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Finals > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What defines prediabetes?

A

HbA1c 42-47mmol/mol

fasting glucose 6.1-6.9

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2
Q

What HbAlc defines diabetes?

A

> 48mmol/mol (6.5%)

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3
Q

What blood glucose defines diabetes?

A

fasting glucose >= 7.0 mmol/l
random glucose >= 11.1 mmol/l
HbA1c >48mmol/mol

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4
Q

What are some complications of diabetes?

A 
lipohypertrophy
vascular disease
nephropathy
neuropathy
retinopathy
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5
Q

How can patients with diabetes reduce complications of diabetic neuropathy

A 
foot check with mirror
comfortable shoes
no barefoot walking
chiropody
treat fungal infections
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6
Q

What is the advice from the DVLA for patients who take insulin?

A

need to inform the DVLA!!!

check blood glucose before driving and every two hours whilst driving
have snack in <5mmol/l
do not drive if <4mmol/l or sx of hypoglycaemia

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7
Q

What does HbA1c show?

A

level of glycated Hb

reflects average plasma glucose over the previous 2 to 3 months and provides a good indicator of glycaemic control.

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8
Q

How often should the HbA1c be monitored in diabetes?

A

every 3 to 6 months

in type 2, when stable and medications stable, can be every 6 months

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9
Q

How can cardiovascular risk be reduced in diabetes?

A

ACEi
statin
aspirin

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10
Q

How are patients monitored for diabetic nephropathy?1

A

yearly urine protein test (Albustix) and serum creatinine

if -ve for protein, test for microalbuminuria

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11
Q

If a diabetic patient is discovered to have proteinuria or micoalbuminuria, what is the appropriate management?

A

ACEi or Angiotensin II receptor antagonist

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12
Q

What can be used to treat painful diabetic neuropathy?

A

duloxetine

pregabalin

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13
Q

How often should patients with IDDM monitor their blood glucose?

A

at least four times a day

on waking, before each meal, before going to bed

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14
Q

What is a multiple daily injection basal-bolus insulin regimen

A

One or more separate daily injections of intermediate-acting insulin or long-acting insulin analogue as the basal insulin
plus multiple bolus injections of short-acting insulin before meals.

This regimen offers flexibility to tailor insulin therapy with the carbohydrate load of each meal.

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15
Q

What is a mixed insulin regimen?

A

One, two, or three insulin injections per day of short-acting insulin mixed with intermediate-acting insulin.

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16
Q

Who can a Continuous subcutaneous insulin infusion (insulin pump) be offered to?

A

adults who suffer disabling hypoglycaemia,
adults who have high HbA1c concentrations (69 mmol/mol [8.5 %] or above) with multiple daily injection therapy (including, if appropriate, the use of long-acting insulin analogues) despite a high level of care

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17
Q

What can persistent poor glucose control in insulin therapy be due to?

A

poor adherece
injection technique,
injection site problems,
blood-glucose monitoring skills,
lifestyle issues (including diet, exercise and alcohol intake),
psychological issues,
organic causes such as renal disease, thyroid disorders, coeliac disease, Addison’s disease or gastroparesis.

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18
Q

What can increase a diabetic’s insuln requirement?

A

Infection,
stress,
accidental or surgical trauma

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19
Q

What can decrease a diabetic’s insuln requirement?

A

physical activity,
intercurrent illness,
reduced food intake,
impaired renal function,

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20
Q

What are the warning signs of hypoglycaemia?

A

sweating, anxiety, hunger, tremor, palpitations, dizziness

confusion, drowsiness, visual problems, seizures, coma

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21
Q

What are the daily blood glucose targets when self testing for IDDM?

A

5-7 mmol/l on waking and

4-7 mmol/l before meals at other times of the day

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22
Q

How does metformin work?

A

increased insulin sensitivity

decreases liver gluconeogenesis

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23
Q

What are the important side effects if metformin?

A

GI upset

lactic acidosis

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24
Q

How do sulfonylureas work?

A

Stimulate pancreatic beta cells to secrete insulin

binding to and antagonising the β-cells K+-ATP channel activity,
increases K+ concentration within the cell
depolarisation.
increases Ca2+ ion entry into the cell
insulin release from β-cells.

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25
Q

What are the important side effects if sulfonylureas?

A

weight gain
hypoglycaemia
hyponatraemia

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26
Q

How do thiazolidinediones work?

A

Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake

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27
Q

What are the important side effects if thiazolidinediones?

A

weight gain

fluid retention

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28
Q

How do DPP-4 inhibitors (-gliptins) work?

A

Increases incretin levels which inhibit glucagon secretion

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29
Q

What are the important side effects if gliptins?

A

increased risk pancreatitis

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30
Q

How do SGLT-2 inhibitors (-gliflozins) work?

A

inhibits reabsorption of glucose in the kidney

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31
Q

What are the important side effects if SGLT-2 inhibitors?

A

urinary infections

increased risk DKA

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32
Q

How do GLP-1 agonists work?

A

Incretin mimetic which inhibits glucagon secretion and increases insulin secretion from pancreas

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33
Q

What are the important side effects if GLP-1 agonists?

A

Nausea and vomiting

Pancreatitis

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34
Q

How are GLP-1 agonists taken?

A

SC

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35
Q

What is the target HbA1c for type 2 diabetes?

A

<48mmol (6.5%)

If on drug associated with hypoglycaemia, aim for <53mmol/mol (7%)

If on two or more hypoglycaemic agents, aim for <53 (7%)

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36
Q

If a patient is being treated with oral hypoglycaemic, at what point would you consider adding another agent?

A

HbA1c >58 (7.5%)

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37
Q

How is hypoglycaemic treatment intensified?

A

metformin

\+
sulfonylurea
thiazolidinedione
DDP-4 inhibitor
SGLT-2 inhibitor

then + 2 of them

consider insulin

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38
Q

When can GLP-1 agonists be prescribed?

A

If triple therapy with metformin hydrochloride and two other oral drugs is tried and is not effective, not tolerated or contra-indicated,

prescribed as part of a triple combination regimen with metformin hydrochloride and a sulfonylurea.

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39
Q

When is metformin contraindicated?

A

lactic acidosis

high risk of lactic acidosis: chronic cardiac failure

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40
Q

What is the first line treatment for NIDDM if metformin is contraindicated?

A

DDP4 inhibitor
Pioglitazone
a sulfonylurea (glibenclamide, gliclazide, glimepiride, glipizide, or tolbutamide).

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41
Q

What medications can trigger DKA?

A 
steroids, 
thiazides
sodium-glucose co-transporter 2 (SGLT2) inhibitors
alpha blockers
beta blockers
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42
Q

What are the key investigation findings in DKA?

A

hyperglycaemia >11
ketonaemia >3
acidosis <7.3

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43
Q

What are the key investigations in suspected DKA?

A

bedside: urine dipstick, ECG
bloods: FBC, U+E, glucose, ABG, troponin I, amylase
micro: blood cultures
Imaging: CXR, AXR

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44
Q

What is the immediate management of DKA?

A

fluid resuscitation
insulin - 50 units actrapid at 0.1unit/kg/hr
K+ replacement?
check pH, biarb, glucose and K+ hourly

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45
Q

What is HONK?

A

hyperosmolar non-ketotic coma

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46
Q

What are the key results defining HONK/HHS?

A

hypovolaemia
hyperglycaemia
low ketones <3mmol
high osmolarity >320mosmol/kg

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47
Q

What causes HONK/HHS?

A

develops in T2DM as a result of a combination of:
illness,
dehydration
an inability to take normal diabetes medication

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48
Q

What causes there to be hyperosmolarity and dehydration in HONK/HHS?

A

Hyperglycaemia causes an osmotic diuresis
due to glucose accumulating in the tubules of the kidney, reducing reabsorption of water in the kidneys, increasing urine output.

hyperosmolarity of the blood leads to an osmotic shift of water into the intravascular compartment,

resulting in severe intracellular dehydration

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49
Q

Why is there no ketosis in HONK/HHS

A

basal insulin is sufficient to prevent ketosis, but not enough to reduce blood glucose

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50
Q

What is the initial management in HONK/HHS?

A

A to E
IV fluids - 0.9% sodium chloride
insulin infusion
potassium replacement

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51
Q

What are the key investigations in HONK/HHS?

A

Bedside: ECG, urinalysis
Bloods: Glucose U and Es, HCO3-, amylase, ABG, calculate serum osmolarity
Micro: blood cultures
Imaging: CXR

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52
Q

What are the risks during pregnancy for a diabetic woman?

A 
miscarriage
pre-eclampsia
premature labour
worsening of diabetic retinopathy/nephropathy
spontaneous abortion
polyhydraminos
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53
Q

Wat are the risks to the fetus during pregnancy of a diabetic woman?

A 
macrosomia
congenital heart defects/neurological defects
late intrauterine death
stillbirth
Erb's palsy
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54
Q

How can diabetic women decrease their risk of complications during pregnancy?

A

no unplanned pregnancies
good glycaemic control for 12 weeks at least before conception
good control during pregnancy - careful to avoid hypos
folic acid for 12weeks prior and up until 12 weeks fetal age
ne[hropathy and retinopathy screening

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55
Q

What are the key finding on fundoscopy in diabetic retinopathy??

A 
micoaneurysms
haemorrhages
hard exudates
neovascularisation
cotton wool spots
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56
Q

What are hard exudates seen in fundoscopy?

A

lipoprotein infiltrates due to leakage from blood vessels

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57
Q

What are cotton wool spots seen in fundoscopy?

A

build up of axonal debris due to poor aconal metabolism

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58
Q

What causes diabetic retinopathy?

A

microvascular occlusion leading to retinal ischaemia

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59
Q

What are the stages of diabetic retinopathy?

A

background
pre-proliferative
proliferative

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60
Q

What are the changes seen in background diabetic retinopathy on fundoscopy?

A

hard exudates
microaneuyrsms
haemorrhages

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61
Q

What are the changes seen in pre-proliferative diabetic retinopathy on fundoscopy?

A

cotton wool spots
haemorrhage
venous bleeding

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62
Q

What are the changes seen in proliferative diabetic retinopathy on fundoscopy?

A

neovascularisation

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63
Q

How can diabetic retinopathy be prevented?

A

good glycaemic control
blood pressure control
lipid control
smoking cessation

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64
Q

State Wagner’s grading of diabetic foot ulcers

A

Grade 1: Superficial diabetic ulcer
Grade 2: Involves ligament, tendon, joint capsule or fascia, No abscess or osteomyelitis
Grade 3: Deep ulcer with abscess or osteomyelitis
Grade 4: Gangrene to portion of forefoot
Grade 5: Extensive gangrene of foot

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65
Q

What are the causes of primary hypothyroidism?

A 
hashimoto's
iodine deficiency
primary atrophic hypothyroidism
drug induced
iatrogenic - radiotherapy or surgery
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66
Q

What drugs can cause hypothyroidism

A

carbimazole
amiodarone
lithium
iodine

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67
Q

What are the causes of secondary hypothyroidism?

A

hypopituitarism

hypothalmic disorders

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68
Q

State some key examination findings in hypothyroidism

A

delayed relaxation of reflexes
hair loss
congestive heart failure
carpal tunnel syndrome

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69
Q

What problems can hypothyroidism cause in pregnancy

A 
eclampsia
anaemia
premature birth
low birth weight
still birth
post partum haemorrhage
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70
Q

How should a patient with hypothyroidism be investigated?

A

Bedside: ECG
Bloods: TSH, FT4, FBC, HbA1c (assoc T1DM), serum lipids, TPO Ab
Imaging: USS neck if goitre

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71
Q

What test results indicate primary hypothyroidism?

A

TSH >10mU/l

low FT4

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72
Q

What test results indicate subclinical hypothyroidism?

A

raised TSH

normal FT4

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73
Q

What test results indicate secondary hypothyroidism?

A

low/normal TSH

low FT4

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74
Q

When can TFT results be misleading?

A 
pregancy
after tx for hyperthyroidism
after starting levothyroxine
poor compliance with levothyroxine
drugs - dopamine, glucocorticoids, amiodarone
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75
Q

What is the differential diagnosis in hypothyroidism?

A 
sick euthyroid
diabetes
coeliac
hypopituitarism
anaemia
chronic liver disease
fibromyaligia
dementia
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76
Q

What do patients on carbimazole need to be checked for

A

Patient should be asked to report symptoms and signs suggestive of infection, especially sore throat.
A white blood cell count should be performed if there is any clinical evidence of infection.
Carbimazole should be stopped promptly if there is clinical or laboratory evidence of neutropenia.

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77
Q

What is a key side effect of carbimazole

A

agranulocytosis

bone marrow supression

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78
Q

What is a common side of effect of carbimazole?

How can this be treated?

A

rash/pruritis
antihistamines
do not need to stop treatment

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79
Q

Can carbimazole be used during pregnancy?

A

yes at lowest possible dose that prevents hyperthyroidism

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80
Q

What monitoring is carried out in carbimazole therapy?

A

before: FBC, LFT
at first: TFTs every 4-6wks until stable
During: TFTs every 3m,

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81
Q

What is the cut off for a normal urine ACR in diabetes?

A

> 3 = microalbuminuria

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82
Q

Describe the actions of PTH

A

increased bone resorption
increased calcium reabsorption in kidneys
increased hydroxylation of vitamin D

leads to increased Ca2+ and lowphosphate

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83
Q

What can cause hypocalcaemia

A 
hypoparathyroidism
- surgical
- autoimmune
Decreased vitamin D
- liver or kidney failure
- reduced intake
- lack of sunlight
Phosphate retention
- kidney disease
Ca2+ deficiency
- pancreatitis
- rhabdomyolysis
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84
Q

What are the features of hypocalcaemia

A 
tetany
Chvostek's sign
Trosseau's sign
seizures
perioral paresthesia
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85
Q

What are the features of hypocalcaemia on ECG

A

prolonged QT interval

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86
Q

What is Chvostek’s sign

A

tap on parotid - facial nerve
facial muscles twitch

+ve in hypocalcaemia

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87
Q

What is Trosseau’s sign

A

brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
carpal spasm - wrist flexion and fingers drawn together

+ve in hypocalcaemia

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88
Q

What are the key investigations in hypocalcaemia

A

Bedside: ECG
Bloods: Ca2+, phosphate, PTH, vit D, Mg2+

89
Q

Describe the treatment of hypocalcaemia

A

emergency = intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
ECG monitoring

mild - oral calcium

chronic kidney disease - alfacalcidol

90
Q

What can cause hypercalcaemia

A

primary hyperparathyroidism
malignancy

sarcoidosis
vit D toxicity
thiazides
lithium
Paget's disease + immobility
thyrotoxicosis
91
Q

Which cancers are most likely to cause hypercalcaemia due to bone metastasis

A

lung
breast
myeloma

92
Q

Which cancers release PTHrP?

A

squamous lung cancer
gynae
GU

93
Q

What are the symptoms of hypercalcaemia

A 
bone pain
constipation, N+V, 
calcium oxalate kidney stones
dehydration
slow/absent reflexes
muscle weakness
confusion, hallucinosis, coma
94
Q

What are the signs of hypercalcaemia on ECG

A

bradycardia

short QT interval

95
Q

What investigations should be carried out in hypercalcaemia

A

Bedside: ECG
Bloods: FBC, U+E (cancer), PTH, vit D, albumin, phosphate, alkaline phosphatase, LFTs
Imaging: CXR

96
Q

What are the characteristic investigation findings in hypercalcaemia produced by malignancy

A

low PTH

raised alkaline phosphotase

97
Q

Describe the treatment of hypercalcaemia

A

IV fluids - 0.9% sodium chloride

bisphosphonates eg

underlying cause

steroids if sarcoidosis

98
Q

State the HPA axis for cortisol

A

CRH from hypothalamus
ACTH from anterior pituitary
cortisol from zona fasciculata of cortex of adrenal glands

99
Q

What are the effects of cortisol?

A

rasied blood glucose
- gluconeogenesis
- lipolysis
- proteolysis
increased sensitivity to peripheral adrenaline
decreased inflammatroy response (T lymph)

100
Q

What are the causes of cushing’s syndrome

A

ACTH dependent

  • pituitary adenoma - increased ACTH
  • ectopic ACTH - small cell lung, carcinoid

ACTH independent

  • exogenous steroids
  • adrenal adenoma
  • adrenal carcinoma
101
Q

What are the symptoms of Cushing’s disease

A 
increased weight
depression/psychosis
proximal weakness
amennorhea
ED
acne
lots of infections
102
Q

What are the signs of Cushing’s disease

A 
central obbesity
proximal wastage
abdominal striae
high blood pressure
Moon face
Supraclavicular fat pad
easy bruising
high BP
high glucose
103
Q

What investigations should be carried out in suspected Cushing’s disease

A

Bedside - 24hr urine cortisol
Bloods - 9am and midnight cortisol, plasma ACTH, FBC, U+E, glucose
Micro
Imaging: CAP CT if ectopic is suspected
Special Tests: 1mg overnight dexamethasone suppression test, high dose dexamethasone supression test, CRH test

104
Q

Describe the low dose dexamethasone suppression test and the expected results

A

dexamethasone should suppress ACTH secretion

healthy patient: cortisol is supressed
Cushing’s syndrome: no change in cortisol levels

105
Q

What can cause a false positive raised cortisol level?

A

pregnancy, anorexia, exercise, psychoses, alcohol and alcohol withdrawal. Strenuous exercise and illness raise cortisol secretion.

106
Q

Describe the treatment of Cushing’s disease

A

pituitary adenoma - transspenoidal removal, radiotherapy
adrenal adenoma - adrenectomy, radiotherapy
ectopic - removal if possible!

107
Q

What kind of acid/base problem does Cushing’s cause?

A

hypokalaemic metabolic alkalosis

108
Q

Why does Cushing’s cause a hypokalaemic metabolic alkalosis

A

cortisol cross reacts with mineralocrticoids - aldosterone

leads to increased K+ excretion, increased sodium retention and increased H+ excretion

109
Q

Describe the high dose dexamethasone suppression test and the expected results

A

should decrease ACTH and therefore cortisol levels

healthy: cortisol supressed
pituitary adenoma - supressed cortisol
ectopic - cortisol stays same

110
Q

What is a phaeochromocytoma?

A

tumour of chromaffin cells of adrenal medulla

secretes catecholamines - adrenaline and noradrenaline

111
Q

What is the 10% rule in phaeochromocytoma

A

10% familial
10% bilateral
10% malignant
10% extrarenal

112
Q

What is an extrarenal phaeochromocytoma called?

A

paraganglionoma

113
Q

What are the signs and symptoms of phaeochromocytoma?

A 
EPISODIC
palpitations
anxiety
sweating
high HR

high BP

114
Q

What investigation is crucial in phaeochromocytoma?

A

24hr urine metanephrines and VMA

plasma metanephrines

115
Q

What is the treatment for phaeochromocytoma

A

presurgery:
alpha blockade - phenoxybenzylamine
beta blockade - propanolol

adrenalectomy

116
Q

What are the causes of adrenal failure?

A

primary
Addison’s disease, TB, metastatic carcinoma

secondary
acute steroid withdrawal
physical stress whilst taking steroids

117
Q

What are the symptoms and signs of Addison’s disease

A 
fatigue
weakness
pigmentation
weight loss
reduced appetite
N+V
postural hypotension
118
Q

Why does hyperpigmentation occur in Addison’s

A

increase in POMC in order to raise ACTH

also leads to raised melanocyte stimulating hormone

119
Q

What investigations are important to do in suspected addison’s/

A

ECG, urinalysis
FBC, U+E, ABG, glucose, cortisol and ACTH levels
Synacthen test

120
Q

What are the common investigation findings in addison’s

A

low sodium, high potassium, low blood pressure, metabolic acidosis

121
Q

Why does metabolic acidosis occur in Addison’s

A

impaired H+ excretion due to laco of stimulation of H+ ATPase

122
Q

What are the actions of aldosterone in the kidney

A

stimulate Na+/K+ATPase and H+ATPase in DCT

leads to increased sodium, decreased potassium and decreased H+

123
Q

What are some truggers of an Addisonian crisis

A

infection
trauma
stopping steroids
surgery

124
Q

What are teh expected results of the synacthen test in Addison’s

A

in teh test they give ACTH
normally expect to see rise in cortisol

in Addison’s there is little/no rise

125
Q

What is the treatment for Addison’s disease (non-acute)

A

hydrocrotisone and fludrocortisone for life

126
Q

What is the treatment for an Addisonian crisis

A

hydrocortisone 100 mg im or iv
1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
continue hydrocortisone 6 hourly until the patient is stable.
oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

127
Q

How should an intercurrent illness be managed in Addison’s

A

double hydrocortisone dose

128
Q

What is the pathophysiology of Hashimoto’s

A

anti TPO Ab

lymphocytic and plasma cell infiltration

129
Q

What are the symptoms of hypothyroidism

A 
lethargy
low mood
cold intolerance
weight gain
constipation
mennhoraggia
myalgia
cramps
weakness
130
Q

What are the diseases associated with hypothyroidism

A

diabetes
pernicious anaemia
Addison’s

131
Q

Is there a goitre present in primary atrophic hypothyroidism or Hashimoto’s thyroiditis? Why?

A

PAH - no goitre due to diffuse lymphocytic infiltration and atrophy

HT - goitre due to lymphocytic and plasma cell infiltration

132
Q

What are the causes of hyperthyroidism?

A

primary:
Graves
toxic mulitnodular goitre
toxic adenoma

post partum thyroiditis
levothyroxine excess
de Quervian’s
amiodarone

133
Q

Describe the pathophysiology of Graves

A

IgG autoantibodies bind to TSH receptors, stimulating thyroid, stimulating thyroxine release and thyroid growth

134
Q

Why is there eye disease in Grave’s

A

the autoantibodies react with the orbital autoantigens, leading to inflammation and swelling of orbital contents

135
Q

What is de Querviann’s

A

post viral self limiting subacute thyroiditis causing hyperthyroidism

136
Q

What are the symptoms of hyperthyroidism

A 
irritability
anxiety
sweating
palpitations
weight loss
increased appetite
difficulty sleeping
diarrhoea
heat intolerance
137
Q

What signs are seen in Grave’s disease but not other causes of hyperthyroidism

A

exophthalmos,
ophthalmoplegia
pretibial myxoedema
thyroid acropachy

138
Q

What is thyroid acropachy

A

clubbing, painful finger and toe swelling, periosteal reaction in limbs

139
Q

What is pretibial myxoedema

A

oedematous swellings above lateral malleolus)

140
Q

What are the signs of hyperthyroidism

A 
warm moist skin
palmar erythema
fine tremor
fast pulse
AF
thin hair
goitre
thyroid nodules
141
Q

What investigations should be carried out in hyperthyroidism

A

ECG
FBC, U+E, ESR, CRP, TFTs, thyroid autoantibodies
isotope scan (toxic multinodular/subacute)
visual fields and acuity

142
Q

What is the treatment for hyperthyroidism

A
  1. carbimazole.
    propanolol for control of symptoms
  2. radioiodine treatment
  3. thyroidectomy
143
Q

What is block-replace treatment of hyperthyroidism

A

give carbimazole and levothyroxine at same time. reduces risk of iatrogenic hypothyroidism

144
Q

what are the risks of thyroidectomy

A

recurrent laryngeal nerve palsy - hoarse voice
hypoparathyroidim
hypothyroidism

145
Q

Describe the titration method of treating hyperthyroidism

A

15–40 mg daily continue until the patient becomes euthyroid, usually after 4 to 8 weeks,
then reduced gradually to 5–15 mg daily
therapy usually given for 12 to 18 months.

146
Q

What is a thyroid storm

A

hyperthyroid crisis with Fever, anxiety, agitation, confusion and tachycardia, and occasionally heart failure

147
Q

What are the causes of hyperlipidaemia

A

primary:
common primary hyperlipidaemia
familial combined hyperlopidaemia
familial hypercholesterolaemia

secondary
due to diabetes, Cushing’s, hypothyroidism, CKD, chornic liver disease, steroids

148
Q

What is the function of LDLs

A

transport cholesterol from liver/bowels to tissue

149
Q

What is the function of chylomicrons

A

transport lipids form gut to liver after a meal

150
Q

what is the function of VLDLs

A

transport lipids from liver to tissues

151
Q

what is the function of HDLs

A

transport lipids from tissues to liver

152
Q

How is cholesterol excreted from the body

A

bile salts

153
Q

What are the blood lipid levels in familial hypercholesterolaemia

A

raised LDLs

154
Q

What are the blood lipid levels in familial combined hyperlipidaemia

A

rasied LDLs and VLDLs

low HDLs

155
Q

What are the blood lipid levels in common primary hypercholesterolaemia

A

raised LDLs

156
Q

What are the blood lipid levels in secondary hyperlipidaemia

A

rasied LDLs

157
Q

What are the signs of hyperlidiaemia

A

tendon xanthoma
xanthelasma
corneal arcus

158
Q

Who is at greater risk of hyperlipidaemia

A

FH
corneal arcus <50y
xanthoma
xanthelasma

159
Q

Who should you screen for hyperlipidaemia knowing they will be at increased risk of CVD

A 
known CVD
smoking
diabetes
CKD
FH CVD <65y
HTN
obesity
160
Q

Who should primary prevention of CVD with hyperlipidaemia be offered to?

A

those with a QRISK score >10% 10yr risk
those with diabetes (>40y, had for >10y, nephropathy, otehr CVD risk factors)
those with CKD

161
Q

What drug is used for the primary prevention of CKD in hyperlipidaemia

A

20mg atrovastatin OD at night

162
Q

Who should secondary prevention of CVD with hyperlipidaemia be offered to?

A

those with pre-existing IHD, PVD or cerbrovascular disease

163
Q

What drug is used for the secondary prevention of CKD in hyperlipidaemia

A

80mg atorvastatin OD at night

164
Q

What is the mechanism of action of statins

A

inhibition of HMG-CoA reductase, leading to decreased synthesis of cholesterol from HMG-CoA
leads to increased LDL receptor synthesis in liver
leads to increased LDL uptake, therefore less LDLs in blood

165
Q

How should you follow up a newly prescribed statin

A

3 months later
full lipid profile

if the non HDl cholesterol has not decreased by >40%, increase the dose!

166
Q

What are some lifestyle interventions used in hyperlidiaemia

A

cardioprotective diet
exercise
stop smoking
weight loss

167
Q

Describe the characteristic blood results of primary hyperparathyroidism

A

PTH (Elevated)
Ca2+ (Elevated)
Phosphate (Low)

168
Q

Describe the characteristic blood results of secondary hyperparathyroidism

A

low vit D
raised PTH
low calcium
raised phosphate

169
Q

Describe the characteristic blood results of tertiary hyperparathyroidism

A 
Ca2+ (Normal or high)
PTH (Elevated)
Phosphate levels (Decreased or Normal)
Vitamin D (Normal or decreased)
Alkaline phosphatase (Elevated)
170
Q

State the pathophysiology of secondary hyperparathyroidism

A

background of chronic renal failure
vitamin D not able to be hydroxylated
low Ca2+
PTH stimulated to be released

171
Q

Describe the characteristic blood results of primary hypoparathyroidism

A

low calcium, high phosphate

low PTH

172
Q

What is the treatment of hypoparathyroidism

A

alfacalcidol

173
Q

What are the causes of primary hypoparathyroidism

A

removal in thyroid surgery

174
Q

DEscribe the pathophysiology of Paget’s disease

A

increased bone turnover
increased numbers of osteoblasts and osteoclasts
remodelling of bone, bone enlargement and deformity

175
Q

What are the signs and symptoms of Paget’s disease

A

asymptomatic!
deep boring pain
bony deformity and enlargement

176
Q

What are the most common sites for Paget’s to occur?

A 
lumbar spine
skull
pelvis
femur
tibia
177
Q

What are the complications of Paget’s disease

A

pathological fractures
OA
hypercalcaemia
nerve compression due to bony overgrowth

178
Q

What are the signs of Paget’s disease on xray

A

localized bone enlargement
patchy cortical thickening
sclerosis, osteolysis and deformity

179
Q

What are the typical blood test results in Paget’s disease

A

normal calcium and phosphate

ALP rasied

180
Q

What is the treatment of Paget’s disease

A

analgesia

bisphosphonates eg alendronic acid

181
Q

What is the bisphosphonates mechanism of action

A

adsorbed onto hydroxyapatite crystals in bone, slowing both their rate of growth and dissolution, and therefore reducing the rate of bone turnover.

182
Q

DEscribe the pathophysiology of osteoporosis

A

low bone mass and structural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture.

183
Q

Why does osteoporosis occur in old age?

A

bone breakdown by osteoclasts increases and is not balanced by new bone formation by osteoblasts

184
Q

Describe how bone mass changes with age

A

reached in the third decade and starts to decline in the fifth decade for men and women.
In women, this decline accelerates after the menopause for a period of between 5 and 10 years.

185
Q

What are the risk factors for secondary osteoporosis

A 
steroid use
hyperthyroidism, hyperparathyroidism
Alcohol and tobacco
Thin <22
Testosterone low
Early menopause
Renal or liver failure
Erosive/inflam bone disease
Dietary calcium low
186
Q

What are some causes of fragility fracture

A 
osteoporosis
Paget;s disease
bone metastasis 
multiple myeloma
osteomalacia
187
Q

How should suspected osteoporosis be investigated?

A

calcium, phosphate, PTH, alk phos

calculate FRAX or QFracture score

188
Q

What is the next step in management depending on the results of the FRAX score calculation

A

low risk - reassure
intermediate risk - do DEXA scan
high risk - start bisphosphonates

189
Q

How is hte DEXA scan calculated

A

bone mineral density is compared to that of a young healthy adult
T score = number of standard deviations away from youthul average

190
Q

What would the results of the DEXA scan be in osteoporosis

A

T score -2.5 or worse

191
Q

What is the lifestyle advice for management of osteoporosis

A 
stop smoking
stop alcohol
weight bearing exercise
balance exercise - reduced risk of falls
home-based fall prevention programme
192
Q

How should a bisphosphonate be taken?

A

with whole glass of water
whilst upright - stay for 30mins
wait 30mins before eating or taking other drugs

193
Q

What are the side effects of bisphosphonates

A

photosensetivity
GI upset
oesophageal ulcers

194
Q

How long should bisphosphonates be taken for?

A

no evidence for further benefit on taking for more than 3YRS

195
Q

What rare but important problems should patients be asked to look out for when taking bisphosphonates

A

osteonecrosis of jaw
osteonecrosis of external auditroy canal - ear pain, discharge from ear or an ear infection
oesophageal reactions

196
Q

Which drugs are used in the treatment of osteoporosis

A

first line: alendronic acid
second line: risedronate or etidronate

vitamin D and calcium if deficient

197
Q

What is osteomalacia

A

normal amount of bone, but loss of mineral content

excess uncalcified osteoid and cartilage

198
Q

What is the difference between rickets and osteomalacia

A

both are the lack of mineral content in bone

rickets occurs during the process of bone growth
osteomalacia occurs after epiphyses have fused

199
Q

What are the signs and symptoms of rickets

A

growth retardation
bow legs
hypotnonia
unwell!

200
Q

What are the signs and symptoms of osteomalacia

A

bone pain and tenderness
fractures
proximal myopathy

201
Q

What are the causes of osteomalcia

A

vitamin D deficinecy
renal osteodystrophy - lack of hydroxylation vit D
liver disease

202
Q

What are the investigations carried out in osteomalacia

A

Calcium, PTH, phosphate, vit D, ALP
xray
bone biopsy

203
Q

What are the typical xray findings in ostemalacia

A

loss of cortical bone
Looser’s zones = translucent bands
ragged Metaphyseal surfaces in ricket’s

204
Q

What is the treatment for osteomalacia

A

dietary deficiency = vitamin D!

malabsorption or liver = vitamin D2

renal disease = alfacalcidol (1alpha hydroxylated vitamin D) or calcitriol (1,25-hydrocyvitamin d3)

205
Q

State the metabolism of vitamin D

A

7-dehydrocholesterol made from production of cholesterol
converted to cholecalciferol (D3) in skin
hydroxylated in liver to 25-hydrocyvitamin d3
hydroxylated in kidney to 1,25-hydrocyvitamin d3

206
Q

What are they typical blood results in osteomalacia

A

low serum calcium,
low serum phosphate,
raised ALP
raised PTH

207
Q

What information shold be given to patients when prescribing metformin

A

take at the same time each day with a meal or snack
can cause GI upset but usually subsides within a few days
do not drink alcohol - increased risk of lactic acidosis
Let a doctor know straightaway if you are being sick or feel very unwell, or if you become unusually tired, or if you feel short of breath and your breathing becomes faster than normal. - lactic acidosis

208
Q

Why is carbimazole not prescribed if a patient has severe liver impairment

A

metabolised in liver

209
Q

Why is carbimazole not prescribed if a patient has had a sever blood disorder

A

risk fo agrannulocytosis adn bone marrow supression

210
Q

What affect does carbimazole have on warfarin

A

carbimazole enhances the anticoagulant effect of warfarin because it is also a vit K antagonist

211
Q

What is acromegaly due to?

A

anterior pituitary adenoma leading to increased GH release (can also be due to ectopic)

stimulates increased IGF-1 secretion which leads to hone and soft tissue growth

212
Q

When can GH be raised

A

pregnancy
puberty
stress
sleep

213
Q

what are the symptoms of acromegaly

A 
paresthesia of the extremeties
shoes adn rings no longer fitting
back ache
joint pain
heacache, vidual pribs
decreased libido
amernorrhoea
214
Q

What are the signs of acromegaly

A 
spade hands
large feet
broad nose
coarse facial features
macroglossia
sweaty skin
acanthosis nigracans
215
Q

What are the complications of acromegaly

A 
impaired glucose tolerance
HTN
cardiomyopathy
CVD
increased risk colon cancer
216
Q

What is the diagnostic test for acromegaly?

What are the expected results?

A

oral glucose tolerance test
check GH at intervals after glucose intake

normally, GH would be supressed by hyperglycaemia
in acromegaly, GH remains raised in hyperglycaemia

217
Q

What investigations should be done in acromegaly

A

ECG, visual fileds and acuity
glucose, calcium, phosphate
MRI head - look for pituitary lesion
OGTT

218
Q

what is teh treatmetn of acromegaly

A
  1. transphenoidal removal
  2. somatostatin analogues eg octreotide
  3. GH receptor antagonist - pegvisomant

Finals (32 decks)

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