Endocrine Flashcards

(203 cards)

1
Q

In patients with PCOS, how is type 2 diabetes managed?

A
  • Lifestyle measures
  • Metformin (up to max dose of 1g BD)
  • SGLT-2 inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What do SLGT-2 inhibitor names end with?

A

‘gliflozin’

e.g. Dapagliflozin, sitagliptin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name some medications which may cause gynecomastia

A
  • spironolactone (most common drug cause)
  • cimetidine
  • digoxin
  • cannabis
  • finasteride
  • GnRH agonists e.g. goserelin, buserelin
  • oestrogens, anabolic steroids
  • metoclopramide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What causes gynecomastia?

A

Usually caused by an increased oestrogen : androgen ratio, casued by:
- syndromes of androgen deficiency (Kallman’s, Kleinfelter’s)
- testicular failure e.g. mumps
- liver disease
- testicular cancer
- ectopic tumour secretion
- hyperthyroidism
- haemodialysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is adrenal insufficiency / Addison’s disease diagnosed?

A

Short synacthen test
- dose of ACTH given, normally adrenals respond by creating cortisol, in primary adrenal insufficiency the adrenals don’t respond

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the 9AM cortisol test good for?

A
  • steroid deficiency
  • excluding primary adrenal insufficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

In primary aldosteronism, the adrenals produce too _________ aldosterone

A

much

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What plasma aldosterone / renin ratio would suggest adrenal gland dysfunction?

A

elevated ratio (more aldosterone)

20 or 30 : 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the first line investigation for Acromegaly?

A

Serum IGF-1

(insulin-like growth factor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Name some clinical features of acromegaly

A
  • Coarse facial features (frontal bossing, large jaw)
  • Large tongue (macroglossia)
  • Enlarged hands and feet
  • Excessively oily skin
  • Headaches and bitemporal hemianopia due to mass of adenoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

In addison’s disease, patients have a ______ level of cortisol

A

low / reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the first line insulin regimen in adults with newly diagnosed type 1 diabetes?

A
  • Twice daily basal insulin detemir (long acting)
  • Insulin aspart bolus with meals (rapid acting insulin analogue)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name some differences between DKA and HHS on ABG result

A
  • DKA has ketone body production, HHS doesn’t
  • DKA presents with systemic acidosis, HHS doesn’t
  • DKA develops over hours / 1-2 days, HHS develops over days to weeks
  • DKA more common in type 1, HHS typically in type 2 or previously unrecognised diabetes
  • HHS higher mortality rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Excess parathyroid hormone has what effect on phosphate excretion?

A

also excess

high parathyroid = high phosphate

(rule of E’s?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the BMI ranges for each of the weight classes?

A

Underweight = <18.49
Normal = 18.5 - 25
Overweight = 25 - 30
Obese class 1 = 30 - 35
Obese class 2 = 35 - 40
Obese class 3 > 40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What drug should be considered as an adjunct for weight loss in obese class 2 patients who are pre-diabetic?

A

Liraglutide (GLP-1 agonist), given OD as a subcut injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name 3 features of MEN-1 (multiple endocrine neoplasia type 1)

A
  • peptic ulceration
  • galactorrhoea
  • hypercalcaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Name a syndrome associated with MEN-1

A

Zollinger-Ellison
Have a gastrinoma (gastrin secreting tumour), casues increased acid production, can cause hormone secreting tumours in the pituitary and parathyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Zollinger-ellison has a __________ inheritance pattern

A

autosomal dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why are SGLT-2 inhibitors contraindicated in patients with recurrent thrush?

A

Due to them causing an increased amount of glucose being secreted in the urine - prone to infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What drug class is Sitagliptin?

A

DPP-4 (deipeptidyl peptidase-4) inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Risk factors for Grave’s disease

A
  • Age 30-60
  • Smoking
  • Female sex (x5-10 more common)
  • FHx of thyroid disorders
  • Vitamin D deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What should be prescribed by the GP in new cases of Grave’s disease?

A

Propanolol (symptom management)

+ referal to endocrinology where they would start something like Carbimazole as usually only initiated under their care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cortisol is controlled by 2 structures in the brain called the _________ and the _______ gland.

A

hypothalamus
pituitary gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Explain how cortisol is released from the adrenal glands
- Hypothalamus releases cortisol-releasing hormone (CRH) - CRH stimulates the anterior pituitary to release adrenocorticotrophic hormone (ACTH) - ACTH stimulates teh adrenal glands to release cortisol
26
How are cortisol levels kept within the normal range?
Cortisol travels to the body tissues and carries out its effects, also travels to the brain and supresses the hypothalamus and pituitary. Negative feedback loop
27
What is Addison's?
When the adrenal glands have been damaged, resulting in reduced cortisol and aldosterone secretion. This is called primary adrenal insufficiency. The most common cause is autoimmune
28
What causes secondary adrenal insufficiency?
Inadequate ACTH and a lack of stimulation of the adrenal glands, leading to low cortisol - could be from loss or damage to the pituitary gland
29
Name some conditions which could cause decondary adrenal indufficiency
- Tumours (e.g. pituitary adenomas) - Surgery to the pituitary - Radiotherapy - Sheehan's syndrome - Trauma
30
What is Sheehan's syndrome?
Where post-partum haemorrhage causes avascular necrosis of the pituitary gland
31
What causes tertiary adrenal insufficiency?
Inadequate corticotropin releasing hormone (CRH) release by the hypothalamus. - Ususally from long term steroids (more than 3 weeks), suppresses hypothalamus
32
Presentation of adrenal insufficiency
- fatigue - muscle weakness - muscle cramps - dizziness and fainting - thirst and craving salt - abdo pain - depression - reduced libido
33
Signs of adrenal insufficiency
- broze hyperpigmentation - excessive ACTH, stimulating - this stimulates melanocytes to produece melatonin in the skin creases
34
What is synacthen test?
ACTH
35
What to do in and aderenali crisis?
Addinsonian Crisis: - acute presemtation og presemtat - hypotention - Hyperglalcaemic hypoglycaema,
36
What does the posterior pituitary release?
- oxytocin - ADH / vasopressin
37
Where is growth hormone secrete from?
anterior pituitary gland
38
Wha t are the 2 main causes of acromegaly?
- anterior pituitary adenoma - secondary effect of some cancer medications (lung / pancreatic)
39
Where is the optic chiasm located?
Just above the centre the naevus
40
What is somatostatin?
A statin
41
What is the role of somatosstatin?
Blocks GH from the pituitary
42
What is the first line investigation for acromegaly?
Insulin-growth factor IG-F 1) can be tested using a blood sample
43
What effect do steroids have on diabetes control?
they worsen diabetic control due to their anti-insulin effects
44
What is a phaemchromocytoma?
tumour of adrenal glands, that releases unregulated amounts of catecolamines (e.g. adrenaline)
45
What cells produce adrenaline? Where are these cells found?
- Chromaffin cells - Medulla of the adrenal gland
46
Which NS does adrenaline stimulate?
sympathetic 'fight or flight'
47
What is the symptom pattern in those with phaeochromocytoma?
intermittent symptoms as the adrenaline is secreted in bursts
48
Which genetic conditions predispose to phaeochromocytoma?
- MEN2 (multiple endocrine neoplasia tye 2) - neurofibromatosis type 1 - von hippel-lindau disease
49
What is the 10% rule to describe the tumours found in phaeochromocytoma?
10% bilateral 10% cancerous 10% outside the adrenal gland
50
Presentation of phaeochromocytoma
- fluctuating symptoms (when adrenaline is high) - anxiety - sweating - hypertension - headache - tremors - palpitations - tachycardia
51
Initial tests for phaeochromocytoma
- Plasma free metanephrines - 24 hour urine catecholamines - CT / MRI - tumour of adrenals - Genetic testing
52
Why is measuring the serum catecholamine / adrenaline an unreliable diagnostic investigation for phaeochromocytoma?
- levels fluctuate throughout the day - catecholamines have a short half life of only a minute or so
53
What are metanephrines?
breakdown product of adrenaline, longer half life and more stable levels than catecholamines
54
How is phaeochromocytoma managed?
- Alpha blockers (phenoxybenzamine, doxazosin) - Beta blockers (after established on alphas) - Surgical removal (control symptoms first, avoiding risks associated wth anaesthesia)
55
What is Whipple's triad of symptoms for an insulinoma
- hypoglycaemia with fasting or exercise - recorded low BMs at time of symptoms - reversal of symptoms with glucose
56
Insulinomas are associated with what genetic condition?
MEN type 1
57
Multiple endocrine neoplasia type 1 (MEN-1) is characterised by the 2 P's, what are they?
Parathyroid adenoma Pituitary tumour Pancreatic tumour (e.g. insulinoma)
58
Why do patients with addison's appear tanned?
ACTH (adrenocorticotropic hormone) produced by the pituitary stimulate the adrenals to produce steroid hormones, this has the same precursor molecule as melanocte stimulating hormone (MSH) So increased ACTH causes increased MSH
59
What drug class is dapagloflozin?
SGLT2 inhibitor (sodium-glucose transporter 2 inhibitor)
60
Causes of hypethyroidism
G - Grave's disease I - Inflammation (thyroiditis) S - solitary toxic thyroid nodule T - toxic multinodular goitre
61
Name some causes of thyroiditis
- De Quervain's thyroiditis - Hashimoto's thyroiditis - Postpartum thyroiditis - Drug-induced thyroiditis
62
Presentation of hyperthyroidism
- Anxiety and irritability - Sweating and heat intolerance - Tachycardia - Weight loss - Fatigue - Insomnia - Frequent loose stools - Sexual dysfunction - Brisk reflexes `
63
What is present in Graves disease but not other types of hyperthyroidism?
TSH receptor antibodies
64
Name 4 Grave's disease specific features
- Diffuse goitre (without nodules) - Grave's eye disease, including expothalmus - Pretibial myxoedema - Thyroid acropachy (hand swelling and finger clubbing)
65
Solitary toxic thyroid nodules are usually what type of benign tumour?
benign adenomas
66
How are solitary thyroid nodules treated?
Surgical removal
67
What is De Quervain's thyroiditis?
Also known as subacute thyroiditis, it's a condition causing temporary inflammation of the thyroid gland, in 3 phases (thyrotoxicosis, hypothyroidism, returns to normal)
68
In DeQuervain's thyrotoxicosis, what is involved in the initial 'thyrotoxic phase'?
- Excessive thyroid hormones - Thyroid swelling and tenderness - Flu-like illness (fever, aches and fatigue) - Raised inflammatory markers (CRP and ESR)
69
What is a thyroid storm and how does it present?
Rare presentation of hyperthyroidism, also known as thyrotoxic crisis. More severe presentation with fever, tachycardia and delirium Can be life-threatening and requires admission for monitoring
70
What is the treatment for a thyroid storm?
Self-limiting but may need additional supportive care with fluid resuscitation, anti-arrhythmic medication and beta blockers
71
What is prescribed first line for hyperthyroidism?
Carbimazole (usually taken for 12 - 18 months)
72
How is Carbimazole managed once the patient has normal thyroid hormone levels?
They continue on Carbimazole and either: - the carbimaole dose is titrated down to maintain levels (known as 'titration block') - a higher dose blocks all production, and levothyroxine is added and titrated to effect (known as 'block and replace')
73
What condition should you look out for in patients taking carbimazole?
Pancreatitis (e.g. severe epigastric pain radiating to the back)
74
What is the second line treatment for hyperthyroidism?
Propylthiouracil
75
Name some risks of taking propylthiouracil
severe liver reactions including death
76
What dangerous process can both carbimazole and propylthiouracil cause and what signs should you look out for?
Agranulocytosis with dangerously low WCCs (makes them vulnerable to infections) Look for sore throat as a presenting complaint
77
How does radioactive iodine treat hyperthyroidism?
- Drink a single dose of radioactive iodine - Thyroid gland takes this up, and the emitted radiation destroys a proportion of the thyroid cells. - The reduction in number of cells results in a decrease in thyroid hormone production. - Remission can take 6 months, after which the thyroid is often underactive, requiring long-term levothyroxine
78
What strict rules are there around radioactive iodine treatment?
- women must not be pregnant or breastfeeding and must not get pregnant within 6 months of treatment - men must not father children within 4 months of treatment - limit contact with people after the dose, particularly children and pregnant women
79
How are the adrenaline-related symptoms of hyperthyroidism managed?
Beta blockers - Propanolol rather than bisoprolol
80
What is subclinical hyperthyroidism?
T3 and T4 = normal TSH = low has absent / mild symptoms
81
What is Grave's disease?
Autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism. Antibodies stimulate TSH receptors on the thyroid
82
What age is toxic multinodular goitre most common in?
>50 years old
83
Which tumours is MEN1 associated with?
3 P's: - Pituitary - Parathyroid (hyperplasia) - Pancreatic
84
Phaeochromocytoma is a tumour of the ___________
adrenal glands
85
Phaeochromocytoma is associated with the MEN ______ gene
MEN 2 (multiple endocrine neoplasia type 2)
86
MEN type 2a associated tumours:
Medullary tyroid cancer (70%) 2 P's: - Parathyroid - Pheochromocytoma
87
MEN type 2b
Medullary thyroid cancer Phaeochromocytoma Marfoid body habitus Neuromas
88
Which drug class has been linked to necrotising fasciitis of the genitalia or perineum (Fournier's gangrene)?
SGLT2 inhibitors !! wtf
89
What levels of these hormones would you expect in Kallman's syndrome? LH FSH Testosterone
LH = low FSH = low Testosterone = low
90
Vitamin D increases absorption of ________ in the intestines
calcium
91
What helps convert vitamin D into its active forms?
Parathyroid hormone
92
Symptoms of hypERcalcaemia
Stones, bones, groans, moans - Kidney stones - Painful bones / aches - Abdomonal groans (constipation, nausea and vomiting) - Psychiatric moans (fatigue, depression and psychosis)
93
What is primary hyperparathyroidism?
casued by an uncontrolled parathyroid hormone production by a tumour of the parathyroid glands
94
Secondary hyperparathyroidism is casued by ...
- insufficient vitamin D / CKD - reduces calcium absorption in the intestines, kidneys and bones - results in hypOclacaemia - parathyroid glands react to low calcium by releasing more parathyroid hormone Ca = low PTH = high
95
What causes tertiary hyperparathyroidism?
Untreated secondary hyperparathyroidism = hyperplasia of pth glands when cause of secondary is treated the pth levels remain high as the glands got used to producing higher amount
96
What is hypothyroidism?
Inadequate output of thyroid homrones by the thyroid gland
97
Hashimotos thyroiditis - explain
Hashimotos is casued by an autoimmune condition and causes inflammation
98
What antibodies are present when patrents have grave's disease?
Anti TPO (thyroid-peroxidase) anti thyroglibulin levels
99
Name some medications that cause hypothyroidism
Lithium Amioderone
100
What is hypopituitarism?
when the pituitary doesn't produce enough thyroid hormones (e.g. TSH or ACTH)
101
Name some causes of hypopituitarism
Tumours Infections Vascular Radiation
102
What is Sheean syndrome?
necrotic pituitary gland after massive blood loss in child birth
103
Features of hypOthyroidism
- dry skin - constipation - fatigue - coarse hair / loss - weight gain - ammenorhoea
104
What causes primary hypOthyroidism?
thyroid gland insufficiency (low ths, high anterior hormones) pituitary releases lots of tsh to try get it working again,, but often fails
105
management of primary hypothyroidism
- replace thyroid hormone - oral levothyroxine (synthetic t4) metabolises
106
What are the tsh, t3 and t4 levels in secondary hypothyroidism?
low tsh, low t3, low t4
107
Managememt of hypothyroid
Replace thyroid hormone using oral levothyroxine (synthetic t4 which metabolises into t3, so get both)
108
What is De Quervain's thyroiditis?
Viral infection causes fever, neck pain and tenderness, dysphagia and hypERthyroidism Hyperthyroid phase --> hypothyroid phase --> normalises
109
How is DeQuervain's thyroiditis managed?
Self-limiting disease, should get batter on its own Can give NSAIDs, B-blockers if required
110
First line management of hypERthyroidism
Carbimazole (under specialist) normal thyroid function after 4-8 weeks
111
What are the 2 different regimens that you can prescribe Carbimazole in?
1) Continue maintanence dose once have normal thyroid function and titrate to normal levels = titration block 2) Block all production of thyroid hormone with Carbimazole and replace them with levothyroxine = block and replace
112
What is the second line medication prescribed for hypERthyroidism?
Propylthiouracil
113
Risks associated with taking propylthiouracil
Small risk of hepatic reactions
114
How does radioactive iodine work to treat hypERthyroidism?
Radioactive iodine drink Taken up by the thyroid gland Destroys thyroid cells Reduces thyroid hormone (can take up to 6 months and maybe cause hypOthyroid which needs management with levothyroxine)
115
Strict rules around taking radioactive iodine
- Avoid getting pregnant for at least 6 months - No close contact with pregnant women or small children - Try not to be in close contact with anyone in the first few days
116
Why are beta blockers given in hyperthyroidism?
to block the adrenaline related symptoms such as; - tachycardia - anxiety - sweating - tremor
117
Which beta blocker would you choose for symptom management in hypERthyroidism and why?
Propanolol as it's non-selective so would cover all systemic symptoms, rather than ones which are just cardioselective
118
What are the 3 types of hyperparathyroidism?
- Primary - Secondary - Tertiary
119
Define primary hyperparathyroidism and what causes it?
Caused by a tumour of the parathyroid glands - leads to increased PTH - leads to increased Ca absorption - leads to hypercalcaemia
120
How many parathyroid glands are there?
4
121
What do the parathyroid glands detect?
Calcuim levels (low)
122
Parathyroid galnds release ________ in responce to low calcium
PTH (parathyroid hormone)
123
How does parathyroid hormone increase serum calcium levels?
It increases calcium absorption in 3 main places: - Intestinal absorption - Increased reabsorption in the kidneys / reduced excretion - Increase osteoclast activity (breaking down bonw, so ca can go into blood)
124
Where in the kidney detects BP?
Juxtoglomerular cells in the afferent arteriole
124
What does PTH do to vitamin D?
Tells the kidneys to convert vitamin D into its active form, calcitriol
125
Renin is produced by the kidneys when the BP is _______
low
126
Angiotensinogen is produced by the ____________
liver
127
angiotensinogen is converted to angiotensin 1, with the help of ________
renin
128
The conversion between angiotenisin I and II is aided by which hormone?
ACE (angiotensin converting enzyme)
129
What is the role of angiotensin II?
it stimulates the release of aldosterone from adrenal glands
130
What type of hormone is aldosterone?
mineralocortocoid steroid hormone
131
What does aldosterone do to these electrolyes? Na+ = K+ = H+ =
Na+ = increases (reabsorption in distal tubule) K+ = increases (secretion in distal tubule) H+ = increases (secretion in the collecting ducts)
132
What is Conn's syndrome?
Primary hyperaldosteronism
133
What can cause primary hyperaldosteronism?
- Adrenal adenoma - Bilateral adrenal hyperplasia - Familial hyperaldosteronism - Adrenal carcinoma
134
Primary hyperaldosteronism os cuased by a problem with the _________
adrenal gland producing too much aldosterone
135
Secondary hyperaldosteronism is caused by ______________
excessive renin stimulating the adrenals to release more aldosterone
136
What can cause the BP in the kidneys to be lower than in the rest of the body?
- renal artery stenosis - renal artery obstruction - heart failure
137
Management of hyperaldosteronism
Aldosterone antagonists (e.g. Eplerinine / Spironalactone) Treating the cause (stenting renal artery...)
138
What is type 1 diabetes?
a condition where the pancreas stops being able to produce adequate insulin
139
What happens when body cells cannot absorb enough glucose?
they lack energy, cells think there is no glucose available
140
Which viruses may trigger type 1 diabetes?
Coxsackie B Enterovirus
141
What is the triad for hyperglycaemia in T1DM?
- polyuria (excessive urination) - polydipsia (excessive thirst) - weight loss (mainly through dehydration)
142
What levels should we aim to keep bloog glucose levels?
4.4 - 6.1 mmol/L 4 = floor
143
Where is insulin produced?
By beta cells in the Islets of langerhans cells in the pancreas
144
What are the 2 main roles of insulin?
- Allow cells to absorb glucose for energy - Causes muscle and liver cells to absorb glucose from the blood and store it as glycogen (glyconeogenesis)
145
What cells produce glucagon?
Alpha cells in the islets of langerhans of the pancreas
146
What happens in glUCOneogenesis?
Body tells liver to convert proteins and fats onto glucose
147
What is ketogenesis?
it occurs when there is insufficient glucose supply and glycogen stroes are exhausted, such as in prolonged fasting. The liver takes fatty acids and coverts them into ketones.
148
Can ketones cross the blood brain barrier?
yes
149
What characteristic examination finding would tell you a patient had ketosis?
acetone breath
150
DKA is caused by inadequate __________
insulin
151
When is it common for patients to have DKA?
- initial presentation of T1DM - existing T1DM who is unwell with an infection for example - existing T1DM who is not adhering to their medication regime
152
Name the 3 features of DKA
- ketoacidosis - dehydration - potassium imbalance
153
How do the kidneys act to counteract the high ketone levels in DKA?
by producing bicarbonate (to try and maintain a normal pH)
154
What causes polyuria and polydipsia?
High blood glucose levels (hyperglycaemia) overwhelm the kidneys, and glucose leaks into the urine. The glucose in the urine draws water out by osmotic diuresis. This causes increased urine production (polyuria) and results in severe dehydration. Dehydration results in excessive thirst (polydipsia).
155
Insulin normally drives which electrolyte into cells?
potassium
156
Hypokalaemia can lead to __________
low serum potassium and fatal arrhythmias
157
Presentation of DKA
- hyperglycaemia - dehydration - ketosis - metabolic acidosis (with low bicarb) - potassium imbalance
158
How is DKA diagnosed?
- Hyperglycaemia (blood glucose > 11/mmol/L) - Ketosis (e.g. getting blood ketones above 3mmol) - Acidosis (pH 7.3)
159
What is the most dangerous complication of DKA?
Dehydration
160
Acronym to remeber the diabetic ketoacidosis acronym?
- Fluids - Insulin - Glucose - Potassium - Infection - Chart fluid balance - Ketones - minto blood ketones
161
What are the autoantibodies for T1DM?
- Anti-islet cell antibodies - Anti GAD antibodies - Anti- insulin
162
What is serum c peptide?
a measure of insulin production. It is low with low insulin production and high with high insulin production
163
Explain the methods of insulin delivery
- Background bolus = background, long acting insulin 30 mins before eating)
164
What can cause liposstryophy?
Injections in the same site which have all been stabbed long term
165
Name some disadvantages of a continuous insulin pump
- difficulties learning to use - having it attached at all times - blockages in infucion set - small risk of infection
166
What does HbA1c measure?
Glycolated haemoglobin (how much glucose is attached to Hb molecule) Average glucose level over past 2-3 months
167
Name some macrovascular complications of having diabetes
- Coronary artery disease - Peripheral ischaemia - Stroke - Hypertension
168
Name some microvascular complications of diabetes
- peripheral neuropathy - retinopathy - kidney disease, particularly glomerulonephrosis
169
Name some infection related com-lications of diabetes
- UTIs - Pneumonia - Skin and soft tissue infections (feet) - Fungla infections (particularly oral / vaginal candidiasis)
170
When awaiting surgery to remove a pheochromocytoma, what should be prescribed for symptom management?
1st - alpha blocker (phenoxybenzamine) 2nd - beta blcoker (propanolol)
171
Name some causes of raised prolactin (the P's)
- Pregnancy - Prolactinoma - Physiological - PCOS - Primary hypothyroidism - Phenothiazines, metoclopramide, domperidone
172
Which antibodies can help detect between type 1 and type 2 diabetes?
anti-GAD present in type 1 measureing c-peptide levels
173
What are the steroid sick day rules?
Double the dose during intercurrent illness
174
Which antibodies are present in Grave's disease?
IgG antibodies to theTSH receptor
175
What effect can Ferrous sulfate have on Levothyroxine?
iron tabs can reduce the absorption of levothyroxine should be taken 4 hours apart
176
Effect of cortisol in the body (systemic)
- increase alertness - reduced immune system - reduced inflammation - reduced bone formation - increased blood glucose - increased metabolism - increased HR, BP, CO
177
When does cortisol peak?
Morning Stressful stimuli
178
Cortisol is a ______corticoid
glucocorticoid
179
Aldosterone is a _____corticoid
mineralocorticoid
180
Name some medications that act as glucocorticoids (like cortisol)
- Prednisolone - Hydrocortisone - Dexamethasone
181
What is the role of aldorsterone?
Regulate electrolyte balances Regulate BP
182
What effect do mineralocortocoids (like aldosterone) have on Na+, K+ and H+?
Sodium retention Potassium secretion Hydrogen secretion
183
Effect of sodium retention in the kidneys
Increased sodium (reabsorbed) Water follows by osmosis More fluid retained in body Increased intravascular volume Increases BP
184
What medication is used to replace aldosterone?
Fludrocortisone
185
Fludrocortsione is prescribed for
- Aldosterone insufficiency - Postural hypotension
186
Causes of chshing's syndrome (CAPE)
Cushings disease (pituitary adenoma, increased ACTH, increased cortisol) Adrenal adenoma (secretes excessive cortisol) Paraneoplastic syndrome (ACTH released by small cell lung cancer, increased cortisol) Exogenous steroids (long-term steroids)
187
Primary adrenal insufficiency is caused by
Addison's (problem with adrenal glands)
188
Secondary adrenal insufficiency is caused by
Removal or damage to the pituitary gland (low acth, low cortisol release)
189
What causes tertiary adrenal insufficiency?
Problem with hypothalamus, usually due to long term glucocorticoid use which supresses the production of CRH in the hypothalamus
190
Direct actions of PTH
- gets bones to release calcium - kidneys reabsorb more calcium - forms calcitriol (active form of vitamin d, as helps with calcium absorption in GI tract)
191
Normal calcium reference range
2.1-2.6 mmol/l
192
What is the guidance on taking metformin during ramadan?
1/3 of the normal metformin dose should be taken before sunrise (Suhoor) and 2/3 should be taken after sunset (Iftar)
193
What type of hypersensitivity reaction is type 1 diabetes?
Type 4 (cell-mediated immune response) T-cells attack the pancreas
194
Which HLA genes are associated with type 1 diabetes?
HLA-DR3 HLA-DR4
195
How does DKA effect K+ levels?
Causes hypERkalaemia - Increased H+ (acidity), so cells take them in via H+/K+ pump, and K+ is pumped out of cells into the extracellular fulid - Lack of insulin means Na+/K+ ATPase pumps don't take K+ ito cells, leaving it also in the extracellular fluid - Overall stored K+ is low but high in blood
196
Symptoms of DKA
- N+V - mental status changes - cerebral oedema
197
Treatment of DKA
- fluids for dehydration - insulin to lower blood glucose - electrolytes (K+)
198
What is HHS?
Hyperosmolar hyperhlycaemic state (increased plasma osmolarity from dehydration and increased concentration)
199
What is happening to cells in HHS?
High glucose in the blood = high plasma osmolarity = causes water to leave the cells into the blood = cells dehydrated = increased urination / dehydration
200
Microvascular complications from diabetes (pathophysiology of it)
- hyaline atherosclerosis - thickened basement membranes, harder for O2 to diffuse across, leads to hypoxia
201
Vascular complications of diabetes
- diabetic retinopathy (cotton wool spots and flare haemorrhages) - kidney damage --> nephrotic syndrome - peripheral neuropathy - ulcers
202
What medications should be stopped when a patient presents with DKA?
- SGLT2 inhibitors - Gliclazide - Insulin