Other than GH what other substance does somatostatin inhibit release of?

A

Gastric acid

95
Q

What is the role of glucagon?

A

Increase glucose production in liver

96
Q

What does increasing glucagon levels do to GH, cortisol and C peptide?

A

Increase them

97
Q

What drug diabetes drug is contraindicated in renal failure and low eGFR?

A

Metformin because it can lead to lactic acidosis

98
Q

Which medications can renal failure diabetics use?

A

DPP4 inhibitors - linagliptin - the liptins.

99
Q

How do DPP4 inhibitors work?

A

Blocking the degradation of GLP-1 therefore sustaining insulin release consequently reducing blood sugar.

100
Q

What level of plasma osmolality triggers ADH release?

A

280, thirst starts to be felt at 290

101
Q

What does ADH release cause?

A

More water to be reabsorbed in kidneys which leads to hyponatraemia as the sodium in the serum can get diluted. Urine osmolality increases whilst serum osmolality decreases.

102
Q

What can cause SIADH?

A

Strokes
Subarachnoid haemorrhage
Trauma to head
Psychosis
Small cell lung cancer - ectopic release of ADH (vasopressin)
Infection
Carbamazepine
Cyclophosphamide

103
Q

What is 2hr plasma glucose in diabetics?

A

11.1 or more

104
Q

What is HbA1c in diabetics?

A

48 mmol or more

105
Q

What would be a random plasma glucose in a diabetic?

A

More than 11.1

106
Q

What happens to macrophage and neutrophil function in badly controlled glycaemic control in diabetics?

A

It’s impaired. Chemotaxis, phagocytosis and intracellular killing is impaired.

107
Q

What would be the presenting symptoms of a somatostatinoma?

A

Diarrhoea
Weight loss
Gallstones
DM
inhibit pancreatic hormones and gastrointestinal hormones. Thus, somatostatinomas are associated with mild diabetes mellitus, steatorrhoea and gallstones, and achlorhydria.

108
Q

What is plasma aldosterone: renin ratio in Conn’s?

A

It’s increased

109
Q

What class of drugs can be used to treat acromegaly?

A

Somatostatin analogues

110
Q

What other conditions can somatostatin analogues treat?

A

Carcinoid syndrome, VIPomas

111
Q

What are some examples of somatostatin analogues?

A

Octreotide
Lareotide

112
Q

What is triad of symptoms in a VIPoma?

A
  1. Achloridyha
  2. Watery diarrhea
  3. Hypokalaemia
113
Q

How does psychogenic polydipsia present?

A

Water seeking behaviour and excessive water drinking sometimes accompanied by hyponatraemia and water intoxication

114
Q

What does DI do to sodium levels?

A

Increases sodium because of water loss from a deficiency in ADH or renal insensitivity of the hormone

115
Q

What test can be used to diagnose diabetes insipidus?

A

Water deprivation test (desmopressin stimulation test)
The patient avoids all fluids for up to 8 hours before the test (water deprivation). After water deprivation, urine osmolality is measured. If the urine osmolality is low, synthetic ADH (desmopressin) is given. Urine osmolality is measured over the 2-4 hours following desmopressin.

In primary polydipsia, water deprivation will cause urine osmolality to be high. Desmopressin does not need to be given. A high urine osmolality after water deprivation rules out diabetes insipidus.

In cranial diabetes insipidus, the patient lacks ADH. The kidneys are still capable of responding to ADH. Initially, the urine osmolality remains low as it continues to be diluted by the excessive water lost in the urine. After desmopressin is given, the kidneys respond by reabsorbing water and concentrating the urine. The urine osmolality will be high.

In nephrogenic diabetes insipidus, the patient is unable to respond to ADH. The urine osmolality will be low both before and after the desmopressin is given.

116
Q

What hormone in high levels in men can cause infertility?

A

Testosterone, esp exogenous supply. It suppresses GnRH and so FSH and LH drop causing a decrease in spermatogenesis

117
Q

Where is the left adrenal gland positioned in relation to the crus of diaphragm?

A

Left adrenal gland is posterior and left of left crus of diaphragm

118
Q

What medications can be used in overactive thyroid?

A

Propylthiouracil or carbimazole

119
Q

What are the risk associated with carbimazole?

A

Agranulocytosis
Angioedema
Lymphadenopathy
Acute pancreatitis

120
Q

How long should a women wait before becoming pregnant after radioactive iodine treatment? and men?

A

At least 6 months and men at least 4

121
Q

If there is a super high testosterone level in females what must be done as next management steps?

A

Referral via cancer pathway to rule out a androgen secreting tumour

122
Q

Except from, potassium, fluids and fixed rate insulin what else should DKA patients be given?

A

LMWH due to VTE risk

123
Q

Which hormone decreases appetite? Which hormone increases appetite?

A

Leptin
Ghrelin

124
Q

What is adiponectin?

A

Adiponectin is a hormone your adipose (fat) tissue releases that helps with insulin sensitivity and inflammation. Low levels of adiponectin are associated with several conditions, including obesity, Type 2 diabetes and atherosclerosis.

125
Q

What may be a niche sign in a child that there is type one diabetes?

A

Previously bed trained child may start wetting bed again

126
Q

In cushing’s disease which hormone is high?

A

Cortisol due to high ACTH - dexamethasone suppression would work to lower these levels.

127
Q

When DKA patient glucose levels drop below 12mmol on there fixed rate insulin what fluid should be swapped instead of saline?

A

Instead of saline swap to 5% dextrose to avoid hypoglycaemia caused by the fixed rate insulin

128
Q

1st line investigation or phaeochromocytoma is?

A

24 urine collection of catecholamines

129
Q

What symptoms may present with osteomalacia?

A

Bone and joint pain
Muscle weakness
Fractures

130
Q

What causes osteomalacia?

A

Abnormal bone mineralization of osteoid due to vitamin D deficiency

131
Q

What defect is responsible for congenital adrenal hyperplasia?

A

21-Hydorxylase deficiency

132
Q

What are the symptoms of congenital adrenal hyperplasia?

A

Increased ACTH leads to increased sex hormones and mineral corticoids, therefore, female babies may have ambiguous genitalia and male babies may have penile enlargement and hyperpigmentation. Also K+ will be high and sodium will be low.

133
Q

What are the symptoms of a thyroid storm?

A

High temp
Tachycardic
Agitated

134
Q

What is 1st line treatment of a thyroid storm?

A

Carbimazole

135
Q

When is carbimazole contraindicated?

A

neutropenia and agranulocytosis

136
Q

What 3 medications can be given during a thyroid storm and what is there purpose?

A
  1. Propylthiouracil + iodine = blocks synthesis of thyroid hormones
  2. Hydrocortisone = prevents conversion of t4 to t3
  3. Propranolol =decreases BP
137
Q

Which cell’s secrete glucagon?

A

alpha islet cells

138
Q

Why can carbamazepine cause SIADH?

A

Because it stimulates V2 vaspopressin receptors - protein complex G

139
Q

What glucose amount suggest hyperosmolar hyperglycaemic state (HHS)?

A

Glucose 30 or over

140
Q

What is pH is HHS?

A

Greater than 7.3

141
Q

What is the pathophysiology of HHS?

A

Decrease in insulin and increase in counter regulatory hormones : cortisol, GW, Glucagon. So glucose increases and this leads to osmotic diuresis

142
Q

What is blood pressure like in HHS?

A

It’s low

143
Q

What can trigger HHS?

A

Infection, stroke ,MI, Vomiting, High dose steroids

144
Q

How is HHS managed?

A

Fluidrecuss, insulin ONLY if there is ketonemia(more than 1mmol). Replace Potassium . If there is ketonemia then used fixed rate insulin at 0.5/kg/hr

145
Q

What are the complications of HHS and how are they then prevented?

A
  1. DVT/PE : LMWH
  2. Cerebral oedema: may occur due to the rapid correction of hyperglycaemia therefore resulting in a lower plasma osmolality due to to fluid recuss: rehydrate slowly
146
Q

What is the treatment of reifenstien?

A

The man has XY but is resistant to androgens so they may have both parts. Therefore treat with androgens as it increases chances of fertility

147
Q

What are most cases of acromegaly due to vs. what’s a the small minority due to?

A

95 % = pituitary adenoma
5% = ectopic release of GH from a carcinoid tumour

148
Q

When is a prolactinoma suspected?

A

If prolactin is above 250 ng/ml

149
Q

What is preferred imaging for a Prolactinoma?

A

MRI

150
Q

What’s the most common cause of hyperthyroidism?

A

Graves

151
Q

What’s the most common form of secondary hypertension?

A

Primary hyperaldosteronism

152
Q

What signalling pathway does GH use?

A

Tyrosine kinase receptor that uses the JAK/STAT pathway

153
Q

If sodium is high what happens to renin?

A

It goes low

154
Q

What’s important to remember in Conn’s when looking at the electrolytes?

A

K+ may be normal instead of low so don’t just focus on that for diagnosis

155
Q

What can be used to decrease secretion of prolactin?

A

Bromocriptine - dopamine agonist

156
Q

What’s the treatment for hyponatraemia in SIADH?

A

800ml fluid restriction over 24 hours

157
Q

Desmopressin is artificial?

A

ADH- vasopressin

158
Q

What is 2nd line diabetic medication if there is poor tolerance or SE from metformin?

A

Gliclazide

159
Q

What is pseudohypoparathyroidism?

A

Failure of target cells to respond to PTH so PTH increases, Calcium decreases and phosphate increases

160
Q

What are the ACTH levels in adrenocortical tumours?

A

Low/ undetectable due to negative feedback from super high cortisol concentrations

161
Q

When should SIADH not be diagnosed?

A

Presence of:
- Hypovolaemia
- Hypotension
- Addison’s
Fluid overload
Hypothyroid

162
Q

Why must you always give an alpha blocker before a beta blocker?

A

It can cause hypertensive crisis if beta blocker isgiven first

163
Q

What type of capillaries are in endocrine organs?

A

Fenestrated capillaries

164
Q

What is kallman’s syndrome?

A

Hypogonadotropic hypogonadism due to defect in GnRH action and release due to failure of GnRH secreting neurones to migrate from nose during embryonic development

165
Q

What would be the hormone results in kallman’s?

A

Low: GnRH, Low LH, Low FSH, Low oestrgoen

166
Q

What are the features of kallman’s?

A

Anosmia
Absent/delayed puberty
Unilateral kidney agenesis
Bimanual synkinesis
Cleft lip

167
Q

What is renin levels in addison’s and why?

A

They are high. Because low aldosterone causes high renin

168
Q

In what condition is doing a renin: aldosterone ratio useful and what would you expect?

A

Conn’s as renin would be low due to high aldosterone

169
Q

What is peutz jeghers?

A

A genetic disorder causing polyps and perioral freckling

170
Q

What is a side effect of GLP-1 agonists like exenatide?

A

Delayed gastric emptying - don’t give this medication if pt have a problem with diabetic gastroparesis

171
Q

What are some rare side effects of statins?

A

Raised creatinine kinase
Hair loss

172
Q

What are some causes of raised creatinine kinase?

A

Steroid use
Hypothyroid
Alcohol excess
Rhabdomyolysis

173
Q

What is regarded as impaired fasting glucose?

A

6.1-6.9

174
Q

What is regarded as impaired glucose tolerance ?

A

7.8 -11.1, 2 hours post 75g oral glucose

175
Q

What is sheehans syndrome?

A

postpartum pituitary gland necrosis, occurs when the pituitary gland is damaged due to significant blood loss and hypovolemic shock or stroke, originally described during or after childbirth l

176
Q

Is aldosterone dependent on pituitary function?

A

NO

UKMLA (12 decks)

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