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)
2
Q
Give an example of a peptide hormone?
A
- Insulin
3
Q
Give an example of an amine hormone?
A
Dopamine and adrenaline
4
Q
Give an example of an iodothyronine hormone?
A
Thyroxine
5
Q
What is an example of a cholesterol hormone?
A
Oestrogen or Vit D
6
Q
Where do peptide hormones act?
A
Cell membrane
7
Q
What are two hormones that act on the nucleus of a cell ?
A
Thyroid hormone
Oestrogen
8
Q
What 6 peptide hormones are produced by the anterior pituitary?
A
LH FSH TSH ACTH Prolactin GH
9
Q
What two hormones are produced by the posterior pituitary gland?
A
ADH
Oxytocin
10
Q
What inhibits the secretion of prolactin?
A
Dopamine
11
Q
What is the imaging of choice to use in a patient with a suspected pituitary tumour?
A
MRI
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
13
Q
What cell is insulin released from?
A
B cells in the pancreas
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
15
Q
Give 3 secondary causes of Diabetes?
A
Pancreatitis
Cushing’s Disease
Haemochromatosis
16
Q
What is the triad for presentation of a patient with Type 1 Diabetes?
A
Weight loss + fatigue
Polydipsia
Polyuria
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
18
Q
What value does the HbA1c need to be to get diagnosed with T2DM?
A
HbA1c > 48
19
Q
What is the pathophysiology behind diabetic ketoacidosis?
A
- SO you get autoimmune breakdown of the beta cells in the pancreas. This leads to less insulin made.
- You get breakdown of glycogen in the liver. High glucose causes dehydration.
- Peripheral lipolysis leads to increased FFA that are broken down to make acetyl co A which is converted to ketones in the mitochondria.
- Leads to metabolic acidosis with respirator compensation
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.
21
Q
What are the two principles behind the pathophysiology of Type 2 DM?
A
- Insulin resistance
2. Insulin deficiency
22
Q
What class of drug is metformin part of ?
A
- Biguanide
23
Q
What is the pharmacology behind orlistat?
A
Intestinal lipase inhibitor
24
Q
What are some of the symptoms of hypoglycaemia?
A
HE IS TIRED
headache Irritability Sweating Tachycardia Impaired vision Restlessness Excessive hunger Dizziness
25
What is the value of glucose for a diagnosis of Hypoglycaemia?
< 4.00
26
How would you manage someone with hypoglycaemia?
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
27
What is hyperosmolar hyperglycaemic state?
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
28
How would someone with hyperosmolar hyperglycaemic state present?
1. Severe dehydration
2. Decreased consciousness
3. Symptoms of hyperglycaemia.
4. The Hyperosmolarity predisposes them to MI, stroke etc.
29
What will the level of K+ be like in a patient with hyperosmolar hyperglycaemic state?
1. LOW K+ level
30
How would you manage a patient with hyperosmolar hyperglycaemic state?
1. IV fluids
2. LMWH to reduce the risk of thromboembolism
3. Replace lost K+ ions
31
Why is it needed for a patient with hyperosmolar hyperglycaemic state to be started on a LMWH like enoxoparin?
They are in a hyperosmolar state. Meaning they have a hypercoag state so at increased risk of thromboembolism
32
What diabetic medication should you avoid in people with diabetic nephropathy? + why?
Metformin
Increased risk of lactic acidosis
33
What is the best test for assessing whether a person has diabetic nephropathy?
Urine albumin: creatinine ratio >3
34
Explain the presentation differences between a patient who has a neuropathic foot ulcer vs a patient who has a neuro ischaemic foot?
Neuropathic Foot: warm, dry with bounding pulses. With reduced sensation
Neuroischaemic foot: cool and pink with atrophic skin and absent pulses
35
What is the other name used for Charcot Foot?
What are 3 factors that trigger Charcot foot?
1. Neuropathic joint
| 2. Mechanical Vascular and Biological Factors
36
How would a Charcot joint normally present?
What imaging would you want to do?
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
37
How do you treat Charcot Foot ? 3 ways
1. Take weight off of the foot
2. Treat the bone disease with Vit D and Bisphosphonates
3. Surgery
38
Is Charcot foot an emergency?
YES
39
Why do you need to check LFTs in a patient with diabetes?
They have an increased incidence/risk of NAFLD and NASH.
40
What are two things you would test a diabetic’s urine for?
Microalbuminuria
Proteinuria
41
Mx of Diabetics in Surgery:
Elective (good control)
Elective (poor control) or fasting
Emergency Surgery
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
42
What happens in the colloid of the thyroid gland?
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.
43
Would you be more concerned about a diffuse or nodular thyroid lump?
Nodular: associated with adenomas, cysts and cancer
Diffuse is normally just associated with goitres etc.
44
What are 4 common causes of hyperthyroidism?
Grave’s Disease
Toxic multinodular goitre or toxic adenoma
Drug induced hyperthyroid: iodine, lithium or amiodarone
De Quervain’s thyroiditis: normally secondary to infection.
45
What is De Quervain’s Thyroiditis?
Transient inflammation of the thyroid normally secondary to acute viral infection.
You get malaise, fever and a pain in the neck.
46
How do you treat DQ thyroditis?
Aspirin
Prednisolone
47
What might you find on blood investigations of a patient with hyperthyroidism?
TSHR- ab if Graves’ disease
Low TSH and high T3 and high T4
48
How do you manage hyperthyroidism?
1. BB propranolol
2. Carbimazole if ? Hypo after a time you can start them on thyroxine as well.
3. Radioactive iodine therapy
4. Surgery
49
What does Graves’ disease do to the eyes?
It causes retro orbital inflammation.
Presents as exophthalmos, photophobia, eye pain and Diplopia
50
What skin changes can you get in Graves’ disease?
Pre tibial myxoedema
51
What is the management of an acute presentation of graves eye disease?
IV methyl pred
Surgical decompression
52
What is thyrotoxicosis?
This is when you have excess thyroid hormone in the blood
sx: tachycardia, restlessness, hyperpyrexia and delirium/coma
53
How do you manage thyrotoxicosis?
Carbimazole
Propranolol
Potassium iodide
IV hydrocortisone
54
What are the two major causes of hypothyroidism?
1. Iodine deficiency
| 2. Autoimmune conditions such as hashimoto
55
Give some signs of Hypothyroid?
BRADYCARDIC
```
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
```
56
What antibodies are present in a patient with hashimoto disease?
TPO antibodies
57
What is a myoedema crisis?
How do you manage it?
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
58
What is the most common type of thyroid cancer in young people?
Papillary
59
What is the most common thyroid cancer in middle age people?
Follicular
60
Where can thyroid cancer throw mets to?
Bone and Lungs
61
How do most people present when they have thyroid cancer?
Thyroid nodule or lump *hard and irregular in shape*
Dysphagia and hoarseness of voice (due to compression of the recurrent laryngeal nerve)
62
What is the diagnostic method use for thyroid cancer?
TFTS
US
Fine needle aspiration
63
How do you treat thyroid cancer?
1. Radio iodine therapy
2. Admin lots of levothyroxine
3. Surgery
64
What are the 3 layers of the adrenal cortex? What do each of them produce?
GFR?
Zona Glomerulosa: mineralcorticoids like aldosterone
Zona Fasciulata: glucocorticoids like cortisol
Zona Reticularis: sex hormone like androgens
65
What is made in the adrenal medulla?
Epinephrine and norepinephrine
66
What is the difference between cushing’s disease and Cushing’s syndrome
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
What are 3 functions of cortisol?
Increased carb and protein breakdown
Increased deposition of fat and glycogen
Diminished host immune response
Increased Na + retention and K+ loss
68
Name two ACTH independent and 2 ACTH dependent causes of Cushing’s Disease?
Independent: oral steroids and adrenal adenoma
Dependent: pituitary adenoma!
69
Gives some signs of a person who has cushing’s disease?
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
How is Cushing’s syndrome diagnosed?
1. Serum and urine cortisol levels
2. Overnight dexametasone suppression test
3. 48 hour dexametasone suppression test
4. MRI brain
71
How is Cushing’s syndrome treated?
Iatrogenic: remove steroids
Surgery: remove the causative mass
Medication: ketraconazole
72
What can inhibit the secretion of GH?
Somatostatin
73
What two hormones stimulate the release of GH?
Grehlin
IGF-1
74
What does iGF-1 do to the body?
Stimulates skeletal and soft tissue growth
75
What are some of the signs of a patient who has acromegaly?
Prognathism (protrusion of the lower jaw) and interdental separation
Skin darkening
Large hands and feet. Coarse facial features
76
What are 3 complications of acromegaly?
1. Cardiomyopathy
2. Diabetes
3. Bowel cancer (colon cancer)
4. OSA
77
What does acromegaly do to a patient’s blood glucose levels?
It causes them to have impaired glucose tolerance and thus diabetes
78
What is the gold standard test for diagnosing acromegaly?
1. IGF-1 test
79
Give 3 tests used to diagnose acromegaly?
1. IGF-1 test
2. GTT
3. MRI of head
4. ECHO or ECG
80
What are 3 treatment options for acromegaly?
1. Somatostatin analogue (ocreotide)
2. GH receptor antagonist SC pegvisomant
3. Surgery
81
What is the medical treatment for high prolactin?
dopamine agonist like cabergoline
82
What are 5 causes of hyperprolactinaemia?
1. Pituitary adenoma
2. Ecstasy
3. Pregnancy
4. Breast feeding
5. Hypothyroidism
83
What is Sheehan’s Syndrome an example of?
Hypoprolactinaemia
Secondary to lactrophs undergoing ischaemia and necrosis after PPH.
84
How do you treat Sheehan’s Syndrome or Hypoprolactinaemia?
You treat these conditions with a dopamine antagonist such as metoclopramide
85
What are the two steps in managing a prolactinoma?
1. Dopamine agonist (cabergoline)
| 2. Radiation or surgery
86
What are 4 causes of Addison’s disease?
1. Autoimmune
2. TB
3. Adrenal metastasis
4. Long term steroid use
87
What causes the tanned like appearance of Addison’s disease?
Increased ACTH production
88
Give 5 symptoms of Addison’s Disease
```
Lethargy
Dizzy
Vitiligo
Bronze skin
Abdo Pain
Anorexia
Postural Hypotension
```
89
What are two core diagnostic tests to consider in a patient with suspected Addison’s Disease?
Short ACTH stimulation test: IM tetracosactide
Adrenal antibodies: 21 hydroxylase antibodies
Cortisol an Aldosterone levels will be low
90
What will happen to sodium and potassium in Addison’s Disease?
1. Low Sodium
| 2. High Potassium
91
Why would the WCC be raised in Addison’s Disease?
As they have low cortisol and cortisol has anti-inflammatory effects
92
How would you manage a patient who is in addisonian crisis?
IV hydrocortisone
IV saline
Glucose infusion
93
How does Addisonian Crisis typically present?
Pain in legs, back or stomach
Weakness, Diarrhoea and Vomiting
Low BP and Hypoglycaemia
94
What is a cause of secondary hypoadrenalism?
Long term steroid therapy
95
What will happen to the levels of:
A. Glucocorticoid
B. Mineralcorticoid
In Secondary Hypoadrenalism
Decrease in glucocorticoid
Mineral corticoid production will be intact
96
What is the management of secondary hypoadrenalism>?
Gradually wean odd long term steroids
97
What is Conn’s Syndrome?
This is a syndrome that involves primary hyperaldosteronism independent of the RAAS
98
What does Conn’s cause to happen to the water levels and salt levels in the blood?
Conn’s leads to the patient to have hyperaldosteronism.
This leads to acute fluid retention and increased sodium.
Hypokalaemia
Increased BP.
99
What are 4 symptoms associated with low K+?
Weakness
Cramps
Polyuria
Polydipsia
100
What will be seen on the ECG of a patient with hypokalaemia?
Flat T waves
ST depression
QT prolongation
101
What is the main aetiology of Conn’s Syndrome?
Adrenal adenoma
Malignant HTN.
102
What is the diagnostic method behind Conn’s Syndrome?
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
What is the management of Conn’s Syndrome?
4w of spironolactone to reduce the BP
Then do a laparoscopic adrenalectomy
104
What is the pathophysiology behind diabetes insipidus?
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
What cells does the kidney act on?
Principle cells of the collecting ducts (kidney)
106
How do you calculate osmolarity?
2 Na + Glucose + Urea
107
What will the sodium be like in a patient with DI?
You will have hypernatraemia
Symptoms will include, lethargy, thirst, weakness and irritability
108
What are 3 useful investigations to do in a patient with suspected DI?
Total Urine Volume for the day
Water deprivation test
IM desmopressin. Distinguishes between cranial and renal DI
109
How do you treat Renal DI?
How do you treat cranial DI?
Renal DI? You give thiazide diuretics and NSAIDs
Cranial DI? You give the patient IM desmopressin
110
What will the sodium and potassium levels look like in a patient with SIADH?
You will have
Low Sodium Levels
High Potassium Levels
Lots of water retention
111
How will SIADH present?
```
Anorexia
Weakness
Malaise
Generalised aches
Reduced GCS
Oedema
```
112
What are two managements of SIADH?
Fluid restrict <1000ml and increase Sodium intake
You can also give demeclocycline a potent ADH inhibitor
113
Give an example of a potent ADH inhibitor?
Demeclocycline
114
What will the plasma and the urine osmolarity look like in a patient with SIADH?
Plasma osmolarity: Low
Urine osmolarity: High (lots of sodium)
115
What will the following levels look like in a patient with Primary hyperparathyroidism?
PTH, Calcium, Phosphate, Alk Phosph
PTH: high
Calcium: High
Phosphate: Low
Alk Phosph: Low
116
What will the following levels look like in secondary hyperparathyroidism?
PTH, Calcium, Phosphate, Alk Phosph
PTH: high
Ca2+” low
Phosphate: low
Alk Phosph: low
117
Tertiary hyperparathyroidism. What will the following levels be?
PTH, Calcium, Phosphate, Alk Phosph
PTH: high
Ca: high
Phosphate: high
Alk Phosph: high
118
What is a cause of the primary hyperparathyroidism?
Low Calcium/ Low Vit D
119
What is a cause of secondary hyperparathyroidism ?
CKD
120
What is a cause of tertiary hyperparathyroidism?
Prolonged secondary hyperparathyroidism
Normally due to CKD
121
Where is PTH secreted from?
Chief cells in the parathyroid gland
122
What are 4 things that PTH stimulates?
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
What is the function of Calcitriol?
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
What type of cell secretes Calcitonin?
released by C cells
125
WHat is the function of calcitonin?
To lead to a decrease in plasma Calcium and Phosphate
126
What investigations would you do in someone suspected of high calcium?
Urine electrophoresis or plasma electrophoresis
Check for 24 hour urinary Ca2+
CT/MRI body
TSH to exclude hyperthyroidism
127
What is Trousseau’s Sign?
This is when you get a spasm in the arm induced by inflating the BP cuff above systolic BP
128
What is Chvostek’s Sign? How does it present?
When you tap on the parotid gland it causes ipslateral facial muscle twitching
129
What are some other symptoms you may get with hypocalcemia?
You can get numbness and tingling of the mouth and extremities
Cramps and Tetany
Increased excitability of the muscles and the nerves
130
What is a common class of drug that leads to hypocalcaemia?
Anti-epileptics
131
What are the different types of Hypoparathyroidism?
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
What is the management of acute hypocalcium ?
IV calcium glu o ate
ADcal and if hypoparathyroid: calcitriol given
133
What are some useful diagnostic investigations you would like to do in a patient with suspected hypoparathyroid or low calcium?
Vit D and Calcium blood levels
PTH and phosphate levels
Urinary calcium (24 hours)
134
What level is classed as hyperkalaemia?
Above 5.5
135
What are three causes of hyperkalaemia?
Spironolactone
ACE inhibitors
Vigorous exercise.
136
What would you see on an ECG of a patient with High K+?
Tall tented T waves, small P waves and wider QRS complexes
137
What is seen on ECG for a patient with low Ca2+?
You will see prolonged QTc
138
ECG changes in a patient with hypercalcaemia?
Short QTc
139
What symptoms will you see in a patient with Hypokalaemia?
```
Muscle weakness
Hypotonia
Hyporeflexia
Tetany
Constipation
```
140
ECG changes in hypokalemia include?
T wave inversion
Long PR interval
Depressed ST segments
141
What type of cells do carcinoid tumours originate from?
Enterochromaffin cells
142
When is a carcinoid tumour referred to as syndrome?
Once the liver gets involved
143
What substances can carcinoid tumours secrete?
1. Substance P
2. Bradykinin
3. glucagon
4. Insulin
5. ACTH
6. Serotonin: leads to carcinoid like symptoms.
144
What are 5 symptoms of carcinoid syndrome?
```
Vasodilation
RUQ pain
Hypotension
tachycardia
Bronchi constriction
Hyperglycaemia
```
145
What is the management of carcinoid syndrome?
Octreotide and surgery
146
What is a pheochromocytoma?
Catecholamine secreting tumour of the adrenal medulla.
147
What two genetic disorders is pheochromotyoma associated with?
VHL and NF1
148
What are the signs and symptoms of a phaeochromocytoma?
```
Headache
Tremor
Palpitations
Weight loss
Anxiety
```
149
What diagnostic test would you want to do in a suspected pheochromocytoma?
1. Plasma metanephrines
2. Urine collection (look for catecholamines)
3. Imaging of CT
150
What should be given pre treatment via surgery for a phaechromocytoma?
Alpha and Beta Blockers
151
What is pituitary apoplexy?
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
What are two causes of pituitary apoplexy?
Sheehan’s syndrome
Infarction or haemorrhage of the pituitary gland.
153
How does a pituitary apoplexy present?
Sudden onset severe headache
Decreased consciousness
Nausea and vomiting
visual impairment
154
How would you manage pituitary apoplexy?
You would start them on high dose hydrocortisone and do surgery.
Long term supplements of pituitary hormones may be needed.
155
What is the management of myxoedema crisis?
1. Thyroxine
2. IV glucose
3. Gradual rewarming
156
What condition would cause you to have an increased ionised calcium level?
Is this state acidotic or alkalotic?
Renal disease
Acidotic
157
What will the hormone levels look like in primary ovarian failure?
(FSH, LH and oestrogen?)
LH> FSH
| Low oestrogen
158
How do you treat neonatal transient thyrotoxicosis?
Manage the baby with carbimazole
159
What staging criteria is used to judge puberty stages?
Tanner Stage
160
What are some symptoms of Kallman’s syndrome?
Womanly figure
| Anosmia
161
What do the wolffian ducts differentiate into?
Vas deferens
Seminal vesicles
Epididymis
162
What do the Müllerian ducts differentiate to form?
Fallopian Tubes
Uterus
Cervix
163
What are the 4 Stages of sexual development in girls?
Thelarche (breast development)
Pubarche (hair development)
Growth
Menarche (menstruation)
164
If a patient has high LH and low testosterone what is the diagnosis?
Klienfelter’s disease
