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FINALS revision - @medicbotanist > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

For the following glands (exocrine or endocrine) explain whether they are:

A. Duct or Ductless
B. Release hormones directly into the blood or not?

A

Exocrine: Have ducts that transport to the site of the action such as the parotid gland

Endocrine: Don’t have ducts and release hormones directly into the blood (thyroid and adrenal glands)

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2
Q

Give an example of a peptide hormone?

A
  • Insulin
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3
Q

Give an example of an amine hormone?

A

Dopamine and adrenaline

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4
Q

Give an example of an iodothyronine hormone?

A

Thyroxine

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5
Q

What is an example of a cholesterol hormone?

A

Oestrogen or Vit D

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6
Q

Where do peptide hormones act?

A

Cell membrane

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7
Q

What are two hormones that act on the nucleus of a cell ?

A

Thyroid hormone

Oestrogen

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8
Q

What 6 peptide hormones are produced by the anterior pituitary?

A 
LH 
FSH 
TSH 
ACTH 
Prolactin 
GH
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9
Q

What two hormones are produced by the posterior pituitary gland?

A

ADH

Oxytocin

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10
Q

What inhibits the secretion of prolactin?

A

Dopamine

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11
Q

What is the imaging of choice to use in a patient with a suspected pituitary tumour?

A

MRI

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12
Q

What is the
Fasting level of glucose
Random level of glucose- needed for a diagnosis of Diabetes Mellitus?

A

Fasting >7.0

Random >11.1

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13
Q

What cell is insulin released from?

A

B cells in the pancreas

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14
Q

Describe what are the actions of the following Glucose Transporter Channels?

Glut 1
Glut 2
Glut 3
Glut 4

A

Glut 1: non insulin stimulated glucose uptake into cells
Glut 2: found in the beta cells of the pancreas. Detects high levels of glucose and release insulin in response

Glut 3: non insulin mediated glucose uptake in the brain
Glut 4: peripheral action of insulin. In muscle and adipose

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15
Q

Give 3 secondary causes of Diabetes?

A

Pancreatitis

Cushing’s Disease

Haemochromatosis

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16
Q

What is the triad for presentation of a patient with Type 1 Diabetes?

A

Weight loss + fatigue

Polydipsia

Polyuria

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17
Q

What is seen as a sign in patients who have severe insulin resistance?

A

Seen in neck and axillae of patients with insulin resistance.

You get acanthosis nigricans

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18
Q

What value does the HbA1c need to be to get diagnosed with T2DM?

A

HbA1c > 48

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19
Q

What is the pathophysiology behind diabetic ketoacidosis?

A
  1. SO you get autoimmune breakdown of the beta cells in the pancreas. This leads to less insulin made.
  2. You get breakdown of glycogen in the liver. High glucose causes dehydration.
  3. Peripheral lipolysis leads to increased FFA that are broken down to make acetyl co A which is converted to ketones in the mitochondria.
  4. Leads to metabolic acidosis with respirator compensation
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20
Q

What is normally found in a person with T2DM pancreas?

A

Amyloid deposits in beta cells due to an increase in pro inflammatory markers.

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21
Q

What are the two principles behind the pathophysiology of Type 2 DM?

A
  1. Insulin resistance

2. Insulin deficiency

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22
Q

What class of drug is metformin part of ?

A
  1. Biguanide
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23
Q

What is the pharmacology behind orlistat?

A

Intestinal lipase inhibitor

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24
Q

What are some of the symptoms of hypoglycaemia?

A

HE IS TIRED

headache
Irritability 
Sweating 
Tachycardia 
Impaired vision 
Restlessness 
Excessive hunger 
Dizziness
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25
Q

What is the value of glucose for a diagnosis of Hypoglycaemia?

A

< 4.00

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26
Q

How would you manage someone with hypoglycaemia?

A
  1. If conscious give fast acting carb: sugar or fruit juice (CI in CKD and low K+ diets)
  2. Repeat after 10 mins up to 3 times
  3. Not responding give IM glucagon or IV glucose 10%. This is the same management if the patient is found unconscious
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27
Q

What is hyperosmolar hyperglycaemic state?

A

This is associated with type 2 diabetes.

RF: infections, steroids and thiazide diuretics.

They are still producing insulin but insufficient amounts to prevent hepatic glucose production

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28
Q

How would someone with hyperosmolar hyperglycaemic state present?

A
  1. Severe dehydration
  2. Decreased consciousness
  3. Symptoms of hyperglycaemia.
  4. The Hyperosmolarity predisposes them to MI, stroke etc.
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29
Q

What will the level of K+ be like in a patient with hyperosmolar hyperglycaemic state?

A
  1. LOW K+ level
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30
Q

How would you manage a patient with hyperosmolar hyperglycaemic state?

A
  1. IV fluids
  2. LMWH to reduce the risk of thromboembolism
  3. Replace lost K+ ions
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31
Q

Why is it needed for a patient with hyperosmolar hyperglycaemic state to be started on a LMWH like enoxoparin?

A

They are in a hyperosmolar state. Meaning they have a hypercoag state so at increased risk of thromboembolism

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32
Q

What diabetic medication should you avoid in people with diabetic nephropathy? + why?

A

Metformin

Increased risk of lactic acidosis

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33
Q

What is the best test for assessing whether a person has diabetic nephropathy?

A

Urine albumin: creatinine ratio >3

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34
Q

Explain the presentation differences between a patient who has a neuropathic foot ulcer vs a patient who has a neuro ischaemic foot?

A

Neuropathic Foot: warm, dry with bounding pulses. With reduced sensation

Neuroischaemic foot: cool and pink with atrophic skin and absent pulses

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35
Q

What is the other name used for Charcot Foot?

What are 3 factors that trigger Charcot foot?

A
  1. Neuropathic joint

2. Mechanical Vascular and Biological Factors

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36
Q

How would a Charcot joint normally present?

What imaging would you want to do?

A

It would normally present with a red, warm, swollen, deform foot.

Will have pain- but due to neuropathy will be a lot lower than expected

X-Ray and MRI scan

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37
Q

How do you treat Charcot Foot ? 3 ways

A
  1. Take weight off of the foot
  2. Treat the bone disease with Vit D and Bisphosphonates
  3. Surgery
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38
Q

Is Charcot foot an emergency?

A

YES

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39
Q

Why do you need to check LFTs in a patient with diabetes?

A

They have an increased incidence/risk of NAFLD and NASH.

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40
Q

What are two things you would test a diabetic’s urine for?

A

Microalbuminuria

Proteinuria

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41
Q

Mx of Diabetics in Surgery:

Elective (good control)
Elective (poor control) or fasting
Emergency Surgery

A

Elective (good control) normal levels given. Unless on LA and a 20% reduction is given.

Elective (poor control) or fasting: variable rate of insulin infusion. Until eating and drinking normal. Alongside KCL + glucose + NaCl

Emergency Surgery: IV fluids and insulin. But check the ketones, BG constantly

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42
Q

What happens in the colloid of the thyroid gland?

A

In the colloid you get iodine molecules binding to tyrosine

To great T1 or T2

This makes T3 or T4 (thyroxine)

It then once stimulated by TSH moves into secretory cells.

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43
Q

Would you be more concerned about a diffuse or nodular thyroid lump?

A

Nodular: associated with adenomas, cysts and cancer

Diffuse is normally just associated with goitres etc.

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44
Q

What are 4 common causes of hyperthyroidism?

A

Grave’s Disease

Toxic multinodular goitre or toxic adenoma

Drug induced hyperthyroid: iodine, lithium or amiodarone

De Quervain’s thyroiditis: normally secondary to infection.

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45
Q

What is De Quervain’s Thyroiditis?

A

Transient inflammation of the thyroid normally secondary to acute viral infection.

You get malaise, fever and a pain in the neck.

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46
Q

How do you treat DQ thyroditis?

A

Aspirin

Prednisolone

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47
Q

What might you find on blood investigations of a patient with hyperthyroidism?

A

TSHR- ab if Graves’ disease

Low TSH and high T3 and high T4

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48
Q

How do you manage hyperthyroidism?

A
  1. BB propranolol
  2. Carbimazole if ? Hypo after a time you can start them on thyroxine as well.
  3. Radioactive iodine therapy
  4. Surgery
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49
Q

What does Graves’ disease do to the eyes?

A

It causes retro orbital inflammation.

Presents as exophthalmos, photophobia, eye pain and Diplopia

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50
Q

What skin changes can you get in Graves’ disease?

A

Pre tibial myxoedema

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51
Q

What is the management of an acute presentation of graves eye disease?

A

IV methyl pred

Surgical decompression

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52
Q

What is thyrotoxicosis?

A

This is when you have excess thyroid hormone in the blood

sx: tachycardia, restlessness, hyperpyrexia and delirium/coma

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53
Q

How do you manage thyrotoxicosis?

A

Carbimazole
Propranolol
Potassium iodide
IV hydrocortisone

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54
Q

What are the two major causes of hypothyroidism?

A
  1. Iodine deficiency

2. Autoimmune conditions such as hashimoto

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55
Q

Give some signs of Hypothyroid?

BRADYCARDIC

A 
Bradycardia 
Reflex slow 
Ataxia 
Dry (thin hair and skin) 
Yawning and drowsy 
Cold hands 
Ascites 
Round puffy face 
Defeated demeanour 
Immobile lieu’s 
Congestive cardiac failure
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56
Q

What antibodies are present in a patient with hashimoto disease?

A

TPO antibodies

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57
Q

What is a myoedema crisis?

How do you manage it?

A

This is when you have severe hyperthyroidism that can cause confusion and coma , cardiac failure, hypoglycaemia etc.

Management: IV T3, glucose infusion and gradual rewarming

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58
Q

What is the most common type of thyroid cancer in young people?

A

Papillary

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59
Q

What is the most common thyroid cancer in middle age people?

A

Follicular

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60
Q

Where can thyroid cancer throw mets to?

A

Bone and Lungs

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61
Q

How do most people present when they have thyroid cancer?

A

Thyroid nodule or lump hard and irregular in shape

Dysphagia and hoarseness of voice (due to compression of the recurrent laryngeal nerve)

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62
Q

What is the diagnostic method use for thyroid cancer?

A

TFTS
US
Fine needle aspiration

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63
Q

How do you treat thyroid cancer?

A
  1. Radio iodine therapy
  2. Admin lots of levothyroxine
  3. Surgery
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64
Q

What are the 3 layers of the adrenal cortex? What do each of them produce?

A

GFR?

Zona Glomerulosa: mineralcorticoids like aldosterone

Zona Fasciulata: glucocorticoids like cortisol

Zona Reticularis: sex hormone like androgens

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65
Q

What is made in the adrenal medulla?

A

Epinephrine and norepinephrine

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66
Q

What is the difference between cushing’s disease and Cushing’s syndrome

A

CD is when you have inappropriate ACTH secretion due to a tumour.

CS: inapppropriate elevated levels of circulating cortisol. Things like alcohol and long term steroid use mimic this.

67
Q

What are 3 functions of cortisol?

A

Increased carb and protein breakdown

Increased deposition of fat and glycogen

Diminished host immune response

Increased Na + retention and K+ loss

68
Q

Name two ACTH independent and 2 ACTH dependent causes of Cushing’s Disease?

A

Independent: oral steroids and adrenal adenoma

Dependent: pituitary adenoma!

69
Q

Gives some signs of a person who has cushing’s disease?

A

Buffalo hump
Thin skin, bruises easily and has purple striae or acne.
Moon face
Central obesity
Mod changes: depression and psychosis
Gonadal changes: irregular periods or ED
Increased Glucose and infection risk.

70
Q

How is Cushing’s syndrome diagnosed?

A
  1. Serum and urine cortisol levels
  2. Overnight dexametasone suppression test
  3. 48 hour dexametasone suppression test
  4. MRI brain
71
Q

How is Cushing’s syndrome treated?

A

Iatrogenic: remove steroids

Surgery: remove the causative mass

Medication: ketraconazole

72
Q

What can inhibit the secretion of GH?

A

Somatostatin

73
Q

What two hormones stimulate the release of GH?

A

Grehlin

IGF-1

74
Q

What does iGF-1 do to the body?

A

Stimulates skeletal and soft tissue growth

75
Q

What are some of the signs of a patient who has acromegaly?

A

Prognathism (protrusion of the lower jaw) and interdental separation

Skin darkening

Large hands and feet. Coarse facial features

76
Q

What are 3 complications of acromegaly?

A
  1. Cardiomyopathy
  2. Diabetes
  3. Bowel cancer (colon cancer)
  4. OSA
77
Q

What does acromegaly do to a patient’s blood glucose levels?

A

It causes them to have impaired glucose tolerance and thus diabetes

78
Q

What is the gold standard test for diagnosing acromegaly?

A
  1. IGF-1 test
79
Q

Give 3 tests used to diagnose acromegaly?

A
  1. IGF-1 test
  2. GTT
  3. MRI of head
  4. ECHO or ECG
80
Q

What are 3 treatment options for acromegaly?

A
  1. Somatostatin analogue (ocreotide)
  2. GH receptor antagonist SC pegvisomant
  3. Surgery
81
Q

What is the medical treatment for high prolactin?

A

dopamine agonist like cabergoline

82
Q

What are 5 causes of hyperprolactinaemia?

A
  1. Pituitary adenoma
  2. Ecstasy
  3. Pregnancy
  4. Breast feeding
  5. Hypothyroidism
83
Q

What is Sheehan’s Syndrome an example of?

A

Hypoprolactinaemia

Secondary to lactrophs undergoing ischaemia and necrosis after PPH.

84
Q

How do you treat Sheehan’s Syndrome or Hypoprolactinaemia?

A

You treat these conditions with a dopamine antagonist such as metoclopramide

85
Q

What are the two steps in managing a prolactinoma?

A
  1. Dopamine agonist (cabergoline)

2. Radiation or surgery

86
Q

What are 4 causes of Addison’s disease?

A
  1. Autoimmune
  2. TB
  3. Adrenal metastasis
  4. Long term steroid use
87
Q

What causes the tanned like appearance of Addison’s disease?

A

Increased ACTH production

88
Q

Give 5 symptoms of Addison’s Disease

A 
Lethargy 
Dizzy 
Vitiligo 
Bronze skin 
Abdo Pain 
Anorexia 
Postural Hypotension
89
Q

What are two core diagnostic tests to consider in a patient with suspected Addison’s Disease?

A

Short ACTH stimulation test: IM tetracosactide

Adrenal antibodies: 21 hydroxylase antibodies

Cortisol an Aldosterone levels will be low

90
Q

What will happen to sodium and potassium in Addison’s Disease?

A
  1. Low Sodium

2. High Potassium

91
Q

Why would the WCC be raised in Addison’s Disease?

A

As they have low cortisol and cortisol has anti-inflammatory effects

92
Q

How would you manage a patient who is in addisonian crisis?

A

IV hydrocortisone
IV saline
Glucose infusion

93
Q

How does Addisonian Crisis typically present?

A

Pain in legs, back or stomach

Weakness, Diarrhoea and Vomiting

Low BP and Hypoglycaemia

94
Q

What is a cause of secondary hypoadrenalism?

A

Long term steroid therapy

95
Q

What will happen to the levels of:
A. Glucocorticoid
B. Mineralcorticoid

In Secondary Hypoadrenalism

A

Decrease in glucocorticoid

Mineral corticoid production will be intact

96
Q

What is the management of secondary hypoadrenalism>?

A

Gradually wean odd long term steroids

97
Q

What is Conn’s Syndrome?

A

This is a syndrome that involves primary hyperaldosteronism independent of the RAAS

98
Q

What does Conn’s cause to happen to the water levels and salt levels in the blood?

A

Conn’s leads to the patient to have hyperaldosteronism.

This leads to acute fluid retention and increased sodium.

Hypokalaemia

Increased BP.

99
Q

What are 4 symptoms associated with low K+?

A

Weakness
Cramps
Polyuria
Polydipsia

100
Q

What will be seen on the ECG of a patient with hypokalaemia?

A

Flat T waves

ST depression

QT prolongation

101
Q

What is the main aetiology of Conn’s Syndrome?

A

Adrenal adenoma

Malignant HTN.

102
Q

What is the diagnostic method behind Conn’s Syndrome?

A

You give a 0.9% saline infusion and see if there is any aldosterone suppression. In Conn’s Syndrome there shouldn’t be.

MRI abdo/pelvis to investigate if there are any adenomas

103
Q

What is the management of Conn’s Syndrome?

A

4w of spironolactone to reduce the BP

Then do a laparoscopic adrenalectomy

104
Q

What is the pathophysiology behind diabetes insipidus?

A

You get a decreased secretion of ADH or impaired response to ADH.

Renal or Cranial cause.

You will get the patient presenting with polyuria and polydipsia.

105
Q

What cells does the kidney act on?

A

Principle cells of the collecting ducts (kidney)

106
Q

How do you calculate osmolarity?

A

2 Na + Glucose + Urea

107
Q

What will the sodium be like in a patient with DI?

A

You will have hypernatraemia

Symptoms will include, lethargy, thirst, weakness and irritability

108
Q

What are 3 useful investigations to do in a patient with suspected DI?

A

Total Urine Volume for the day

Water deprivation test

IM desmopressin. Distinguishes between cranial and renal DI

109
Q

How do you treat Renal DI?

How do you treat cranial DI?

A

Renal DI? You give thiazide diuretics and NSAIDs

Cranial DI? You give the patient IM desmopressin

110
Q

What will the sodium and potassium levels look like in a patient with SIADH?

A

You will have

Low Sodium Levels

High Potassium Levels

Lots of water retention

111
Q

How will SIADH present?

A 
Anorexia 
Weakness 
Malaise
Generalised aches 
Reduced GCS 
Oedema
112
Q

What are two managements of SIADH?

A

Fluid restrict <1000ml and increase Sodium intake

You can also give demeclocycline a potent ADH inhibitor

113
Q

Give an example of a potent ADH inhibitor?

A

Demeclocycline

114
Q

What will the plasma and the urine osmolarity look like in a patient with SIADH?

A

Plasma osmolarity: Low

Urine osmolarity: High (lots of sodium)

115
Q

What will the following levels look like in a patient with Primary hyperparathyroidism?

PTH, Calcium, Phosphate, Alk Phosph

A

PTH: high

Calcium: High

Phosphate: Low

Alk Phosph: Low

116
Q

What will the following levels look like in secondary hyperparathyroidism?

PTH, Calcium, Phosphate, Alk Phosph

A

PTH: high
Ca2+” low
Phosphate: low
Alk Phosph: low

117
Q

Tertiary hyperparathyroidism. What will the following levels be?

PTH, Calcium, Phosphate, Alk Phosph

A

PTH: high
Ca: high
Phosphate: high
Alk Phosph: high

118
Q

What is a cause of the primary hyperparathyroidism?

A

Low Calcium/ Low Vit D

119
Q

What is a cause of secondary hyperparathyroidism ?

120
Q

What is a cause of tertiary hyperparathyroidism?

A

Prolonged secondary hyperparathyroidism

Normally due to CKD

121
Q

Where is PTH secreted from?

A

Chief cells in the parathyroid gland

122
Q

What are 4 things that PTH stimulates?

A
  1. The activation of Vit D in the kidney to make calcitriol
  2. Increased osteoclast activity
  3. Increased Ca2+ intestinal reabsorption
  4. Increased Ca2+ renal absorption
  5. Increased excretion of phosphate
123
Q

What is the function of Calcitriol?

A

It leads to increased phosphate and calcium absorption in the gut

Inhibits PTH

Enhances bone turnover

Enhances Ca2+ and phosphate reabsorption in the kidney

124
Q

What type of cell secretes Calcitonin?

A

released by C cells

125
Q

WHat is the function of calcitonin?

A

To lead to a decrease in plasma Calcium and Phosphate

126
Q

What investigations would you do in someone suspected of high calcium?

A

Urine electrophoresis or plasma electrophoresis
Check for 24 hour urinary Ca2+
CT/MRI body

TSH to exclude hyperthyroidism

127
Q

What is Trousseau’s Sign?

A

This is when you get a spasm in the arm induced by inflating the BP cuff above systolic BP

128
Q

What is Chvostek’s Sign? How does it present?

A

When you tap on the parotid gland it causes ipslateral facial muscle twitching

129
Q

What are some other symptoms you may get with hypocalcemia?

A

You can get numbness and tingling of the mouth and extremities

Cramps and Tetany

Increased excitability of the muscles and the nerves

130
Q

What is a common class of drug that leads to hypocalcaemia?

A

Anti-epileptics

131
Q

What are the different types of Hypoparathyroidism?

A

Primary: normally autoimmune or Di George syndrome

Secondary: post thyroid surgery
Pseudohypoparathyroid: short 4th and 5th finger, short statue and intellectual impairment.

Psuedopseudohypoparathyroid: get the Same features as a live but no issues with Ca2+

132
Q

What is the management of acute hypocalcium ?

A

IV calcium glu o ate

ADcal and if hypoparathyroid: calcitriol given

133
Q

What are some useful diagnostic investigations you would like to do in a patient with suspected hypoparathyroid or low calcium?

A

Vit D and Calcium blood levels
PTH and phosphate levels

Urinary calcium (24 hours)

134
Q

What level is classed as hyperkalaemia?

135
Q

What are three causes of hyperkalaemia?

A

Spironolactone
ACE inhibitors
Vigorous exercise.

136
Q

What would you see on an ECG of a patient with High K+?

A

Tall tented T waves, small P waves and wider QRS complexes

137
Q

What is seen on ECG for a patient with low Ca2+?

A

You will see prolonged QTc

138
Q

ECG changes in a patient with hypercalcaemia?

139
Q

What symptoms will you see in a patient with Hypokalaemia?

A 
Muscle weakness
Hypotonia 
Hyporeflexia 
Tetany 
Constipation
140
Q

ECG changes in hypokalemia include?

A

T wave inversion
Long PR interval
Depressed ST segments

141
Q

What type of cells do carcinoid tumours originate from?

A

Enterochromaffin cells

142
Q

When is a carcinoid tumour referred to as syndrome?

A

Once the liver gets involved

143
Q

What substances can carcinoid tumours secrete?

A
  1. Substance P
  2. Bradykinin
  3. glucagon
  4. Insulin
  5. ACTH
  6. Serotonin: leads to carcinoid like symptoms.
144
Q

What are 5 symptoms of carcinoid syndrome?

A 
Vasodilation 
RUQ pain 
Hypotension 
tachycardia 
Bronchi constriction 
Hyperglycaemia
145
Q

What is the management of carcinoid syndrome?

A

Octreotide and surgery

146
Q

What is a pheochromocytoma?

A

Catecholamine secreting tumour of the adrenal medulla.

147
Q

What two genetic disorders is pheochromotyoma associated with?

A

VHL and NF1

148
Q

What are the signs and symptoms of a phaeochromocytoma?

A 
Headache 
Tremor 
Palpitations 
Weight loss 
Anxiety
149
Q

What diagnostic test would you want to do in a suspected pheochromocytoma?

A
  1. Plasma metanephrines
  2. Urine collection (look for catecholamines)
  3. Imaging of CT
150
Q

What should be given pre treatment via surgery for a phaechromocytoma?

A

Alpha and Beta Blockers

151
Q

What is pituitary apoplexy?

A

This is a condition where you have a patient that is unaware they have a pituitary tumour. They only know once they develop symptoms of apoplexy.

152
Q

What are two causes of pituitary apoplexy?

A

Sheehan’s syndrome

Infarction or haemorrhage of the pituitary gland.

153
Q

How does a pituitary apoplexy present?

A

Sudden onset severe headache
Decreased consciousness
Nausea and vomiting
visual impairment

154
Q

How would you manage pituitary apoplexy?

A

You would start them on high dose hydrocortisone and do surgery.

Long term supplements of pituitary hormones may be needed.

155
Q

What is the management of myxoedema crisis?

A
  1. Thyroxine
  2. IV glucose
  3. Gradual rewarming
156
Q

What condition would cause you to have an increased ionised calcium level?

Is this state acidotic or alkalotic?

A

Renal disease

Acidotic

157
Q

What will the hormone levels look like in primary ovarian failure?

(FSH, LH and oestrogen?)

A

LH> FSH

Low oestrogen

158
Q

How do you treat neonatal transient thyrotoxicosis?

A

Manage the baby with carbimazole

159
Q

What staging criteria is used to judge puberty stages?

A

Tanner Stage

160
Q

What are some symptoms of Kallman’s syndrome?

A

Womanly figure

Anosmia

161
Q

What do the wolffian ducts differentiate into?

A

Vas deferens

Seminal vesicles

Epididymis

162
Q

What do the Müllerian ducts differentiate to form?

A

Fallopian Tubes

Uterus

Cervix

163
Q

What are the 4 Stages of sexual development in girls?

A

Thelarche (breast development)

Pubarche (hair development)

Growth

Menarche (menstruation)

164
Q

If a patient has high LH and low testosterone what is the diagnosis?

A

Klienfelter’s disease

FINALS revision - @medicbotanist (20 decks)

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