Endo Flashcards

1
Q

Metformin

MOA

Side effects

Contraindications

A

Mechanism of action = Impoves glucose tolerance

  • Activates AMP-activated protein kinase (AMPK)
  • Increases insulin sensitivity
  • Decreases hepatic gluconeogenesis
  • May also reduce gastrointestinal absorption of carbohydrates

Uses

  • T2DM (doesn’t cause hypo or weight gain)
  • PCOS
  • Fatty liver

Adverse effects
Gastrointestinal upsets are common (nausea, anorexia, diarrhoea), intolerable in 20%
Reduced vitamin B12 absorption - rarely a clinical problem
Lactic acidosis* with severe liver disease or renal failure

Contraindications
- !!CKD!!!: NICE recommend that the dose should be reviewed if the creatinine is > 130 µmol/l (or eGFR < 45 ml/min) and stopped if the creatinine is > 150 µmol/l (or eGFR < 30 ml/min)
- May cause lactic acidosis if taken during a period where there is tissue hypoxia. Examples include a recent myocardial infarction, sepsis, acute kidney injury and severe dehydration (D&V)
- Iodine-containing x-ray contrast media: examples include peripheral arterial angiography, coronary angiography, intravenous pyelography (IVP); there is an increasing risk of provoking renal impairment due to contrast nephropathy; metformin should be discontinued on the day of the procedure and for 48 hours thereafter
alcohol abuse is a relative contraindication

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2
Q

Sitagliptin

MOA

Important points

Side effects

A

dipeptidyl peptidase 4 (DPP-4) inhibitor.

Don’t cause weight gain
Don’t cause hypoglycaemia

Side effects
Pancreatitis

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3
Q

Sulphonylurea

MOA

side effects

Examples

A

Stimulate pancreatic beta cells to secrete insulin

Hypoglycaemic episodes
Increased appetite and weight gain
Syndrome of inappropriate ADH secretion - Low Na
Liver dysfunction (cholestatic)

e.g. Gliclazide

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4
Q

Glitazones side effects

A

Weight gain
Fluid retention
Liver dysfunction
Fractures

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5
Q

hypocalcaemia

Symptoms

Causes

A
Tingling
Muscle cramps
Hyperactive deep tendon reflexes
Chovstek + Trousseau
Prolonged QT
Convulsions
Causes
Hypoparathyroid
Low calcium or vitamin D 
infections
some medications, such as phenytoin (Dilantin), phenobarbital, and rifampin
stress
anxiety
intense exercise
irregular magnesium or phosphate levels
kidney disease
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6
Q

What is Exanatide

USe

Adverse effects

A

Glucagon-like peptide-1 (GLP-1) mimetics

  • increase insulin secretion and inhibit glucagon secretion (work as incretin mimetic)
  • Given SC

Typically result in weight loss in T2Dm

Consider adding exenatide to metformin and a sulfonylurea if:
BMI >= 35 kg/m² in people of European descent and there are problems associated with high weight, or
BMI < 35 kg/m² and insulin is unacceptable because of occupational implications or weight loss would benefit other comorbidities.

Adverse effects

  • Main = N&V
  • pancreatitis

Can only continue using if
11 mmol/mol (1%) reduction in HbA1c and 3% weight loss after 6 months to justify the ongoing prescription of GLP-1 mimetics.

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7
Q

What are SGLT2 inhibitors

Use

Examples

Side effects

A

SGLT-2 inhibitors reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.

Use - Diabetes

Examples include canagliflozin, dapagliflozin and empagliflozin.

Important adverse effects include
Urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
normoglycaemic ketoacidosis
increased risk of lower-limb amputation: feet should be closely monitored

Patients taking SGLT-2 drugs often lose weight, which can be beneficial in type 2 diabetes mellitus.

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8
Q

Diagnosis of DKA

Management

A

Key points
glucose > 11 mmol/l or known diabetes mellitus
pH < 7.3
bicarbonate < 15 mmol/l
ketones > 3 mmol/l or urine ketones ++ on dipstick

Management
Fluid replacement: most patients with DKA are deplete around 5-8 litres. Isotonic saline is used initially. Please see an example fluid regime below.

Insulin: an intravenous infusion should be started at 0.1 unit/kg/hour.
Once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started

Correction of hypokalaemia
long-acting insulin should be continued, short-acting insulin should be stopped

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9
Q

What are thiazolinediones

Use

MOA

Example

Adverse effects

A

Thiazolidinediones are a class of agents used in the treatment of type 2 diabetes mellitus. They are agonists to the PPAR-gamma receptor and reduce peripheral insulin resistance. Rosiglitazone was withdrawn in 2010 following concerns about the cardiovascular side-effect profile.

The PPAR-gamma receptor is an intracellular nuclear receptor. It’s natural ligands are free fatty acids and it is thought to control adipocyte differentiation and function.

Example = Pioglitazone

Adverse effects
weight gain
liver impairment: monitor LFTs
fluid retention - therefore CI IN HF
The risk of fluid retention is increased if the patient also takes insulin
INCREASED FRACTURE RISK😒
BLADDER CANCER: recent studies have shown an increased risk of bladder cancer in patients taking pioglitazone (hazard ratio 2.64)

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10
Q

Causes of gynaecomastia

A

Gynaecomastia describes an abnormal amount of breast tissue in males and is usually caused by an increased oestrogen:androgen ratio. It is important to differentiate the causes of galactorrhoea (due to the actions of prolactin on breast tissue) from those of gynaecomastia

Causes of gynaecomastia
physiological: normal in puberty
syndromes with androgen deficiency: Kallman's, Klinefelter's
testicular failure: e.g. mumps
liver disease
testicular cancer e.g. seminoma secreting hCG
ectopic tumour secretion
hyperthyroidism
haemodialysis
drugs: see below
Drug causes of gynaecomastia
spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
gonadorelin analogues e.g. Goserelin, buserelin
oestrogens, anabolic steroids
Digoxin
Isoniazid
Cimetidine
Ketoconazole
Marijuana 
Ethanol + Oestrogen
Azathioprine
Thyroxine

Management = dopamine agonists e.g. bromocriptine

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11
Q

What is Nelson’s syndrome

A

Nelson’s syndrome occurs due to rapid enlargement of a pituitary corticotroph adenoma (ACTH producing adenoma) that occurs after the removal of both adrenal glands (bilateral adrenalectomy) which is an operation used for Cushing’s syndrome. Removal of both adrenal glands eliminates the production of cortisol, and the lack of cortisol’s negative feedback can allow any pre-existing pituitary adenoma to grow unchecked. Continued growth can cause mass effects due to physical compression of brain tissue. Increased production of adrenocorticotrophic hormone (ACTH) can result in increased melanocyte stimulating hormone (MSH) which can result in HYPERPIGMENTATION

Nelson’s syndrome is now rare because bilateral adrenalectomy is now only used in extreme circumstances. After bilateral adrenalectom follow-up should include awareness of Nelson’s syndrome. Monitoring of ACTH level and pituitary MRI are recommended 3-6 months after surgery and regularly thereafter

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12
Q

Diagnosis of IFG and IGT

Difference

A

IFG: A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)

IGT: fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

IFG and IGT denote different denote different abnormalities of glucose regulation (fasting and post-prandial).
- Lower risk of progression to DM in IFG

Management
- Both: Lifestyle advice + annual review

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13
Q

What are gliptins

MOA

Side effects

A

Dipeptidyl peptidase-4 (DPP-4) inhibitors (e.g. Vildagliptin, sitagliptin)

Key points
oral preparation
trials to date show that the drugs are relatively well tolerated with no increased incidence of hypoglycaemia
do not cause weight gain

NICE guidelines on DPP-4 inhibitors
NICE suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems, a thiazolidinedione is contraindicated or the person has had a poor response to a thiazolidinedion

Side effects
Pancreatitis

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14
Q

T1 diabetes blood glucose targets

Management

Illness advice

Other option to multiple daily insulin injections

A

In type 1 diabetics, blood glucose targets:
5-7 mmol/l on waking and
4-7 mmol/l before meals at other times of the day

Aim for 48% HbA1c

Type of insulin
- Offer multiple daily injection basal–bolus insulin regimens, rather than twice‑daily mixed insulin regimens, as the insulin injection regimen of choice for all adults

Twice‑daily insulin detemir is the regime of choice. Once-daily insulin glargine or insulin detemir is an alternative
offer rapid‑acting insulin analogues injected before meals, rather than rapid‑acting soluble human or animal insulins, for mealtime insulin replacement for adults with type 1 diabetes

NICE recommend considering adding metformin if the BMI >= 25 kg/m²

DO NOT STOP using insulin during acute illness

  • Maintain calorie intake
  • Check blood glucose 4 or more times a day and look for ketones; increase insulin dose if glucose rising; advice to get specialist diabetes nurse/gp help if concerned
  • Admit if vomiting, dehydrated, ketotic, a child or pregnant

Insulin pumps (continuous SC insulin) can be considered when disabling hypos have been occurring or person unable to achieve target HbA1c despite careful management

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15
Q

What is pseudo Cushings

A

Pseudo-Cushing’s
mimics Cushing’s
often due to alcohol excess or severe depression
causes false positive dexamethasone suppression test or 24 hr urinary free cortisol
insulin stress test may be used to differentiate

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16
Q

Osmolaritiy

A

2 Na + 2 K + Glucose + Urea (all in mmol/L).

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17
Q

Orlistat criteria for use

A

NICE have defined criteria for the use of orlistat. It should only be prescribed as part of an overall plan for managing obesity in adults who have:

1) BMI of 28 kg/m^2 or more with associated risk factors, or
2) BMI of 30 kg/m^2 or more
3) continued weight loss e.g. 5% at 3 months

Orlistat is normally used for < 1 year

MOA
inhibit pancreatic lipases, which in turn will decrease the absorption of lipids from the intestine

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18
Q

What is Klinefelter’s syndrome

Features

A

Klinefelter’s syndrome is associated with karyotype 47, XXY.

Features
often taller than average
lack of secondary sexual characteristics
small, firm testes
infertile
gynaecomastia - increased incidence of breast cancer
elevated gonadotrophin levels but low testosterone
-  high LH and low testosterone

Diagnosis is by karyotype (chromosomal analysis).

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19
Q

What is hashimotos’ thyroiditis

Features

How to monitor progress

A

Hashimoto’s thyroiditis (chronic autoimmune thyroiditis) is an autoimmune disorder of the thyroid gland. It is typically associated with hypothyroidism although there may be a transient thyrotoxicosis in the acute phase. It is 10 times more common in women

Features
features of hypothyroidism
goitre: firm, non-tender
anti-thyroid peroxidase and also anti-Tg antibodies

Hashimoto’s thyroiditis = hypothyroidism + goitre + anti-TPO

TSH to monitor progress

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20
Q

What is addisonian crisis

Presentation

Causes

Management

A

Causes
Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)
adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
steroid withdrawal

Presentation

  • Shock
  • Hypoglycaemia

Management
- Hydrocortisone 100 mg IM/IV - give 6hrly until stable
- Crystalloid 1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
continue hydrocortisone 6 hourly until the patient is stable.
- Check blood glucose - may need

No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days

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21
Q

Causes of hypogylcaemia

A

Causes of hypoglycaemia can be remembered by the mnemonic EXPLAIN

Exogenous drugs (typically sulfonylureas or insulin)
Pituitary insufficiency
Liver failure
Addison's disease
Islet cell tumours (insulinomas)
Non-pancreatic neoplasms
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22
Q

What is subclinical hypothyroidism

Management

A

Basics
TSH raised but T3, T4 normal
no obvious symptoms

Significance
risk of progressing to overt hypothyroidism is 2-5% per year (higher in men)
risk increased by the presence of thyroid autoantibodies

Management

Not all patients require treatment. NICE Clinical Knowledge Summaries (CKS) have produced guidelines. Note that not all patients will fall within the age boundaries given and hence these are guidelines in the broader sense.

TSH is between 4 - 10mU/L and the free thyroxine level is within the normal range
if < 65 years with symptoms suggestive of hypothyroidism, give a trial of levothyroxine. If there is no improvement in symptoms, stop levothyroxine
‘in older people (especially those aged over 80 years) follow a ‘watch and wait’ strategy, generally avoiding hormonal treatment’
if asymptomatic people, observe and repeat thyroid function in 6 months

TSH is > 10mU/L and the free thyroxine level is within the normal range
start treatment (even if asymptomatic) with levothyroxine if <= 70 years
'in older people (especially those aged over 80 years) follow a 'watch and wait' strategy, generally avoiding hormonal treatment'
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23
Q

What is sick euthyroid

Management

A

Sick euthyroid syndrome = low T3/T4 and normal TSH with acute illness

In sick euthyroid syndrome (now referred to as non-thyroidal illness) it is often said that everything (TSH, thyroxine and T3) is low. In the majority of cases however the TSH level is within the >normal range (inappropriately normal given the low thyroxine and T3).

Changes are reversible upon recovery from the systemic illness and hence no treatment is usually needed.

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24
Q

T1 DM

Cause

Management

Risk

Associated conditions

Genes - hla types

What is LADA

A

Cause
Insulin deficiency from autoimmune destruction of insulin secreting beta cells

Management
NEED INSULIN

Risk

  • DKA
  • Weight loss

Associated conditions
- Other autoimmune (HLA DR3 +/- DR4)

LADA = latent autoimmune diabetes of adults = t1dm with slower progression to insulin dependence in later life

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25
Q

T2DM

Cause

Risk factors

MODY

A

Cause
Decreased insulin secretion +/- Increased insulin resistance

Risk factors

  • Obesity
  • Lack of exercise
  • Calorie and alcohol excess
  • 80% concordance with identical twins (HIGHER THAN T1)

MODY = Maturity onset diabetes of the young

  • AD form of T2DmM affecting young people
  • patients with the most common form are very sensitive to sulfonylureas, insulin is not usually necessar
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26
Q

Causes of DM besides classic T1/T2

A

STEROIDS, anti-his drugs, newer antipsychotics

Pancreatic

  • Pancreatitis
  • Surgery (where >90% pancreas removed)
  • Trauma
  • Pancreatic destruction (haemochromatosis, CF)
  • Pancreatic cancer
Endo
Cushing's disease
Acromegaly
Phaeochromocytoma
Hyperthyroidism
Pregnancy

Others

  • Congenital lipodystrophy
  • Glycogen storage disorders
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27
Q

T2DM diagnosis

A

If the patient is symptomatic:

  • fasting glucose greater than or equal to 7.0 mmol/l
  • random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

If the patient is asymptomatic the above criteria apply but must be demonstrated on TWO SEPARATE OCCASIONS.

Or
a HbA1c of greater than or equal to 48 mmol/mol (6.5%) is diagnostic of diabetes mellitus

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28
Q

Differentiating T1 and T2 DM

A

T1

  • Often starts before puberty
  • HLA D3 and D4 linked
  • cause = autoimmune beta-cell destruction
  • presentation = polydipsia, polyuria, weight loss, ketosis

T2DM

  • older patients usually
  • No HLA association
  • Cause = Insulin resistance/beta-cell dysfunction
  • Presentation = Asymptomatic/complications e.g. MI
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29
Q

Algorithm for T2DM medicationss

A

If HbA1c rises to 48 (6.5%) on lifestyle measures
- 1st line: Standard release metformin
Aiming for HbA1c 48

If HbA1c rises to 58 consider dual therapy:
1. Metformin + DPP4 inhibitor (e.g. sitagliptin)
2. Metformin + Pioglitazone
3. Metformin + SU
4. Metformin + SGLT2 I
Aim for HbA1c 53

If HbA1c rises to 58 consider triple therapy
1. Metformin + DPP4i + SU
2. Metformin + Pioglitazone + SU
3. Metformin + SU/Pioglitazone + SGLT2i
4. Insulin based therapy
Aim for HbA1c 53
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30
Q

General treatment of DM

A

Focus on education and lifestyle advice (eg exercise to ↑insulin sensitivity), healthy eating: —↓saturated fats, ↓sugar, ↑starch-carbohydrate, moderate protein. Foods made just for diabetics are not needed. One could regard bariatric surgery as a cure for dm in selected patients.

Be prepared to negotiate Hba1c target and review every 3–6 months.

Assess global vascular risk; start a high-intensity statin , eg atorvastatin as tolerated, control bp. Give foot-care . (Pre-)pregnancy care should be in a multidisciplinary clinic (ohcs ).

Advise informing dvla and not to drive if hypoglycaemic spells ; loss of hypo-glycaemia awareness may lead to loss of licence; permanent if hgv).

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31
Q

Controlling BP in Diabetes

T1 vs T2

A

T1DM
Treat if BP >135/85 unless albuminuria or 2 or more features of metabolic syndrome in which case 130/80
- ACEi 1st line, ARB if intolerant

T2DM
Target BP <140/80 or 130/80 if kidney, eye or cerebrovascular damage
- ACEi 1st line (except Africo-Carribean where ACEi blue diuretic or CCB)

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32
Q

Looking for complications of DM

A

1) Check injection sites for infection or lipohypertrophy (fatty change): advise on rotating sites of injection if present.
2) Vascular disease: Chief cause of death. MI is 4-fold commoner’. STROKE is twice as common. Address other risk factors—diet, smoking, hypertension. Suggest STATIN (eg atorvastatin 20mg nocte) for all, even if no overt ihd, vascular disease, or MICROALBUMINURIA. Aspirin 75mg reduces vascular events (in context of secondary prevention). Safe to use in diabetic retinopathy.
3) Nephropathy: ( Microalbuminuria is when urine dipstick is −ve for protein but the uA:Cr is ≳3mg/mmol reflecting early renal disease and ↑vascular risk. If ua:cr >3, inhibiting the renin–angiotensin system with an ACEo or sartan, even if bp is normal, protects the kidneys. Spironolactone may also help.

4) Diabetic retinopathy: Blindness is preventable.
Endocrinology - Annual retinal screening mandatory for all patients.
- Refer to an ophthalmologist if pre-proliferative changes or if any uncertainty at or near the macula (the only place capable of 6/6 vision).
- Pre-symptomatic screening enables laser photocoagulation to be used, aimed to stop production of angiogenic factors from the ischaemic retina. Indications: maculopathy or proliferative retinopathy.

5) Cataracts: May be juvenile ‘snowflake’ form, or ‘senile’—which occur earlier in diabetic subjects. Osmotic changes in the lens induced in acute hyperglycaemia reverse with normoglycaemia (so wait before buying glasses).
6) Rubeosis iridis: New vessels on iris: occurs late and may lead to glaucoma.
7) Metabolic complications:
8) Diabetic feet: Look for neuropathy + ischaemia + foot ulcers - test with 10g monofilament fibre, check ankle jerks, Charcot joint?
9) Neuropathy: Symmetrical sensory neuropathy, Mononeuritis multiplex (CN 3, 6), Amytrophy, Autonomic neuropathy

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33
Q

Diabetic retinopathy stages

A

1) Background retinopathy:
Microaneurysms (dots), haemorrhages (blots), and hard exudates (lipid deposits). Refer if near the macula, eg for intravitreal triamcinolone.

2) Pre-proliferative retinopathy: Cotton-wool spots (eg infarcts), haemorrhages, venous beading. These are signs of retinal ischaemia. Refer to a specialist.
3) Proliferative retinopathy: New vessels form. Needs urgent referral.
4) Maculopathy: (Hard to see in early stages.) Suspect if ↓acuity. Prompt laser, intravitreal steroids, or anti-angiogenic agents may be needed in macular oedema. Pathogenesis: Capillary endothelial change → vascular leak → microaneurysms → capillary occlusion → local hypoxia + ischaemia → new vessel formation. High retinal blood flow caused by hyperglycaemia (and ↑bp and pregnancy) triggers this, causing capillary pericyte damage. Microvascular occlusion causes cotton-wool spots (± blot haemorrhages at interfaces with perfused retina). New vessels form on the disc or ischaemic areas, proliferate, bleed, fibrose, and can detach the retina. Aspirin2 (2mg/kg/d) may be recommended by ophthalmologists; there is no evidence that it ↑ bleeding.

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34
Q

Hypoglycaemia symptoms

Causes

A

Autonomic:

1) Sweating
2) Anxiety
3) Hunger
4) Tremor
5) Palpitations
6) Dizziness

Neuroglycopenic
- Confusion
- Drowsiness
- Visual trouble
- Sezures/Comas
- Rarely focal seizures
Mutism, personality change, restlessness + incoherence

Causes: ExPLAIN AND

  • alcohol (binge no food)
  • Aspirin posioning
  • ACEi/Beta blockers
  • Quinine suplhate
  • Aminoglutethamide
35
Q

Interpreting results in hypoglycaemia

A

Hypoglycaemiac hyperinsulinaemia causes

  • Insulinoma
  • Sulphonylurea
  • Insulin injection (no detectable c-peptide)
  • Non insulina hypoglycaemic syndrome

Insulin low or undetectable, no excess ketones
- Non-pancreatic neoplasm, anti -insulin receptor antibodies

Low insulin, high ketones

  • Alcohol
  • Pituitary insufficiency
  • Addison’s disease
36
Q

Hypoglycaemia management

A

If conscious, orientated, and able to swallow
==> give 15–20g of quick-acting carbohydrate snack (eg 200mL orange juice) and recheck blood glucose after 10–15mins (repeat snack up to 3 times).

If conscious but uncooperative
==> squirt glucose gel between teeth and gums.

In unconscious patients/ low GCS or those not responding to these measures
==> Glucose glucose IV (eg 10% at 200mL/h if conscious; 10% at 200mL/15mins if unconscious), OR
==> give glucagon 1mg IV/IM (will not work in malnourished patients). Expect prompt recovery.

Once blood glucose >4.0mmol/L and patient has recovered, give long-acting carbohydrate (eg slice of toast).

37
Q

What is HHS

Diagnosis

Risks

Management

A

Hyperglycaemia hyperosmolar state

Seen in unwell patients with type 2 dm.
The history is longer (eg 1wk), with marked dehydration

Diagnosis
1) Hypovolaemia
2) Glucose >30mmol/L.
with Ketonaemia stays <3mmol/L and pH >7.3.
3) Osmolality is typically >320mosmol/kg:

Risks
OCCLUSIVE EVENTS are a danger (focal cns signs, chorea, dic, leg ischaemia/rhabdomyolysis)—give LMWH prophylaxis to all unless contraindication

Management
1) Rehydrate slowly with 0.9% saline ivi over 48h, typical deficits are 110–220mL/kg, ie 8–15L for a 70kg adult.

2) Replace K+ when urine starts to flow

Only use insulin if blood glucose not falling by 5mmol/L/h with rehydration or if ketonaemia—start slowly 0.05u/kg/h.

Keep blood glucose at least 10–15mmol/L for first 24 hours to avoid cerebral oedema.
Look for the cause, eg mi, drugs, sepsis, or bowel infarct.

Give LMWH to ALL

38
Q

DKA

Pathology

Typical picture

Triggers

Diagnosis

Tests

A

Excess glucose but lack of insulin so can’t be taken into cells and metabolised
==> Body pushed into starvation like state where ketoacidosis is only mechanism of energy production
CAN BE DEADLY

Typical picture
- Gradual drowsiness, vomiting and dehydration in T1DM

Do glucose in all with unexplained abdominal pain, vomitting, polyuria, polydipsia, lethargy, anorexia, ketotic breath, dehydration, coma or deep breathing (Kussmaul)

Triggers

  • Infection
  • Surgery
  • MI
  • Pancreatitis
  • Chemo
  • Antipsychotics
  • Wrong insulin dose/non compliance

Diagnosis

1) glucose > 11 mmol/l or known diabetes mellitus
2) pH < 7.3 or bicarbonate < 15 mmol/l
3) ketones > 3 mmol/l or urine ketones ++ on dipstick

Tests

  • ECG + CXR
  • Urine dip + MSU
  • Blood : Cap + lab glucose, ketones, pH (use venous blood), U&Es, HCO3- , osmolality, blood culture, FBC
39
Q

Signs that DKA needs transfer to HDU/ICU for monitoring and central venous access

A
  • Blood ketones > 6
  • Venous bicarb <5
  • pH <7.0
  • K <3.5
  • GCS <12
  • O2 sats less than 92% on air
  • sBP <90
  • Pulse <60 or >100
  • Anion gap >16
40
Q

Management of DKA

A

ABC - 2 large bore cannulas

1) Start fluid 1L 0.9% saline over 1 h (if sBP <90 give 500ml bolus and reassess in 15min - if still same give another bolus and call senior)
- 1st 1L over 1h then: 1L over 2h, 1L over 2h, 1L over 4h, 1L over 4 h, 1L over 8
NB: Typical fluid deficit = 100ml/kg

Test: venous blood gas for pH, bicarb; bedside and lab glucose + ketones, u&es, FBC, CRP; CXR, ECG

2) Insulin
- Infuse at 0.1U/kg/h (max 15U)
- Continue pts long term insulin
Aim is fall in ketones of 0.5mmol/L/h pr rise in venous bicarb of 3mmol/L/h with fall in glucose of 3mmol/L/h

Check hourly Blood glucose and ketones
Check VBG: pH, bicarb, K+ at 2h, 4h, 8h, 12h and 24h minimum

3) Continue fluids and assess need for K
Typical deficit = 3-5mmol/kg
DONT ADD K to 1st bag. Thereafter add as per VBG:
>5.5 Nil
3.5-5.5 == 40mmol
<3.5 == HDU/ICU!!!

4) Consider catheter if not passed urine by 1h. aim for 0.5ml/kg/h. Consider NG tube if vomiting or drowsy
- Start ALL on LMWH

5) AVOID HYPOGLYCAEMIA
- When blood glucose <14 - start 10% glucose at 125ml/h to run alongside saline

6) Continue fixed rate insulin infusion until ketones <0.6, venous pH >7.3 and venous bicarb >15

41
Q

DKA Complications

A
Cerebral oedema
Aspiration pneumonia
Hypokalaemia
Hypophosphataemia
Thromboembolism
42
Q

Hypopituitarism

Order of hormones affected

Causes

A

Decreased secretion of anterior pituitary hormones. Order of hormones affected

1) GH
2) Gonadotrophins (FSH + LH)
3) TSH
4) ACTH
5) Prolactin

Causes

1) Hypothalamus: kalman’s syndrome, Tumour, Infection, Inflammation, Ischaemia
2) Pituitary stalk: Tumour, Surgery, Mass lesion (craniopharyngioma), Memingioma, Carotid artery aneurysm
3) Pituitary: Tumour, Irradiation, Inflammation, Autoimmunity, Infiltration (Amyloid, Haemochromatosis, Mets), Ischaemia (Pituitary apoplexy, DIC, Sheehan’s syndrome)

Panhyppituitarism = deficiency of all anterior hormones usually causesd by

  • Irradiation
  • Surgery
  • Pituitary tumour
43
Q

Hypopituitarism features

A

1) GH lack
- Central obesity
- Atherosclerosis
- Loss of strength/balance/well being/exercise ability
- Low CO
- Osteoporosis
- Low glucose

2) Gonadotropin lack
Males: ED, Loss of libido, Loss of muscle bulk, Hypogonadism
Females: Oligo/amenorrhoea, Reduced fertility, Reduced libido, breast atrophy, dyspareunia

3) Thyroid lack
Hypothyroidism

4) Cortocopin lack
Adrenal insufficiency BUT no skin pigmentation as ACTH low

5) Prolactin: Rare, absent lactation

Features of the cause
- Mass effect of tumour

44
Q

Hypopituitarism investigation

A

Basal tests

  • IGF1 (GH)
  • LH + FSH
  • TSH, t4
  • Cortisol
  • Prolactin
  • U&Es

Dynamic tests
1) Short Synacthen test to assess adrenal axis
2) ITT: To assess adrenal and GH axis
CI: Epilepsy, Heart disease, Renal failure
- IV insulin to induce hypoglycaemia ==> Stress to increase cortisol and GH secretion. Glucose must fall below 2.2 and pt should become symptomatic when cortisol + GH are taken
Normal: GH >20, Peak cortisol >550nmol/L
3) Arginine + GH releasing hormone test
4) Glucagon stimulation test is alternative when ITT CI

Management - Refer to endo

  • Hydrocortisone for secondary adrenal failure - MUST BE FIRST
  • Thyroxine if hypothyroid (but TSH useless for monitoring)
  • Oestrogen/testosterone as relavent
  • Gonadotropin therapy needed to induce fertility for M and F
  • GH: Somatotrophin mimics GH
45
Q

What is pituitary apoplexy

Presentation

Management

A

Rapid pituitary enlargement from a bleed into a tumour can cause mass effect
CVD collapse due to acute hypopituitarism and death

Suspect if acute onset headache, meningism, reduced GCS, ophthalmoplegia/visual field defect, especially if known tumour

Management
- Urgent hydrocortisone 100mg IV and meticulouus fluid balance
+/- Cabergoline (dopamine agonist, if prolactinoma)
+/- Surgery

46
Q

Hyperprolactinaemia

Symptoms

Causes

A
Symptoms
Female
- amenorrhoea or oligomenorrhoea
- infertility
- Galactorrhoea
Also low libido, weight gain, dry vagina

Male

  • ED
  • Reduced facial hair
  • Galactorrhoea

May present late with osteoporosis or local pressure effects from the tumour

Causes
1) Excess production from pituitary (prolactinoma)
2) Disinhibition, by compression of pituitary stalk, reducing local dopamine levels
3) Use of a dopamine antagonist
Prolactin 1000-500 can be any by >5000 likely prolactinoma with macro adenoma (>1cm having highest levels)

Physiological: pregnancy; breastfeeding; stress
Drugs: metoclopramide; haloperidol; methyldopa; oestrogens; ecstasy; antipsychotics, Chlorpromazine
Diseases: prolactinoma: micro or macroadenoma; Stalk damage: pituitary adenomas, surgery, trauma; hypothalamic disease: craniopharyngioma

47
Q

Prolactinoma management

A

Dopamine agonists (bromocriptine or cabergoline) = 1st line

Surgery never really needed

48
Q

Acromegaly

Cause

Symptoms

Signs

Tests

Complications

Management

Follow up

A

High secretion of GH from a pituitary tumour (99%) or hyperplasia e.g. ectopic GH releasing hormone from a carcinoid tumour

GH stimulates bone and soft tissue growth through IGF1)

Symptoms

  • Acroparaesthesia
  • Amenorrhoea
  • Headache
  • Sweating/snoring
  • Nothing fits anymore as bigggg

Signs:

  • Big hands, jaw and feet
  • Coarsening face; wide nose
  • Big supraorbital ridges
  • Macroglossia
  • Widely spaced teeth
  • Acanthosis nigricans
  • OSA
  • Carpal tunnel signs in 50%
  • Proximal weakness and arthropathy

Complications

  • Impaired glucose tolerance
  • Vascular: High BP, LVH, Cardiomyopathy, Arrythmias, IHD, Stroke
  • Neoplasia: Increased colon cancer risk

Tests - PULSATILE RELEASE SO DON”T MEASURE BASAL
NB: Normal GH secretion inhibited by high glucose and GH hardly detectable. In acromegaly, GH release fails to suppress

1) IGF1 = 1st line - high
2) OGTT to confirm
In normal patients GH is suppressed to < 2 mu/L with hyperglycaemia
in acromegaly there is no suppression of GH
may also demonstrate impaired glucose tolerance which is associated with acromegaly
3) MRI may detect tumour

Management
TRANSPHENOIDAL SURGERY = 1st line
If it fails
- Somatostatin analogues e.g. Octreotide
- GH receptor antagonist - Pegvisomant
- Radiotherapy - meh

Follow up
- Yearly GH, IGF1 +/- OGTT; visual fields; vascular assessment; BMI

49
Q

What is Diabetes insipidus

Symptoms

Causes

Management

A

Large volumes (>3L/day) of dilute urine due to impaired water resorption by the kidney, because of REDUCED ADH secretion from the posterior pituitary (cranial di) or impaired response of the kidney to ADH (nephrogenic di).

Symptoms
Polyuria, Polydipsia, dehydration
Signs of hypernatraemia

Causes

1) Cranial
- Tumour
- Trauma
- Infiltration
- Haemorrhage
- Infection

2) Nephrogenic
- Drugs: Lithium, Demeocycline
- Metabolic: Low K+, High Ca2+
- CKD
- Post obstructive uropathy

Tests
- Serum osmolality: High; Urine osmolality: Low
- water deprivation test
==> Cranial: Urine osmolality increases AFTER desmopressin
==> Nephrogenic: No increase in urine osmolality after desmopressin

Treatment
Cranial: Desmopressin
Nephrogenic: Bendrofluomethiazide PO/34h

50
Q

Cushings syndrome causes

A

Most common = exogenous
Endogenous most common = Cushing’s disease (Pituitary adenoma)

ACTH dependent cause
• Cushing’s disease: Bilateral adrenal hyperplasia from an acth-secreting pituitary adenoma. Low-dose dexamethasone test leads to no change in plasma cortisol, but 8mg may be enough to more than halve morning cortisol (as occurs in normals).
• Ectopic ACTH production: Small cell lung cancer and carcinoid tumours.
Pigmentation (due to ↑↑acth)
Hypokalaemic metabolic alkalosis (↑↑cortisol leads to mineralocorticoid activity)
Weight loss, hyperglycaemia.
Classical features of Cushing’s are often absent. Dexamethasone even in high doses (8mg) fails to suppress cortisol production.
• Rarely, ectopic crf production: Some thyroid (medullary) and prostate cancers.

ACTH-independent causes (↓acthdue to −ve feedback)
• Iatrogenic: Pharmacological doses of steroids (common).
• Adrenal adenoma/cancer: (May cause abdo pain ± virilization in ♀) Because the tumour is autonomous, dexamethasone in any dose won’t suppress cortisol.
• Adrenal nodular hyperplasia: (As for adrenal adenoma, no dexamethasone suppression.)
• Rarely: Carney complex. McCune–Albright syndrome.

51
Q

Cushings syndrome

Symptoms

Signs

A

Symptoms
↑Weight; mood change (depression, lethargy, irritability, psychosis); proximal weakness; gonadal dysfunction (irregular menses; hirsutism; erectile dysfunction); acne; recurrent Achilles tendon rupture; occasionally virilization if ♀.

Signs
Weight redistribution
-  Central obesity
-  moon face
-  Buffalo hump

Skin changes

  • Thinning
  • Striae
  • Bruises
  • Poor healing

Diabetes

Proximal myopathy

Osteoporosis

Mental changes

HYPERTENSION, hypernatraemia, hypokalaemia

52
Q

Cushings syndrome tests

Management

A

1st line: 9am and midnight plasma ACTH (and cortisol) levels. If ACTH is suppressed then a non-ACTH dependent cause is likely such as an adrenal adenoma
- Normally cortisol <50nmol; no suppression in Cushings syndrome

2nd line tests
Low and high dose dexamethasone suppression

Cortisol result Interpretation
Not suppressed by low-dose dexamethasone
==> Cushing’s syndrome not due to primary causes, i.e. likely secondary to corticosteroid therapy

Not suppressed by low-dose, but suppressed by high-dose dexamethasone
==> Cushing’s disease

Not suppressed by low- or high-dose dexamethasone ==> Ectopic ACTH syndrome likely

Management

  • Iatrogenic: Stop meds if possible
  • Cushings disease: Trans-sphenoidal removal of tumour
  • Adrenal adenoma: Adrenalectomy
  • Ectopic ACTH: Surgery if tumour local and hasn’t spread
53
Q

Addisons disease

Causes

Symptoms

Signs

Investigations

A

Primary adrenocorical insufficiency
- Glucocorticoid + mineralocorticoid deficiency

Causes

  • 80% autoimmune in the UK
  • TB WW
  • Adrenal mets (from lung, breast, renal cancer)
Symptoms
Lean, tan
Tired
Muscle weakness and fatigue 
Hypotension
Abdo pain
Depression
Dehydrated

Signs

  • Hypotension
  • Hyperkalaemia
  • High ACTH due to cortisol deficiency ==> increased pigmentation
  • Crisis: collapse, shock, pyrexia

Investigations
Definitive = ACTH stimulation test (short Synacthen test). Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM. Adrenal autoantibodies such as anti-21-hydroxylase may also be demonstrated.

If an ACTH stimulation test is not readily available then sending a 9 am serum cortisol can be useful:
> 500 nmol/l makes Addison’s very unlikely
< 100 nmol/l is definitely abnormal
100-500 nmol/l should prompt a ACTH stimulation test to be performed

Management
Hydrocortisone: usually given in 2 or 3 divided doses. Patients typically require 20-30 mg per day, with the majority given in the morning dose
+ fludrocortisone

54
Q

What Is primary hyperaldosteronism

Symptoms

Causes

Tests

Management

A

Excess release of aldosterone, independent of RAS ==> Sodium and water retention + less renin release

Symptoms
- Often asymptomatic or signs of hypokalaemia: Weakness, cramps, paraesthesia, pyuria, polydipsia

Causes:
1) Adrenal adenoma = Conn’s syndrome
2) Bilateral adrenocortical hyperplasia = 1/3
Others: Adrenal carcinoma

Hypernatraemia, hypokalaemia

Tests:

  • PLASMA ALDOSTERONE TO RENIN RATIO: High
  • HRCT abdomen and adrenal vein sampling is used to differentiate between unilateral and bilateral sources of aldosterone excess
  • Adrenal Venous Sampling (AVS) can be done to identify the gland secreting excess hormone in primary hyperaldosteronism

Management

  • Conn’s: Laparoscopic adrenalectomy. Spironalactone for 4 weeks pre-op controls BP and K+
  • Hyperplasia: treat medically with Spironolactone or Amiloride
  • Adrenal carcinoma: Surgery
55
Q

What is secondary hyperaldosteronism

A

Due to a high renin from ↓renal perfusion, eg in renal artery stenosis, accelerated hypertension, diuretics, ccf, or hepatic failu

56
Q

Bartter’s syndrome

A

LOH channels

Normal BP
High renin + aldosterone production
Hypokalaemia + Metabolic alkalosis

Rx:

  • K+ replacement
  • NSAIDS + ACEi
57
Q

What is phaeochromocytoma

Silly rule for them

Features

Investigations

Treatment

A

Catecholamine producing tumour arising from sympathetic paraganglia cells, which are chromafin cells found in adrenal medulla

10% malignant
10% extra-adrenal
10% bilateral
10% familial

features
Heart: Tachy, palpitations, dyspnea, angina, Faints, MI/LVF
CNS: Headache, visual disorder, dizzy, tremor, numbness, fits, encephalopathy, Horner’s syndrome, SAH/CNS haemorrhage
Psych: Anxiety, Panic, Confusion, Episodic psychosis
GI: Abdo pain over tumour site, masss
Other:s Sweat/flushes, heat intolerance

Investigations

  • 24h Urine METANEPHRINES
  • Localisation: Abdo CT/MRI

Treatment

  • Alpha blockage e.g. phenoxybenzamine BEFORE others to avoid crisis from unopposed alpha adrenegic stimulation
  • Beta block too if heart disease or tacky e.g. propranolol
  • Consult the anesthatist
58
Q

MEN syndromes

A

MEN 1
Parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia
Pituitary (70%)
Pancreas (50%): e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration)
Also: adrenal and thyroid

Most common presentation = high calcium

Men 2a
Medullary thyroid cancer (70%)
Parathyroid (60%)
Phaeochromocytoma

Men 2b
Medullary thyroid cancer
Phaeochromocytoma
Marfanoid body habitus
Neuromas
59
Q

What is hirsuitism

Causes

Investigations

A

Male pattern hair growth in women

Causes

  • Familial
  • Idiopathic
  • Increased androgen secretion by ovary (PCOS, Ovarian cancer), the adrenal gland (CAH, Cushing’s syndrome, adrenal cancer) or drugs (steroids)
Investigations:
US: bilateral polycystic ovaries in PCOS
Bloods
- High testosterone (if >6 look for androgen producing arenal or ovarian tumour)
- Low sex-hormone binding globulin
- High LH/FSH ratio (not consistent)
- TSH
- Lipids

Management
Healthy eating, optimize weight, shaving; laser photoepilation; wax; creams, eg eflornithine, or electrolysis (expensive/time-consuming, but effective); bleach (1:10 hydrogen peroxide).

  • Oestrogens: combined contraceptive pill (ohcs p[link])—Yasmin® is one choice as its progestogen, drospirenone, is an antimineralocorticoid. Alternatively, co-cyprindiol provided there are no contraindications, such as uncontrolled hypertension and current breast cancer. Stop co-cyprindiol 3–4 months after hirsutism has completely resolved because of increased vte risk. If cocs are contraindicated or have not worked (after 6/12), refer the woman to secondary care for specialist treatment:
  • Metformin (helps with insulin resistance) and spironolactone are sometimes tried.
  • Clomifene is used for infertility (a fertility expert should prescribe).
60
Q

What is virilism

Investigation

A

Onset of amenorrhoea, clitomegaly, deep voice, temporal hair recession and hisuitism

Look for androgen secreting adrenal or ovarian tumour

61
Q

What is erectile dysfunction

A

Erections come from neuronal release of NO, which via cGMP and Ca hyperpolarize and thus relaxes vascular and trabecular SM cells ==> engorgement

Organic causes
1) Smoking
2) Alcohol
3) Diabetes (reduce NO + autonomic neuropathy)
Also endocrine
- Hypogonadism
- Hyperthyroidism
- High prolactin
Neuro
- Cord lesions
- MS
- Autonomic neuropathy
Pelvic surgery
Renal or hepatic failure

Drugs

  • Digoxin
  • beta blocker
  • Diuretics
  • Antipsychotic
  • Antidepressents
  • Finasteride

investigations
- U&Es, LFTs, TSH, FSH, Lipids, Testosterone , Prolatctin
+/- Doppler
- Check penile sensation (if not ok - probably CNS problem)

Management

  • Treat causes
  • Counselling
  • Oral phosphodiesterase (PDE5) inhibitors Sildenafil 25-100mg 1/2-1h pre sex (food and alcohol upset absorption)
62
Q

What are phosphodiesterase inhibitors

Example

Side effects

Contraindications

A

PDE5 inhibitors increase cGMP

E.g. Sildenafil

Side effects

  • Headache
  • Flushing
  • Dyspepsia
  • Stuffy nose
  • Transient blue-green tinging of vision

CI

  • Concurrent use of nitrates
  • BP high or systolic <90/arrhythmia
  • Degenerative retinal disorders
  • Unstable angina/stroke <6months ago
  • MI <90 days ago

Cautions

  • Bleeding (peptic ulcer)
  • Marked hepatic/renal impairment
  • Peyronies disease
  • Risk of priapism (SCD, Myeloma, Leukaemia)
  • Dyspnoea on minimal effort
  • Complex antihypertensive regimens
63
Q

TFT axis

What raises TBG

A

TSH released from anterior pituitary
Stimulates thyroid to produce t3 + t4

NB most plasma t3 and t4 is protein boung (e.g. thyroxine binding globulin -TBG)

Raised TBG (causes raised TOTAL T3+T4)

  • Pregnancy
  • Oestrogen therapy
  • Hepatitis

Low TBG

  • Neoprotic syndrom (protein loss)
  • Malnutrition (protein loss)
  • Drugs (androgens, steroids, phenytoin)
  • Chronic liver disease
  • Acromegaly
64
Q

Thyroid specific tests

A

TSH, free T3, T4

Autoantibodies

  • TPO/ TG: Hashimoto’s or Graves
  • TSH receptor antibody: May be high in Graves

Serum TG:
- Useful in cancer monitoring

US
- Distinguishes cystic from solid nodules

Isotope scan

65
Q

Interpret TFTs

High TSH, low T4

High TSH, normal T4

High TSH, high T4

A

High TSH, low T4
= Hypothyroid

High TSH, normal T4
= Treated hypothyroid or subclinical hypothyroidism

High TSH, high T4
= TSH secreting tumour or thyroid hormone resistance

66
Q

Interpret

Low TSH, High T3/T4

Low TSH, normal T4 and T3

Low TSH low T4

Low TSH, Low T4/T3

A

Low TSH, High T3/T4
= Hyperthyroidism

Low TSH, normal T4 and T3
= Subclinical hyperthyroid

Low TSH low T4
= Central hypothyroidism (hypothalamic or pituitary disorder)

Low TSH, Low T4/T3
= Sick euthyroid or pituitary disease

67
Q

Thyrotoxicosis

Symptoms

Signs

A

Symptoms

  • Weight loss; Increased appetite
  • Diarrhoea
  • Overactive
  • Sweats; Heat intolerance
  • Palpitations; Tremor
  • Irritability; Labile emotions
  • Oligo-menorrhoea +/- infertility

Signs

  • Pulse: Fast/Irregular
  • Warm moist skin
  • Fine tremor
  • Thin hair
  • Lid lag; lid retraction
  • May be goitre, thyroid noodles or bruit depending on cause
68
Q

Signs of Graves disease

A

Eye: Exophthalmous appearance pf protruding eyes), Proptosis (eyes protrube beyond the orbit) Ophthalmoplegia (especially of upward gaze) - due to muscle swelling and fibrosis

Pretibial myxoedema: Odematous swellings over lateral malleoli

Thyroid acropachy

69
Q

Graves disease investigations

Presentation

Triggers

Associated conditions

Management options
- Their risks

A

Low TSH (suppressed)
High T3 and T4
TSH R ab +ve in 90%
TPO and TG antibodies in 75%

Presentation

  • Hyperthyroid
  • SMOOTH thyroid enlargement

Triggers: Stress, infection, childbirth

Associated: Other AI disease e.g. Vitiligo, T1DM, Addison’s disease

Management
Treatment options include titration of anti-thyroid drugs (ATDs, for example carbimazole), block-and-replace regimes, radioiodine treatment and surgery. Propranolol is often given initially to block adrenergic effects

ATD titration
Carbimazole is started at 40mg and reduced gradually to maintain euthyroidism
Typically continued for 12-18 months
patients following an ATD titration regime have been shown to suffer fewer side-effects than those on a block-and-replace regime

Block-and-replace
Carbimazole is started at 40mg
thyroxine is added when the patient is euthyroid
treatment typically lasts for 6-9 months

The major complication of carbimazole therapy is agranulocytosis

Radioiodine treatment
Contraindications include pregnancy (should be avoided for 4-6 months following treatment) and age < 16 years. Thyroid eye disease is a relative contraindication, as it may worsen the condition
the proportion of patients who become hypothyroid depends on the dose given, but as a rule the majority of patient will require thyroxine supplementation after 5 years

Surgery
- Usual thyroidectomy total - Its become hypothyroid so require lifelong thyroid replacement

70
Q

Toxic multi nodular goitre

Causes

Investigations

A

Thyroid gland that contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism.

Causes
- Seen in elderly + iron deficient areas

Investigations

  • TSH supressed, High T3/T4
  • Nuclear scintigraphy reveals patchy uptake.

Management
Radioiodine therapy.
- CI: Pregnancy, active hyperthyroid (risk of thyroid storm), lactation

71
Q

Complications of thyroid surgery

A

1) Recurrent laryngeal nerve damage

2) Hypoparathyroidism: Low PTH ==> Low Ca, High Ph

72
Q

De Quervan’s thyroiditis

Cause

Phases

Investigations

A

Subacute thyroiditis (also known as De Quervain’s thyroiditis and subacute granulomatous thyroiditis) is thought to occur following viral infection and typically presents with hyperthyroidism.

There are typically 4 phases;
phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
phase 2 (1-3 weeks): Euthyroid
phase 3 (weeks - months): Hypothyroidism
phase 4: Thyroid structure and function goes back to normal

Investigations
Thyroid scintigraphy: globally REDUCED uptake of iodine-131
ESR + CRP: HIGH

Management

  • Usually self-limiting - most patients do not require treatment
  • Thyroid pain may respond to aspirin or other NSAIDs
  • in more severe cases steroids are used, particularly if hypothyroidism develops
73
Q

Initial presentation of DM - how to figure out if T1 or T2

A

Consider measuring C-peptide after initial presentation if there is difficulty distinguishing type 1 diabetes from other types of diabetes. Be aware that C-peptide concentrations have better discriminative value the longer the interval between initial presentation and the test.

74
Q

Tertiary hyperparathyroidism blood findings

A
PTH = raised 
Calcium = raised 
Vitamin D = normal 
Phosphate = low-normal
ALP = raised
75
Q

Most common cause of primary hyperparathyroidism

Symptoms

A

80%: solitary adenoma
15%: hyperplasia
4%: multiple adenoma
1%: carcinoma

Symptoms
polydipsia, polyuria
peptic ulceration/constipation/pancreatitis
bone pain/fracture
renal stones
depression
hypertension
76
Q

Diabetic neuropathy management

A

first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin

If the first-line drug treatment does not work try one of the other 3 drugs
Tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
pain management clinics may be useful in patients with resistant problems

NB: Amitryptilline can cause urinary retention

77
Q

How many units of insulin in 1ml

A

100

78
Q

Effect of iron on thryroid

A

Reduces the absorption of thyroxine

79
Q

Effect of haemolytic anaemia on hba1c

A

Underestimates glucose levels

80
Q

Splenectomy effect on HbA1c

A

Falsely high HbA1c due to increased life span of RBCs

81
Q

Myxoedema coma management

A

Levothyroxine is used to replace the low levels of thyroid hormone causing the patient’s symptoms.
+
Hydrocortisone is given to treat adrenal insufficiency. Patients suffering from a myxoedemic coma due to secondary hypothyroidism are at risk of hypopituitarism due to the location of the lesion. Thus patients are treated as presumed adrenal insufficiency until it has been ruled out.

82
Q

Thyrotoxic storm treatment

A

Thyrotoxic storm is treated with beta blockers, propylthiouracil and hydrocortisone

83
Q

FRAX score use

What does it look at

A
FRAX
estimates the 10-year risk of fragility fracture
valid for patients aged 40-90 years
based on international data so use not limited to UK patients
assesses the following factors: 
- age
- sex
- weight
- height
- previous fracture
- parental fracture
- current smoking
- alcohol intake
- glucocorticoids
- rheumatoid arthritis
- secondary osteoporosis

Interpreting FRAX score

WITHOUT BMD: results (10-year risk of a fragility fracture) will be given and categorised automatically into one of the following:

  • low risk: reassure and give lifestyle advice
  • intermediate risk: offer BMD test
  • high risk: offer bone protection treatment

Therefore, with intermediate risk results FRAX will recommend that you arrange a BMD test to enable you to more accurately determine whether the patient needs treatment

If the FRAX assessment was done witha bone mineral density (BMD) measurement the results (10-year risk of a fragility fracture) will be given and categorised automatically into one of the following:

  • reassure
  • consider treatment
  • strongly recommend treatment
84
Q

CAH

A

21-hydroxylase deficiency features
- virilisation of female genitalia
- precocious puberty in males
60-70% of patients have a salt-losing crisis at 1-3 wks of age

11-beta hydroxylase deficiency features

  • virilisation of female genitalia
  • precocious puberty in males
  • hypertension
  • hypokalaemia

Dx for both = ELEVATED 17-hydroxyprogesterone

Rx

  • Glucocorticoid replacement
  • MR replacement (fludracortisone)
  • Females may need suergery

Salt losing crisis = Vom/weight loss, hypotension, hyponatraemia, hyeperkalaemaia, floppy/unresponsive