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Endocrine > IPE > Flashcards

IPE Flashcards

1
Q

What is meant by ACTH dependent and independent in relation to cushing’s syndrome?

A

ACTH independent - due to negative feedback ACTH falls at high levels of cortisol- no suppression at any dose of Dexamethasone
ACTH dependent - increased ACTH is causing the increased cortisol eg in Cushing disease or ectopic ACTH secretion from tumour - dexamethasone suppresses the ACTH release and leads to fall in levels

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2
Q

What are the signs of low Ca?

A 
Spasm
Perioral parathesia 
Anxious 
Sezuires
orientation impaired
Cardiomyopathy and can lead to Torsades Des Pointes
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3
Q

What is the main cause of primary hyperparathyroidism?

A

Pituitary adenoma

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4
Q

Apart from the effects of the hormones what are the other signs and symptoms that a patient with hypopituitary may present with?

A

Mass effect signs - headaches

Vision - bitemporal hemianopia

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5
Q

How much of what is given if IV treatment is needed in a hypoglycaemic patient?

A

100ml of 20% dextrose

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6
Q

What are the eye signs in all thyrotoxicosis not just graves?

A

Lid lag and lid retraction

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7
Q

What tests should be done in those with suspected thyrotoxicosis?

A 
TFT - increased T4 and decreased TSH
TSH receptor antibodies 
increased Ca and LFTs
Isotope scan 
eye test- fields, acuity and movement
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8
Q

What is a thyroid storm and how is it treated?

A 
Increased temperature, confusion, coma, AF and acute abdomen 
May also be in heart failure 
Treatment 
- Fluid and NG
- Bloods and culture
- Propanolol and consider digoxin
- Carbimazole and then Ludwig iodine 
- Hydrocortisone 
- Tx underlying cause
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9
Q

Along with treating the hormone problem what can also be prescribed to reduce the symptoms of thyrotoxicosis?

A

Propanolol

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10
Q

What investigations would you do in a patient where you were suspecting DI?

A

Bloods - U&Es, Ca and blood glucose
Urine and plasma osmolarity
Diagnosis is made with a water deprivation test with desmopressin

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11
Q

Explain the presentation of a myoxedema coma?

A 
Looks hypothyroid
hypothermic 
Hypoglycaemia
Heart failure
Coma and sezuires
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12
Q

What are the precipitants of myxoedema coma?

A 
Radio-iodine
Thyroidectomy 
Pituitary surgery
infection 
trauma and stroke
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13
Q

What is the management of a myxoedema coma?

A 
Bloods 
Correct any hypoglycaemia 
T3/T4 slowly corrected - may precipitate an MI
Hydrocortisone 
Rx hypothermia and Hf
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14
Q

In those with a high prolactin what bloods should be done?

A

Basal prolactin
Pregnancy test
TFTs

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15
Q

How is the diagnosis of glucose made?

A
  • Symptoms AND raised venous glucose on ONE occasion (fasting > 7mmol/l or random > 11.1mmol/l).
  • Raised venous glucose on TWO occasions (fasting, random, or oral glucose tolerance test)
  • HbA1c > 48mmol/L/6.5% (however, this isn’t used in children, pregnancy or Type 1)
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16
Q

What are the different types of DM?

A

Type 1 – this is usually childhood/adolescent in onset but can occur at any age. It is due to insulin deficiency from autoimmune destruction of the pancreatic beta cells. It presents with polydipsia, polyuria and weight loss. These patients are prone to ketoacidosis which is a medical emergency. There are also autoantibodies present: islet cell antibodies and anti-glutamic acid decarboxylase. Latent autoimmune diabetes of adults (LADA) is a form of type 1 diabetes mellitus, so if an older patient is ketotic with poor response to oral hypoglycaemics remember LADA.
Type 2 – this usually presents in older patients that are overweight. It is due to insulin resistance as well as beta cell dysfunction. There is a very high prevalence of this due to changes in lifestyle (as well as better diagnosis). It is associated with obesity, alcohol intake, lack of exercise and calorie excess.

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17
Q

What are the risks of gestational diabetes?

A

miscarriage, pre term labour, pre eclampsia, congenital malformations, macrosomia and a worsening of diabetic complications.

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18
Q

What are the risk factors for gestational diabetes?

A

over 25 years old, family history, heavier weight, non-Caucasian, HIV positive and previous gestational diabetes.

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19
Q

What should be used to control diabetes in pregnancy?

A

Metformin and insulin

no other hypoglycaemics

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20
Q

What is metabolic sydrome?

A
  • Central obesity (BMI > 30, or high waist circumference) AND 2 of:
  • BP > 130/85, triglycerides > 1.7 mmol/l, HDL < 1.03 (males)/ 1.29 (females) mmol/l, fasting glucose > 5.6 mmol/l or diabetes mellitus.
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21
Q

What are the 2 life threatening complications of T1DM?

A

Hypoglycaemia and DKA

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22
Q

What must a T1DM have for good care?

A
  • Phone support – a trained nurse available to give advice.
  • Knowledge of diet modifications and to avoid binge drinking (delayed hyperglycaemia)
  • Partner/parent/housemate knows how to abort hypoglycaemia
  • Education on how to self adjust doses in light of exercise, finger prick result and calorie intake
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23
Q

How often is blood glucose testing recommended for patients with T1DM?

A

4 times per day

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24
Q

What are the common insulin regimes?

A
  • Basal bolus regime – before meals rapid acting insulin and a bed time long acting analogue. This involves a lot of injections, but offers good control and the opportunity for a more flexible lifestyle.
  • Biphasic regime – twice daily pre mixed insulin, useful in patients with a regular lifestyle.
  • Once daily before bed long acting insulin – a good regime when switching from tablets in a type 2 diabetic.
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25
Q

What are the sick day rules for T1DM?

A
  • Increase frequency of blood glucose monitoring to four hourly or more frequently – continue normal insulin regime
  • Encourage fluid intake aiming for at least 3 litres in 24hrs
  • If struggling to eat may need sugary drinks to maintain carbohydrate intake
  • It is useful to educate patients so that they have a box of ‘sick day supplies’ that they can access if they become unwell
  • Check for ketonuria and adjust insulin dose accordingly (know to seek medical attention if they get too high)
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26
Q

What is the first line management for T2DM?

A

Lifestyle changes
Offer a statin
Control BP
Footcare

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27
Q

What is the first line medication choice for T2DM?

A

biguinide - metformin

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28
Q

How does insulin work?

A

increases insulin sensitivity and helps with weight

29
Q

What are the SEs of metformin?

A

Nausea, diarrhoea, abdo pain, lactic acidosis

Metallic taste

30
Q

When are biguinides contraindicated?

A

eGFR <30

31
Q

When should another agent be added to metformin in T2DM?

A

HbA1c >7.5%

32
Q

What is an example of a sulphonylurea?

A

Gliclazide

33
Q

What are the side effects of Sulphonylureas?

A

WL

Hypoglycaemia

34
Q

What is the mechanism of action of pioglitazone?

A

increases insulin sensitivity- increased fat and muscle glucose uptake

35
Q

What are the side effects of pioglitazone?

A 
hypoglycaemia
fractures
Fluid retention
increased LFTs
weight gain
36
Q

What are the complications of pioglitazone?

A

HF
osteoporosis
previous bladder tumours

37
Q

What is a sitagliptin?

A

DPP 4 inhibitor - augment insulin release-

DPP4 usually breaks down GLP 1 which is released from the gut to increase insulin after food

38
Q

What is good about gliptins?

A

Avoid hypoglycaemic events

39
Q

Give some examples of SGLT2 inhibitors and where they work

A

Dapagliflozin
Empafliflozin

work in the kidney

40
Q

What are some of the side effects of SGLT2 inhibitors

A

increased UTIs and thrush and WL

41
Q

What are the microvascular complications of diabetes?

A

retinopathy
nephropathy
neuropathy

42
Q

What are the macrovascular complications of diabetes?

A

MI, stroke and PVD

43
Q

What is the screening process for retinopathy in diabetics?

A

Annual screening is mandatory

44
Q

What is back ground retinopathy in diabetics?

A

Microaneurysms
haemorhages
hard exudates

45
Q

What is pre proliferative changes in diabetics?

A

Cotton wool spots - infarcts
haemorhages
venous bleeding

All indicate ischaemia and need specialist management

46
Q

What is proliferative change in diabetic retinopathy?

A

new vessels formed

47
Q

How can we tell between ischaemic and neuropathic feet in diabetics?

A

Neuropathy vs ischaemia – many patients will have both.
• Neuropathy – reduced sensation in stocking distribution, absent ankle jerks, neuropathic deformity: pes cavus, claw toes, loss of transverse arch, rocker bottom sole.
• Ischaemia – absent foot pulses, do Doppler pressure measurements/angiography.

48
Q

What are the different types of diabetic neuropathies?

A
  • symmetrical sensory polyneuropathy - glove and stocking
  • mononeuritis multiplex
  • autonomic neuropathy
49
Q

What are the elements of autonomic neuropathy?

A

postural hypotension, gastroparesis, urine retention, erectile dysfunction and diarrhoea.

All relate to vagus nerve effects

50
Q

What is the treatment of symmetrical sensory polyneuropathy in diabetics?

A

Treatment of the pain is paracetamol, then amitriptyline, then duloxetine, then gabapentin/pregabalin and finally opioids. Avoiding weight bearing helps.

51
Q

What is a DKA?

A

this occurs in Type 1 diabetics (very rarely Type 2). The body cannot use glucose, so reverts to an alternative metabolic pathway of ketoacidosis, as it is the only way the body can produce energy. The combination of severe acidosis and hyperglycaemia can be deadly.

52
Q

What is the presentation of a DKA?

A

drowsiness, vomiting and dehydration. They may also have abdominal pain, polyuria, polydipsia, ketotic breath (acetone production) and reduced GCS

53
Q

What can trigger a DKA?

A

infection (UTI), surgery, MI, pancreatitis, chemotherapy, antipsychotics and wrong insulin dose/non compliance.

54
Q

What are the indications of a severe DKA? How does this change the management

A

blood ketones > 6 mmol/l, O2 sats < 92% on air, venous bicarbonate < 5 mmol/l, systolic BP < 90 mmHg, pH < 7.1, pulse > 100 or < 60, GCS < 12 or K < 3.5 mmol/l.

Consider ITU referral

55
Q

What is the management of DKA?

A
  1. ABCDE assessment, two large bore cannulas. Start fluids, 0.9% saline – 500ml bolus.
  2. ABG for pH, bicarbonate and lab glucose, ketones and U&Es (Na and K).
  3. Give insulin! 50 units actrapid to 50ml of 0.9% saline. Infuse continuously at 0.1 units/kg/hour. Aim for a fall in ketones of 0.5mmol/l/hour or rise in bicarbonate of 3mmol/l/hour with a fall in glucose of 3mmol/l/hour. If these targets are not being reached, increase insulin by 1 unit per hour.
  4. Check pH, bicarbonate, glucose and K+ at 1 hour, 2 hours and then 2 hourly.
  5. Assess need for K+ replacement.
  6. Avoid hypoglycaemia! Once glucose is <14mmol/l start 10% glucose at 125ml/hour to run along saline.
  7. Continue the fixed rate insulin until ketones are <0.3mmol/l, pH > 7.3 and bicarbonate > 18 mmol/l.
  8. Find and treat the trigger!
56
Q

What are the rules relating to DM and the DVLA?

A

• If on insulin then patient can drive a car as long as they have hypoglycaemic awareness, not more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months and no relevant visual impairment. Drivers are normally contacted by DVLA.
• If on oral therapy or exenatide no need to notify DVLA. If tablets may induce hypoglycaemia (e.g. sulfonylureas) then there must not have been more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months.
• If diet controlled alone then no requirement to inform DVLA.
If they feel hypoglycaemic when driving, the patient should pull over and have a sugary drink/snack and then check blood glucose again. They must wait 45 minutes once the blood glucose is above 4mmol/l before driving again.

57
Q

What is a hyperglycaemic hyperosmolar state?

A

Typically in a T2DM
About 1 week history of marked dehydration and glucose >35mmol/L
Do not become acidotic as no switch to ketone metabolism

58
Q

What is the management of a hyperglycaemiac hyperosmolar state?

A

Rehydrate slowly with 0.9% saline over 48 hours and replace K+ once they start to urinate if needed. Only use insulin if blood glucose is not falling by 5mmol/l/hour or if there is ketonaemia. Keep blood glucose at least 10-15 mmol/l for the first 24 hours to avoid cerebral oedema. There is also a risk of DVT, so give LMWH prophylaxis unless contraindicated.

59
Q

What do you lknow about transient D in CF?

A

hard to diagnose due to transient nature- patients have a 5 day implant in order to measure their glucose level. Hard to treat due to transient nature- treat with insulin and teach patients to monitor their carbohydrates intake in order to appropriately adjust insulin.

60
Q

What are some secondary causes of hyperglycaemia?

A
  • Medications - STEROIDS, b blockers, adrenaline, thiazide diuretics and some antipsychotics
  • Acute stress events - stroke, MI, sepsis, encephalitis
  • Endocrine dysfunction
  • Pancreatic disease and chronic pancreatitis
  • Thyroid, adrenal or pituitary gland dysfunction
  • Endocrine tumours increasing production of growth hormones, glucocorticoids, catecholamines, glucagon and somatostatin
61
Q

What antibodies are seen in T1DM?

A

Anti-islet and anti-GAD

62
Q

When should metformin be omitted in hospitalised patients?

A

Ketoacidosis
Lactic acidosis
peri -operatively
if using iodine contrast agents

63
Q

What type of drug is acarbose and how does it work?

A

decreased break down of starch into sugar

64
Q

What are the SEs of acarbose?

A

Flatulence
Diarrhoea
Abdo pain

65
Q

What type of drug is Exenatide and what is important about administration?

A

GLP1 agonist - mimics GLP-1

SC

66
Q

What are the side effects of exenatide?

A

Gi disturbances and indigestion
Pancreatitis
WL

67
Q

What are the symptoms of diabetic retinopathy?

A

painless gradual reduction of central vision as oedema builds and haemorrhage will result in a sudden loss of vision over the area of the haemorrhage – dark, painless floaters in the vision which may regress over the next few days

68
Q

How does gastroparesis present and whats its management?

A

early satiety
GORD
Bloating
erratic blood glucose

management - metaclopramide, domperidone and erthryomycin

69
Q

What is the pathophysiology behind a charchot deformity?

A

Progressive degeneration of a weight bearing joint (normally the ankle) thought to result from neuropathy
Repeated microtrauma, unfelt because of the patient’s neuropathy, leads to progressive destruction and damage to the bones and joints
Increased osteoclastic resorption of bone due to increased blood flow, weakens the bone and causes its destruction
Reduced autonomic nervous system regulation of blood flow – less vasoconstriction

Endocrine (1 decks)

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