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Aisha > Dunedin- Endocrine > Flashcards

Dunedin- Endocrine Flashcards

1
Q

What antibodies are associated with LADA or slowly evolving immune mediates diabetes of adults?

A

GAD (glutamic acid decarboxylase)

note- insulin not required at diagnosis
often >35 years

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2
Q

What is fulminant Type 1 diabetes

A

20% of acute onset T1DM in Japan
abrupt onset <7 days
frequent flulike and gastrointestinal symptoms
ketoacidosis at diagnosis
no c-peptide secretion

negative for islet autoantibodies

increased levels of pancreatic enzymes

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3
Q

What is ketosis prone type 2 diabetes?

A

diabetes that typically presents with ketosis and evidence of severe insulin deficiency

goes into remission and doesnt need insulin treatment

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4
Q

What Is the mode of inheritance of monogenic diabetes?

A

autosomal dominant

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5
Q

What type of monogenic diabetes is most common? and what is the gene related?

A

Type 3, gene HNF1a

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6
Q

How can you treat MODY3?

A

sulfonylurea

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7
Q

How do you treat MODY 2 (GCK)?

A

dont need to

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8
Q

How do you treat MODY MODY5, MODY6, MODY7, MODY8?

A

Insulin

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9
Q

List some strongly diabetogenic drugs

A

glucocorticoids, immunosuppressives, antipsychotics

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10
Q

List some weakly diabetogenic drugs

A

Thiazides, B-blockers, statins

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11
Q

Post-transplant diabetes/NODAT (new onset diabetes after transplantation)

Is it more common with solid or non-solid Organs?

A

Solid organs

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12
Q

What drugs are linked to NODAT (new onset diabetes after transplant)? is there any viruses linked to it?

A

Glucocorticoids
calcineurin inhibitors (tacrolimus >cyclosporin)

HCV or CMV virus

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13
Q

Why do immune checkpoint inhibitors cause diabetes?

A

Beta cells have PDL-1 receptors
often presents with DKA

does not reverse! life-long insulin

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14
Q

When to think about MODY?

A

if they act like T1DM but antibodies negative
often young and well

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15
Q

What is the lifetime risk of T1DM depending on family members affected?

A

Sibling 8%
Father 5%
Mother 3%
Mono Twin:
* 150-fold increased risk
* 50% concordance (greater the younger age that 1st twin affected)

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16
Q

What are common haplotype of T1DM?

A

1st chromosome - DR3
2nd chromosome DR4-DQ8

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17
Q

List some Genes related to T1DM?

A

Insulin VNTR (variable number tandem repeats)
PTPN22 (protein tyrosine phosphate)
CTLA4
IL2RA (interleukin-2 receptor-alpha)

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18
Q

List some viral precipitants for T1DM

A

enteroviruses esp coxackie viruses
congenital rubella infection

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19
Q

Briefly describe the pathogenesis of T1DM?

A

B cell destruction, further excaberated by the release of pro inflammatory cytokines

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20
Q

Describe what islet cells look like in T1DM?

A

Marked heterogeneity of islet lesions:
– Normal (no inflammation and normal beta cells)

Intense insulitis (marked infiltration of inflammatory cells)
* CD8 + T cells main inflammatory cell
* Only 10-30% show insulitis at any time.
* Can persist for many years (>10yr) after diagnosis

– Pseudoatrophic (lack of beta cells and no inflammatory cells)

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21
Q

Describe autoantibodies to T1DM

A

note, these are not actually relevant to the pathogenesis
and they also go away over time

– Insulin autoantibodies (IAA)
– Glutamic Acid Decarboxylase antibodies (GAD)
– Islet cell tyrosine phosphatase-2 (IA-2)
– Tetraspanin-7
– Zinc Transporter-8 (ZnT8)

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22
Q

What is teplizumab?

A

anti-CD3 monoclonal antibody

in stage 2 diabetes, and delays Type 1 diabetes by 2years.

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23
Q

Describe some stage 3 studies/drugs for T1DM

A

verapamil, teplizumab, baricitinib

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24
Q

What are some benefits of short acting insulin analogues?

A
  • better control of postprandial hyperglycaemia
  • reduced late hypoglycaemia and nocturnal hypoglycaemia
  • decreased severe hypoglycaemia by 30%
  • no evidence of reduced complication and only very small reduction in HBA1c
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25
Q

How long does Glargine (Lantus) last for?

A

24 hours, begins to wane at 15 hours

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26
Q

How to reduce risk of nocturnal hypoglycaemia with glargine (Lantus)?

A

give with breakfast

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27
Q

Should you split Glargine?

A

similar results with splitting however splitting causes weight gain.

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28
Q

How long does insulin detemir work?

A

20 hours
given twice daily
reduces hypoglycaemia compared with isoprene

less weight gain
binds to albumin

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29
Q

How long does Insulin degludec work?

A

40 hours

less nocturnal hypoglycaemia than evening glargine

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30
Q

How long does insulin isodec work?

A

half life of 8 days. given once a week

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31
Q

What is 500/100 rule in diabetes?

A

carbohydrates ratio: 500/total daily unit of insulin

insulin sensitivity factor: 100/total daily unit of insulin

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32
Q

What is the daily insulin requirement?

A

0.5unit/kg- 50% as basal and 50% as prandial

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33
Q

Describe glycaemia targets for T1DM, and in the case of continuous glucose monitoring.

A

pre-prandial: 4.4-7.2 mmol/L
post-prandial: <10mmol/ml

Time in range 4-10mmol/L: >70%

Time below range <5%

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34
Q

What is the “dawn phenomenon”

A

Rise in blood glucose levels in the morning “dawn” as we have higher GH and cortisol.

when you are giving insulin in the morning it cant respond to that but pumps were good in overcoming dawn phenomenon.

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35
Q

What is the somogy effect?

A

high BSL in the morning due to hypoglycaemic event in the night.

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36
Q

How much does closed-loop pump improve time in range compared to non-closed loop pump?

A

10%

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37
Q

What are methods of cell replacement therapy in T1DM?

A

Whole pancreas transplant
Islet cell transplantation
Stem cell therapy

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38
Q

What are the different levels of hypoglycaemia?

A

Level 1: glucose 3-3.9
Level 2: glucose <3mmol/L
Level 3: hypoglycaemia with altered mental status and/or physical status

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39
Q

What is the normal response to hypoglycaemia?

A

reduce insulin secretion
increased glucagon secretion
increased adrenaline secretion
increased GH and cortisol secretion
behavioural secondary to SNS activation

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40
Q

What are symptoms of hypoglycaemia?

A

Autonomic
- adrenergic: palpitations, tremor, anxiety
- cholinergic: sweating, hunger, parasthesia

Neuroglycopenic
- brain glucose deprivation: confusion, fatigue, weakness, visual changes, seizure, loss of consciousness

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41
Q

Describe the pathophysiology of T2DM

A

Characterised by both insulin resistance and initial hyperinsulinaemia followed by progressive beta cell dysfunction

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42
Q

What is the action of insulin?

A

suppression of lipolysis
stimulation of glucose uptake

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43
Q

When you gain weight, what occurs to adipose tissue?

A

hypertrophy more prominent than hyperplasia

creates hypoxic conditions and adipocyte death

macrophages are recruited to clear the dead adipocytes

dysfunctional adipocytes and macrophages release FFA’s and cytokines e.g. TNFalpha, IL-6

FFAs and these cytokines are toxic to Beta cells

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44
Q

What are some methods of prevention of T2DM?

A

lifestyle intervention
Metformin
pioglitazone
liraglutide

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45
Q

Describe the different diabetic drugs in terms of mechanism, cardiovascular effects, adverse effects

A
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46
Q

What are the diabetic drugs proven to be cardioprotective?

A

SGLT2, GLP-1 agonist

+/- metformin

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47
Q

What is the MOA of SGLT2 inhibitor?

A

Inhibiting glucose reuptake in
proximal tubule

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48
Q

What is the MOA of sulphonylurea? main risk?

A

SU receptor on beta cells stimulating insulin secretion

hypoglycaemia risk, some have increased CV risks

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49
Q

What is the MOA of metformin? S/E?

A

insulin sensitiser
AMP kinase activation

S/E GI symptoms, vit B12 deficiency

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50
Q

What is the MOA of GLP1 agonist

A

Stimulating insulin
inhibiting glucagon secretion
Induces satiety
Delays gastric emptying

better stroke reduction
risk of pancreatitis and medullary thyroid cancer

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51
Q

What are some of the new incretins?

A

orforglipron, cagrilinitide+semalgutide, retratrutide

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52
Q

What are the risk of complications in diabetes in order?

A

Retinopathy >nephropathy > neuropathy > microalbuminuria

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53
Q

Other factors that can affect HBA1c

A

Increased A1c: iron deficiency, B12, deficiency, decreased eryhtopoiesis

Decreased A1c: use of erythropoietin, iron or B12, reticulocytosis, chronic liver disease

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54
Q

What can occur to retinopathy if sudden improvement in BSL?

A

worsening retinopathy if advanced baseline retinopathy and higher HbA1c

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55
Q

Describe screening for diabetic retinopathy

A

screening with retinal photography
- from diagnosis of T2
- within 5y diagnosis for T1DM

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56
Q

What is the treatment for diabetic retinopathy treatment?

A

treat HTN
lower lipids (fenofibrate)
pan retinal photocoagulation (in severe PDR or vision threatening)
anti-VEGF in macular oedema eg ranibizumab

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57
Q

Describe the pathology of diabetic kidney disease

A

thickened GBM
mesangial expansion
podocyte injury
glomerulosclerosis
tubulointerstital fibrosis

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58
Q

Describe natural history of diabetic nephropathy

A

1) increase GFR (kidney hypertrophy)

2) microalbuminuria, hypertension (mesangial matrix expansion, glomerular basement membrane thickening, arteriolar hyallinosis)

3) proteinuria, nephrotic syndrome, decreased GFR (mesangial nodules- kimmesltiel-wilson, tubulo-interstital fibrosis)

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59
Q

How to treat diabetic kidney disease

A

Glycemic control
BP control
RAS inhibition
SGLT2

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60
Q

How do SGLT2s act in diabetic kidney disease?

A

when you use SGLT2 you get an increase of sodium which gets to the macula dense which causes vasoconstriction of afferent arterioles and dilation of efferent which reduces perfusion of glomerulus

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61
Q

What are the common fibres affected in diabetic neuropathy?

A

large fiber neuropathy and small fibre neuropathy common

can also get proximal motor neuropathy, acute mono-neuropathy, compression palsies

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62
Q

Does tight glycemic control in diabetes reduce CV outcomes?

A

NOPE

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63
Q

What is the management of metabolic associated fatty liver disease?

A

lifestyle intervention
metformin may reduce risk of HCC
pioglitazone –> has side effects but good
Liraglutide
SGLT2

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64
Q

What is the effect of gestational diabetes on childhood?

A

more likely to have impaired glucose tolerance in childhood

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65
Q

What is the effect of inadequate glycemic control in the first trimester?

A

Increased risk of diabetic embryopathy:
– anencephaly, microcephaly, congenital heart disease,
renal anomalies, and caudal regression
– Risk directly proportional to HbA1c

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66
Q

What are the glucose targets in pregnancy?

A

fasting plasma glucose < 5.3 mmol/L and
1-h postprandial glucose 7.8 mmol/L or 2-h postprandial 6.7 mmol/L)

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67
Q

Can we use HBA1c in pregnancy?

A

No- HbA1c levels are reduced during pregnancy due to increased rbc turnover

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68
Q

How to prevent risk of pre-eclampsia in patients with type 1 or type 2 diabetes?

A

low-dose aspirin 100–150 mg/day starting at 12 to 16 weeks of gestation

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69
Q

What are the major categories of lipoproteins and their specific apoproteins?

A

chylomicrons - Apo B48
VLDL, IDL, LDL- Apo B100
HDL- Apo-A

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70
Q

What is the mode of inheritance of familial chylomicronaemia syndrome?

A

autosomal recessive disorder
LPL deficiency in 80% of cases

get extreme hypertriglyercaemia

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71
Q

Why is the inheritance of familial hypercholesterolaemia?

A

autosomal dominant
usually see heterozygous, homozygous rare

lack of LDL receptor and APOB , can get gain of function of PCSK9

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72
Q

What is the management of treatment of familial hypercholesterolaemia?

A

Statins
if LDL-C >2.6 still, add in ezetimibe

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73
Q

Describe the diagnosis if familial hypercholesterolaeia

A

Simon Broome Criteria

Definite
* Total cholesterol >7.5mmol/L or LDL> 4.9mmol/L
PLUS one of the following:
* Tenon xanthomas in the patient or 1st or 2nd degree relative
* DNA based mutation of LDLR, apoB or PCSK9

Possible
* Total cholesterol >7.5mmol/L or LDL> 4.9mmol/L
PLUS one of the following:
* MI in 1st degree relative <60 years or 2nd degree relative <50 years
* Raised total cholesterol >7.5mmol/L in a 1st degree relative

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74
Q

What is the MOA of thiazolidenione (e.g. pioglitazone)?

A

PPARgamma receptor activation

S/E Increased risk of heart failure, weight gain, fluid retention and fractures

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75
Q

What is the MOA of alpha glucosidase inhibitor (e.g. Acarbose)

A

Reduce CHO absorption from intestine

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76
Q

What is the mechanism of familial hypertriglyceridaemia?

A

Increased VLDL particle
get increased triglycerides

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77
Q

What is the genetic mutation in familial lipoprotein lipase deficiency?

A

Lipoprotein lipase mutation, APO C-II deficiency

get increased triglycerides and decreased HDL

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78
Q

What conditions can cause secondary hyperlipidaemia?

A

Diabetes mellitus
obesity
hypothyroidism
chronic kidney disease
alcohol excess
cholestasis

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79
Q

List the types of hyperlipidaemia:

A

Type 1:

Type 2: Familial hypercholesterolaemia (IIa)
- this is what we usually refer to.

Familial combined hypercholesterolaemia (IIb)
- overproduction of VLDL by the liver –> raised liver and triglycerides

Type 3: dysbetalipoproteinaemia
- homozygous carrier status (autosomal recessive)
- usually have a precipitating events
- total cholesterol >10, triglyceride >10, xanthomas in 50%

Type 4: Primary hypertriglyceridaemia
- autosomal dominant, polygenic
- reduced lipolysis of triglycerides + hepatic overproduction of VLDL
- Note Chylomicrons NOT PRESENT

Type 5: Mixed hypertriglyceridaemia
- polygenic
- presence of chylomicrons after 12-14 hours of fasting
- elevated levels of VLDL

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80
Q

Describe pituitary anatomy

A
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81
Q

How big is a pituitary microadenoma?

A

<1cm in diameter

majority non-functioning
hypodense after gadolinium due to reduced blood supply

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82
Q

What is the size of a pituitary macroademoma? How to tell if it is function

A

> 1cm in diameter

if change in
- prolactin
- TSH, FT4
- UFC (urianry free cortisol)
- IG-1

Note, even in non-functioning prolactin can be raised

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83
Q

What are causes of pituitary mass lesions other than pituitary tumours?

A

Rathke’s cyst
Chordomas
craniopharyngioma
Meningioma
option gliomas
hypothalamic masses
metastases
carotid artery aneurym
infiltrative disease (sarcoidosis, histiocytosis, tuberculosis, lymphoma)
lymphocytic hypohpysitis

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84
Q

What is an easy way to distinguish between craniopharyngioma and other pituitary masses?

A

BRAFV600E mutation exists in most cases

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85
Q

Describe the pituitary development

A

Lactotroph, somatotroph, and thyrotroph are classified as PIT1 lineage

Corticotroph as TPIT lineage

Gonadotroph as SF1 lineage

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86
Q

How to manage pituitary apoplexy?

A

Often presents as subarachnoid haemorrhage, severe headache, and can get visual changes

manage with steroids

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87
Q

What are causes of hypophysitis?

A

Primary
1) Lymphocytic 70% (often in pregnancy or postpartum)
2) Granulomatous 20$
3) IgG4 related
4) Xanthomatous

Secondary
1) immune checkpoint inhibitor induced
2) Anti-PIT1 antibody syndrome
3) Inflammatory or infectious disorders (sarcoidosis, tuberculosis, histiocytosis)

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88
Q

What is a common cause of inflammatory/infiltrative changes in the infundibulum (pituitary)

A

sarcoidosis

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89
Q

What immune medications are most likely to cause hypophysitis?

A

Anti CTLA-4 + antiPD1/PDL-1 > Anti-CTLA-4 > Anti PD1 > Anti-PDL1

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90
Q

What is the pathophysiology of ICPi- induced hypophysitis?

A
91
Q

Describe the difference in pituitary hormone deficiencies depending on which immune therapy is used

A

CTLA-4 inhibitor-induced IH –> total anterior pituitary hypofunction

PD-1/PD-L1 inhibitor –> isolated ACTH deficiency

92
Q

What hormones are released by the pituitary gland?

A
93
Q

Testing for Acromegaly

A

Acromegaly is a GH producing pituitary tumour.

Screening test: IGF-1

Oral glucose tolerance test (in a normal person, GH reduces in glucose tolerance test, this is a test of exclusion)

94
Q

What subtype of acromegaly is more aggressive?

A

Sparsely granulated subtypes are aggressive and occur in younger patients

Densely granulated somatotropin is more insidious

95
Q

What are some somatostatin receptor ligands that can be used in pituitary adenoma/acromegaly?

A

Ocreotide and lanreotide
Pasiroetide

S/E
cholelithiasis, bradycardia, alopecia

Pasireotide –> reduces insulin and incretin levels so can cause hyperglycaemia. GLP agonists work well

In general these are better in densely granulated, women, SSR2 expression

Reduces response in younger patients, T2 hypersensitivity, sparsely granulated, ALP expression, High Ki-67 index

96
Q

What are treatments for acromegaly?

A

Surgery
Somatostatin receptor ligants

Pegvisomant (modified growth hormone molecule)
- note, normally growth hormones binds to two receptors to work. pegvistomant is targeted in peripheries, so GH is still high but IGF-1 can be normal
- also good in diabetes

Cabergoline
- GH secreting tumours hae D2 receptors, 30% normalise IGF1 levels

Radiotherapy

97
Q

What are clinical features of adult GH deficiency

A

*Altered body composition (increased abdominal adiposity, decreased lean body mass, decreased bone mineral density)

*abnormal lipid profile: elevated total and LDL cholesterol

  • decreased muscle strength and aerobic capacity
  • poor quality of life: low energy, reduced functional capacity, social isolation
98
Q

How to diagnose GH deficiency?

A

Glucagon response <3Ug/L diagnostic
If BMI >30 use lower cut off

99
Q

How does growth hormone replacement therapy affect other hormones?

A

*increases conversion of cortisol to cortisone (therefore inactivates it)
* increases metabolism of T4 to T3
*women taking oral oestrogen’s are relatively resistant to growth hormone

100
Q

What is macroprolactinaemia ?

A

this is prolactin that is bound together by immunoglobulin. occurs in some people and increases half life of prolactin in circulation.

you can check this by doing PEG precipitation which takes out any anticoagulation

101
Q

What are causes of hyperprolactinaemia?

A

Spurious: macroprolactinaemia

Physiological: sleep, stress, pregnancy, breast-feeding

Pharmacological
- DA receptor blockers
- Metaclopramide, domperadone
- opioids
- H2 antagonists
- SSRI- fluoxetine
- oestrogen

Pathologic:
- hypothalamic/pituitary stalk lesions- craniopharyngioma, infiltrative disease, stalk section
- pituitary disease- prolactinoma’s, mixed tumours, non-functioning tumours , primary hypothyroidism

102
Q

What is the pathophysiology of hyperprolactinaemia?

A

Inhibits kisspeptin production in the hypothalamus which in turn inhibits GnRH secretion

Increased hypothalamic dopaminergic tone –> suppresses GnRH pulsatility, blocks the oestrogen induced LH surge

Gonadal steroid production inhibition

Galactorrhoea (not all women get this because of oestrogen deficiency)

103
Q

What prolactin levels indicate a macroprolactinoma vs a non-functioning tumour?

A

> 2000 is macro
<2000 is non-functioning

104
Q

Management of hyperprolactinaemia?

A

Dopamine agonists
Cabergoline (fever side effects because more specific to D2 receptor)

note with cabergoline, some people dont have recurrence even after stopping

105
Q

Indications for neurosurgery in patients with prolactinomas

A
106
Q

What electrolyte derrangmenets can result in a similar picture to diabetes insipidus?

A

Hypercalcaemia and hypokalaemia as they can down regulate aquaporin-2 channels

107
Q

What is copeptin?

A

derived from the cleavage of pre-pro-vasopressin

strong correlation between copeptin and AVP levels

108
Q

When is growth hormone high?

A

second half of the night

109
Q

What factors inhibit growth hormone?

A

FFAs
Glucose
Obesity

110
Q

What is the pathogenesis of Graves disease?

A

T cells present antigen to B cells
CD40-CD154 interaction

note, iscalimab is an anti CD40 MAB
inhibits autoreactive B activation

111
Q

What are risks of antithyroid drugs?

A

Agranulocytosis
Rash and Arthralgia
Hepatotoxicity with PTU
lupus-like vasculitis
Pancreatitis

112
Q

When is PTU preferred over carbimazole?

A

1st trimester of pregnancy

Thyroid storm (PTU more valuable in preventing conversion of T3 –> T4 in periphery)

113
Q

When to avoid giving radiotherapy in Graves disease?

A

active Graves orbitopathy
pregnancy
breastfeeding

114
Q

Graves orbitopathy may run an independent course to the thyrotoxicosis. True or false?

A

True

115
Q

What is the pathophysiology of Graves orbitopathy?

A

TSH receptors on retro-orbital fibroblasts –> TSH receptor antibodies stimulate fibroblasts to secrete glycosaminoglycans –> swelling of retroorbital tissue (muscles and adipose tissue) –> pushes the eye forward (exophthalmos) –> impairs extraocular muscle relaxation (diplopia) –> impairs venous drainage of eyelids (peri orbital oedema) and conjunctiva (chemises) –> optic nerve compression may cause dysthyroid optic neuropathy (DON) and visual loss

116
Q

Treatment of Graves Orbitopathy?

A

Stop smoking
maintain euthyroidism
Avoid radio iodine

Eye specific measures:
-lubricants
- selenum 100ug BD

Mod-Severe
- IV methylprednisone +/- cyclosporin, rituximab or orbital radiotherapy
- Tociluzimab
- teprotumamab (anti-IGF1 receptor)

DON (dysthyroid optic neuropathy) and visual loss –> high dose IV methylpred and if unresponsive urgent surgical decompression

117
Q

Describe the pathogenesis of toxic multinodular goitre and toxic adenoma

A

iodine deficiency leading to hyperplasia –> mutagenesis leading to cell clones containing somatic mutations –> ultimately nodular transformation

118
Q

Describe the treatment of toxic nodular goitre or toxic adenoma

A

Radioactive iodine
surgery

119
Q

Describe how different things present on thyroid scintiscans

A

*Graves –> diffuse uptake
*Multinodular goitre –> patchy uptake
*Toxic nodule –> single area of uptake
* No uptake –> thyroiditis, exogenous thyroid hormones, iodine exposure

120
Q

How to manage thyroiditis

A

Treat symptoms

121
Q

Describe what subacute (De Quervain) thyroiditis is

A

*Post viral infection: granulomatous thyroiditis on pathology
*painful thyroid on palpation
* Biochemical thyrotoxicosis, raised inflammatory markers
* Absent uptake on thyroid scintiscan

122
Q

Describe what silent painless thyroiditis and postpartum thyroiditis is

A

Autoimmune aetiology- thyroid antibodies present
non-painful and inflammatory markers not raised

123
Q

Describe what wolff-chaikoff effect and the Jod-Basedow phenomenon is

A

These phenomenon relate to iodine and the thyroid

wolff-chaikoff effect: large amount of iodine reduces thyroid hormones. return to euthyroid in 24 to 48 hours

Jod-basedow phenomenon: iodine increases thyroid levels. usually have a background of autoimmune disease or nodular goitre. thyrotoxicosis

124
Q

What are the underlying mechanisms that cause iodine induced thyrotoxicosis?

A

Iodine containing agents: kelp tablets, iodinated contrast agents, drugs (Lugols iodine, amiodarone)

1) underlying thyroid disease –> Jod-Basedow phenomenon (transient, managed with anti-thyroid drugs)

2) Underlying normal thyroid –> cytotoxic effect of iodine causing thyroiditis

125
Q

Why does amiodarone induce thyrotoxicosis? What are the types

A

Amiodarone has a lot of iodine in it
it is also stored in fat tissues so can persist for ages

Type 1 AIT –> due to Jod-basedow phenomenon. treat with antithyroid drugs, stop amiodarone.

Type 2 AIT –> destructive thyroiditis, treat with prednisone and beta blockers. self-limited. amiodarone can be continued.

126
Q

What drugs can cause thyroid impairment?

A

*Lithium (hypothyroidism but also graves thyroiditis)
*HAART
*Alemtuzumab- can cause immune reconstitution syndrome
*Immune checkpoint inhibitors
*TKIs (sunitinib, sorafenib)

127
Q

What antibodies are involved in Hashimoto’s thyroiditis?

A

1) Anti-TPO (microsomal) antibodies
2) TSH receptor blocking antibodies

128
Q

When to treat subclinical hypothyroidism?

A

pregnancy
age <70 years and TSH >10mIU/L

129
Q

When to treat subclinical hyperthyroidism?

A

TSH <0.1 mIU/L
TSH 0.1- 0.4 and >65 years
known cardiac disease

130
Q

Which factors are worse for thyroid nodules on US?

A

Composition: Solid
Echogenicity: very hypoechoic
Shape: Taller than wide
Margin: extra-thyroidal extension
Echogenic foci: punctate echogenic foci

micro calcifications are suspicious for papillary cancer

131
Q

What is the most common type of thyroid cancer?

A

Papillary –> excellent prognosis

Other types include
- follicular thyroid cancer: excellent prognosis
- anaplastic thyroid cancer: very aggressive
- medullary thyroid cancer

132
Q

When to use calcitonin to monitor cancer?

A

For medullary thyroid cancer

133
Q

What is the management of thyroid cancer

A

1) surgery- either lobectomy (low risk) or total thyroidectomy
2) radioactive iodine ablative treatment
3) Monitoring- US neck, thyroglobulin (in those who have had a total thyroidectomy)
4) TSH suppression
5) recurrence –> treat by surgery if possible or radioactive iodine

if radioactive iodine resistant –> TKI therapy (lenvatinib)

134
Q

How to treat gestational transient thyrotoxicosis?

A

resolved by 16 weeks when hCG levels have fallen
treatment not required

135
Q

What happens to Graves disease and pregnancy?

A

Often goes into remission during pregnancy but usually relapses postpartum
Treat with PTU in first trimester

136
Q

If you have had radio iodine treatment, how long do you have to wait before conception?

A

6 months

137
Q

How to with hypothyroidism in pregnancy?

A

at time of conception, increase dose of thyroxine by 30% (increased requirements are due to increased TBG levels)

138
Q

What is myxoedema coma and what is the leading cause of death?

A

mortality mainly due to resp failure
hypothermia and reduced level of consciousness
usually precipitating event
obtunded, bradycardic, hypotension, hypoventilation, hypothermia, cool and dry skin

treatment: mechanical ventilation, glucocorticoid therapy, parenteral T4 or T3 treatment

139
Q

What is the treatment of thyroid storm?

A

PTU or carbimazole
beta blockage
potassium iodide- wait at least 1 hour after ATD
glucocorticoids
treat underlying cause

140
Q

What is a TSH receptor?

A

Located on the cell membrane of follicular thyroid cells and is a G protein coupled receptor

141
Q

In circulation, what is thyroid hormone bound to?

A

TBG (75%), transthyretin (10%), and albumin (15%)

142
Q

What is active, T3 or T4?

A

T3 is active

143
Q

What are some physiological effects of thyroid hormone?

A

*Thermogenesis- regulated basal metabolic rate
*activates Na/K/ATPase in cell membrane
*regulates Ca-ATPase in the sarcoplasmic reticulum of muscle cells
*increases the expression of uncoupling protein in BAT

144
Q

What is the most common cause of adrenal insufficiency?

A

Tuberculosis in developing world

Autoimmune adrenalitis in developed world

145
Q

Describe the pathogenesis of autoimmune adrenalitis

A

cytotoxic CD8 T cells and helper CD4 T cells with reactivities against 21-hydroxylase

146
Q

What is autoimmune polyendocrine syndrome

A

A form of adrenal insufficiency

15% are APS-1: adrenal insufficiency, hypoparathyroisim and chronic mucocutaneous candidiasis. AIRE gene mutation

85% APS-2: adrenal insufficiency + autoimmune thyroid disease (Schmidt’s syndrome) + Type 1 diabetes (Carpenter’s syndrome)

Both can get primary ovarian infufficiency

147
Q

What is adrenoleukodystrophy? mode of inheritance?

A

a cause of adrenal insufficiency

X-linked
ALD gene mutation
very long chain fatty acid accumulation

148
Q

What are investigations in adrenal insufficiency?

A

*Synacthen test abnormal (<400nmol/L)
*ACTH measurement- high
*aldosterone low
*renin raised
* DHEAS low
* 21 hydroxylase antibodies +ve

In antibody negative cases –> measure VLCFAs, image the adrenals for TB, metastases, lymphoma, and test for antiphospholipid syndrome

149
Q

How much is a physiological requirement of glucocorticoid?

A

15-25mg hydrocortisone a day

common regimen: 10mg mane, 5mg midday, 5mg 4pm

increased requirements in 3rd trimester of pregnancy

150
Q

What are the steroid conversions?

A

4 dexamethasone, 25mg pred, 100mg hydrocortisone

151
Q

When is cortisol the highest?

A

in the morning

152
Q

What is a normal mineralocorticoid replacement?

A

start with fludrocortisone 100ug/day

adjust according to plasma renin level

hydrocortisone has some mineralocorticoid activity, but prednisone has minimal and dexamethasone has none

153
Q

Why does fludrocortisone dose need to be increased in pregnancy?

A

Progesterone has an anti-minerolcorticoid effect, and fludrocortisone dose usually needs to increase in the 3rd trimester

154
Q

What is Critical Illness- related corticosteroid insufficiency (CIRCI)?

A

Sustained high levels of cortisol resulting in suppression of ACTH due to negative feedback

no single diagnostic test

treatment: hydrocortisone 40mg IV in the AM, 20mg IV in evening

155
Q

What deficiency is involved in congenital adrenal hyperplasia?

A

autosomal recessive, low cortisol

mutations of the gene CYP21A2 causes steroids 21-hydroxylase deficiency

therefore you get 17a hydroxy progesterone build up

diagnosis: synacthin test and 17OHP levels go higher

156
Q

What is the difference between classical and non-class forms of congenital adrenal hyperplasia?

A

Classic form –> diagnosed at birth, high 17OHP, cortisol lowly. Treatment: glucocorticoids +/- mineralocorticoids

Non-Classic form –> can have normal cortisol production, usually have hirsuitism, irregular periods, acne, infertility. 17OHP 30-300. Antiandrogen therapy

157
Q

How does Crinecefont work in congenital adrenal hyperplasia?

A

A corticotrophic releasing factor type 1 receptor antagonist

reduces ACTH levels and in turn androgen levels

allows for physiologic glucocorticoid replacement

158
Q

How to treat primary aldosteronism?

A

adrenalectomy for unilateral hyperaldosteronism

MRA therapy for bilateral forms of primary aldosteronism

158
Q

How to screen for primary aldosteronism? What drugs to sto

A

Aldosterone: renin ratio

stop B-blockers, ACE-inhibitors/ARB, diuretics, DHP CCB

stop diuretics and Spiro for 6 weeks
all others 2-4 weeks

159
Q

What are some confirmatory tests for primary aldosteronism?

A

Adrenal vein sampling
IV saline test
Captopril test

160
Q

What are familial causes of primary aldosteronism?

A

Type 1: due to chimeric gene CYP11B1 (11B hydroxylase) + CYP11B2 (aldosterone synthase) expressed in zone fasiculata –> treat with steroids

161
Q

When can you bypass adrenal vein sampling in aldosteronism?

A

If Adenoma >10mm + hypokalaemia + <35 years of age

162
Q

What is the management of a aldosterone secreting adenoma?

A

Unilateral aldosterone secreting adenoma
- surgery > MRA

Bilateral adrenal hyperplasia
- MRA treatment: spironolactone or eplerenone
- aim for normal BP and K+ and normal plasma renin
- ENaC blockage: amiloride
- trials of aldosterone synthase inhibitors underway

163
Q

What is the role of hounsfield units in adrenal incidentaloma?

A

hounsfield <10 likely non-functioning

suspicious lesions
>4cm in size
>10 HU density on non-contrast CT
<60% washout on delayed (15min) contrast scan
MRI- lack of signal drop out on chemical shift imaging
FDR-PET; SUVmax >5

164
Q

What is the triad of pheochromocytoma?

A

Palpitations, headaches and sweating + Hypertension

165
Q

How to investigate pheochromocytoma?

A

Plasma or urinary metanephrines
>3x ULN

if elevated but <3 xULN then try again or clonidine suppression test. if doesnt get suppressed likely pheo

166
Q

Management of pheochromocytoma?

A

Alpha blockage, then Beta blockage
minimally invasive adrenalectomy

167
Q

Describe approach to suspected Cushing’s syndrome

A
168
Q

Describe screening test for Cushing syndrome

A
169
Q

How to investigate ACTH dependent Cushing’s syndrome

A

MRI pituitary (tumour>10mm)
- CRH test, desmopression test, 8mg dexamethasone test

MRI normal or pituitary tumour <10mm
- bilateral inferior petrosal sinus sampling

170
Q

What are some imaging options for suspected Cushing’s disease?

A

*MRI pituitary
*fine cut whole body CT
*Ga-Dotatate: modified (Tyr3)-octreotide molecule covalently linked to 1,4,7,10-tetraazacyclododecane-1,4,7,10tetraacetic acid (DOTA) combined with the radioactive 68Ga isotope

171
Q

Diagnostic approach to amenorrhoea

A
172
Q

What is that pathophysiology of PCOS?

A
173
Q

What is Rotterdam criteria for PCOS?

A

Need 2 of 3

1) oligo or anovulation
2) clinical and/or biochemical hyperandrogenism
3) Polcystic ovaries on US (20 or more follicles measuring 2-9 diameter), increased ovarian volume >10ml, not recommended for diagnosis <8 years post menarche

174
Q

What are typical lab findings of PCOS?

A
  • elevated testosterone, low SHBG, elevated DHEAS
  • elevated LH/FSH ratio, elevated AMH 2-3x
175
Q

How to treat hirsuitism in PCOS?

A

anti-androgen- cyproterone, spironolactone (with contraception)

176
Q

Describe fertility treatment in PCOS

A

ovulation induction:
*letrozole (aromatase inhibitor)

*clomiphene citrate- oestrogen receptor antagonist

*metformin (not superior to clomiphene)

IVF
Laparoscopic ovarial drilling/diathermy

177
Q

What are investigation findings in functional hypothalamic amenorrhoea?

A

increase cortisol, decrease TSH, Decease T3, decrease IGF-1, decrease leptin

decrease FSH, decrease LH, decrease oestrogen

reduced bone density

178
Q

What is the SRY gene on the Y chromosome?

A

This determines whether you will produce testes or not

179
Q

What is 46XY complete gonadal dysgenesis?

A

Phenotypic female with normal external genitalia including uterus and fallopian tubes (normal mullerian structures)

increase FSH and LH, decrease oestradiol, normal testosterone, 46XY

underdeveloped streak gonads with increased risk dysgermimoma

treatment: HRT, remove streak gonads, fertility

180
Q

What is complete androgen insensitivity syndrome (AIS)

A
  • female external genitalia at birth, but absent mullerian structures (no uterus, fallopian tubes or upper vagina due to MIF produced by fetal testes)
  • present with primary amenorrhoea
  • pubic and axillary hair absent or sparse
  • karyotype 46XY, testosterone N or increased, normal conversion to DHT, LH increased
  • removal of testis to prevent malignant transformation but low risk and necessity/timing of surgery unclear
181
Q

Turner syndrome, genetics + height?

A

45X

short stature
ovarian failure (streak gonads, elevated FSH/LH)

congenital bicuspid aortic valve, coarctation of the aorta

182
Q

How long do you need to have amenorrhoea before you call it menopause?

A

12 months

183
Q

What is Kallmans syndrome?

A

Anosmia + hypogonadotrophic hypogonadism

genes: ANOS1 (or Kal1) X linked recessive Xp22.3

midline defects (cleft lip and palate)
renal agenesis
sensorineural hearing loss
abnormal eye movements
synkinesia

184
Q

What is Klinefelter syndrome?

A

*increase FSH and LH, decrease or low normal testosterone
*semen analysis- azospermia
*DEXA- reduced bone mineral density

185
Q

Describe the calcium handling in the kidney

A

Majority is passively reabsorbed in the proximal tubule and thick ascending limb

Approximately 10% is actively reabsorbed in DCT

There is the calcium sensing receptor in the kidney

186
Q

What is the pathophysiology for Familial hypocalciuric hypercalcaemia?

A

Autosomal dominant
often have hypermagnesaemia
PTH dependent
Inactivating mutation of CaSR
3 variants: CaSR gene, Ga11 gee, AP2S1 gene

correct Mx- do nothing

187
Q

What is the effect of PTH in the kidney?

A

1) calcium reabsorption in the DCT
2) phosphate excretion in the PT
3) stimulates 1 alpha hydroxylase promoting 1, 25 Vit D synthesis

188
Q

What is FGF23 made from?

A

Osteocytes

189
Q

What is the action of FGF23?

A
190
Q

What regulates PTH?

A

1) serum calcium via extracellular calcium sensing receptor –> inhibits release of preformed PTH
2) chronić hypomagnesaemia inhibits PTH release
3) FGF23 inhibits PTH secretion
4) 1,24 vitamin D inhibits PTH secretion
5) Hyperphosphataemia stimulates secretion directly

191
Q

What does PTH act on?

A

Intestine –> increases renal 1,25OH2 Bit D

Kidney –> stimulates Ca reabsorption in distal tubule, stimulates 1alpha hydroxylase, inhibits phosphate reabsorption and bicarbonate reabsorption

Bone –> stimulate bone resorption or formation

192
Q

Management of hyperparathyroidism?

A

Surgery
bisposphonates
cinacalcet –> stimulates calcium sensing receptor

193
Q

Describe the structure of osteoblast

A

Express PTH and Vit D receptors and Alk Phos on cell surface

Produce type 1 collagen, osteocalcin, osteopontin

lay down bone matrix (osteoid) which is then mineralised by deposition of hydroxyapatite

194
Q

What are osteocytes? and their relationship to sclerostin

A

Osteocytes are osteoblasts that remain within corticol bone
act as sensors of mechanical loading
secrete sclerostin tonically that inhibit bone formation

respond to mechanical forces by stopped sclerostin production triggering bone remodelling

195
Q

What are osteoclasts and what do they arise from?

A

Multinucleated Giant cell specialised for bone resorption

arise from monocyte precursors

formation and activation is stimulated by osteoblasts

osteoclasts pump protons, generated by carbonic anhydrase II, into the resorbing compartment to dissolve the bone mineral

Then the collagen-rich bone matrix is degraded by proteases such as cathepsin K and matrix metalloproteinases

196
Q

Discuss what produces Rank ligand?

A

osteocytes and osteoblasts

197
Q

What is RANK and what is OPG?

A

RANK is a receptor for RANKL on osteoclast precursors

OPG is osteoprotegerin - a soluble “decoy” receptor for RANKL

198
Q

When to treat osteoporosis?

A

*T score of -2.5 or less at the femoral neck, total hip, lumbar spine, 33% radius
*fracture of the hip or vertebra regardless of BMD or DXA
* osteopenia at the femoral neck or total hip by DKA with 10-year hip fracture risk >3%
*osteopenia with fracture of proximal humerus, pelvis, or distal forearm

199
Q

How to treat high risk vs very high risk of osteoporosis?

A

High risk –> bisphosphonates
very high risk –> teriparatide or abaloparatide; romosuzumab if not at high CV risk

200
Q

What bone turnover markers to monitor when you start someone on bisphosphonates:

A

CTX at 3 months
P1NP at 6 months

can monitor this in patients on bisphosphonates to establish treatment adherence and response

201
Q

What is the max recommended daily dose of vitamin D?

A

4000 IU

202
Q

What is the role of SERM drugs in fractures?

A

only have benefit in vertebral fractures

203
Q

What is the MOA of bisphosphonates?

A

Bind to hydroxyapatite crystals at sites of active bone remodelling
inhibit bone resorption by inducing osteoclast apoptosis

204
Q

Where is the greatest benefit of bisphosphonates?

A

Greatest effect in sites rich in trabecular bone where baseline turnover is high such as the lumbar spine

205
Q

Describe features of atypical femoral fractures

A

Location: subtrochanteric, femoral shaft or diaphysis

*Usually bilateral
*Atraumatic or minimal trauma
*often a prodome of thigh pain
*biopsy: marked suppression of bone turnover
association with glucocorticoids, RA, PPIs, low vit D

Risk reduces rapidly after stopping bisphosphonate

206
Q

Examples of bisphosphonates vs RankL antibody

A

bisphosphonates: alendronate, risedronate, zoledronic acid

RANKL monoclonal antibody: denosumab

207
Q

What is the MOA of denosumab?

A

RANK L inhibitor
inhibits osteoclastogenesis
causes significant drop in BTO markers (CTX, P1NP)

can get osteonecrosis of the jaww and atypical fractures

208
Q

What is a risk with suddenly stopping denosumab?

A

Rapid loss of BMD on stopping with clusters of vertebral fractures
* Mechanism unclear but may be due to dormant osteoclast precursors that then
undergo synchronous activation on stopping denosmab

209
Q

What is the MOA of teriparatide?

A

Agonist of the PTH type 1 receptor
intermittent PTH preferential stimulates formation
Promotes differentiation of preosteoblasts and inhibits osteoblast apoptosis
Greater effect in trabecular than cortical bone i.e. lumbar spine compared to the hip

210
Q

What is abaloparatide?

A

Analogue of human parathyroid hormone-related peptide
similar to teriparatide

211
Q

What is canonical Wnt pathway?

A

stimulates bone formation

receptor: LRP5/6
co-receptor: frizzled

212
Q

What are sclerostin inhibitors?

A

Sclerostin is produced by osteocytes
sclerostin reduces bone formation. SCLEROSTIN BAD

sclerostin inhibitors inhibit bone resorption by stimulating osteoprotegerin formation

eg romosuzumab

213
Q

Is Denosumab followed by teriparatide good?

A

NO, leads to significant bone LOSS and should be avoided

214
Q

What is the main mechanism of glucocorticoid induced osteoporosis?

A

stop osteoblast formation and cause osteoblast apoptosis

215
Q

What type of fractures are most associated with glucocorticoids?

A

vertebral fractures

the risk of fractures rapidly decreases with glucocorticoids are discontinued

216
Q

When to treat patients for osteoporosis when taking glucocorticoids?

A

1) treat if previous fracture or age >70 years OR prednisone dose >7.5mg/day

2) if no previous fracture and age <70 years and prednisone dose <7.5mg per day. Treat if: DEXA T score <-2.5 OR FRAX MOF >20% or hip fracture >3%

217
Q

Which gene confers the greatest contribution to polygenic obesity from GWAS?

A

FTO gene

218
Q

What is the action of leptin?

A

Secreted by white adipose tissue

low leptin levels are a strong stimulus of food intake (starvation response) but high leptin levels do not induce satiety.

219
Q

What hormones make you full (satiety)? hungry?

A

Satiety: GLP1, PYY3 peptide, cholecystokinin (CKK), Pancreatic polypeptide

Hungry: Ghrelin, neuropeptide Y (NPY), agouti-related peptide, orexin, endocannabinoids, galanin

220
Q

What is a classic MRI finding in charcot arthropathy?

A

MRI- bone marrow oedema, soft tissue oedema, subc

221
Q

Summarise the different insulin and duration of action

A

Insulin isodec- half life of 8 days
insulin degludec- 40 hours (bind to albumin)
Insulin glargine- 24 hours
Insulin detamir- 20 hours (binds to albumin)

222
Q

How to calculate cholesterol levels?

A

HDL + LDL + 20% triglycerides = total cholesterol

223
Q

How to diagnose familial hypercholesterolaemia?

A

Aisha (47 decks)

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