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Year 3 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Type 1 Diabetes Mellitus (T1DM)

A

a metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency secondary to the autoimmune destruction of pancreatic beta cells

Most pts have genetic predisposition e.g. HLA-DR3 & HLA-DR4

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2
Q

Epidemiology of Type 1 Diabetes Mellitus (T1DM)

A

accounts for ~15% of diabetic pts (but ~85% of cases of diabetes in <20 y/o)

presents at age <20yrs in majority of pts (but can occur at any age)

associated with HLA-DR3 & HLA-DR4 and other autoimmune conditions

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3
Q

Presentation of Type 1 Diabetes Mellitus (T1DM)

A

often sudden onset
generally polyuria, lethargy, weight loss, blurred vision, abdo pain

~1/3 pts present with diabetic ketoacidosis (DKA) as first manifestation
-dehydration, polyuria, polydipsia, Kussmaul respiration

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4
Q

Investigations for Type 1 Diabetes Mellitus (T1DM)

A

Random plasma glucose
-≥11.1 mmol/l

Fasting plasma glucose
-≥7.0 mmol/l

Plasma glucose 2h post 75g of glucose
-≥11.1 mmol/l

HbA1c

  • ≥48 mmol/l
  • NB less useful in T1DM due to rapid ↑ of glucose

C-peptide
-↓ / undetectable

Urine dip
-ketones +ve in DKA

Diabetes specific antibodies (+ve in ~80% of pts)

  • Islet cell antibodies
  • insulin autoantibodies
  • anti-GAD

TFTs, lipid profile, U&Es

NB C-peptide & diabetes specific antibodies are generally used in T1DM suspected but pt has atypical features e.g. age >50yrs / BMI ≥25, slow development of hyperglycaemia

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5
Q

Management of Type 1 Diabetes Mellitus (T1DM)

A

pt education with diet & lifestyle advice

Monitor HbA1c every 3-6months (target ≤48mmol/L)

Glucose monitoring

  • at least 4x per day (before every meal & before bed)
  • more frequently if unwell
  • target 5-7mmol/L on waking
  • target 4-7mmol/L before meals / random

Insulin

  • 1st line: offer multiple daily injection basal bolus insulin regime e.g. twice daily insulin determir
  • 2nd line: once daily insulin glargine

Metformin
-consider adding if BMI ≥25

Statins
-most pts offered 20mg statin at some point

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6
Q

Diagnostic criteria for Type 1 Diabetes Mellitus (T1DM)

A

If the patient is symptomatic:

  • fasting glucose ≥7.0 mmol/l
  • random glucose ≥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.

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7
Q

Atypical features of Type 1 Diabetes Mellitus (T1DM)

A

age >50yrs
BMI ≥25
slow development of hyperglycaemia

C-peptide & diabetes specific antibodies are generally used if T1DM suspected but pt has atypical features

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8
Q

Monitoring in Type 1 Diabetes Mellitus (T1DM)

A

HbA1c

  • monitor every 3-6months
  • target ≤48mmol/L

Glucose monitoring

  • at least 4x per day
  • before every meal & before bed
  • more frequently if unwell
  • target 5-7mmol/L on waking
  • target 4-7mmol/L before meals / random

Annual reviews:

  • TFTs
  • U&Es
  • Lipid profile
  • eye screening
  • foot checks
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9
Q

Type 2 Diabetes Mellitus (T2DM)

A

a disorder characterised by progressive deficiency in insulin secretion and ↑ insulin resistance leading to abnormal glucose metabolism

accounts for ~85% of all cases of diabetes

usually presents at age >40yrs
-the incidence in children/adolescents is rising

more common in people of south asian / african / afro-carribbean / middle eastern ancestry

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10
Q

Epidemiology of Type 2 Diabetes Mellitus (T2DM)

A

accounts for ~85% of all cases of diabetes

usually presents at age >40yrs
-the incidence in children/adolescents is rising

more common in people of south asian / african / afro-carribbean / middle eastern ancestry

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11
Q

Risk factors for Type 2 Diabetes Mellitus (T2DM)

A
  • obesity (especially central / truncal)
  • lack of physical activity
  • south asian/african/afro-carribbean/middle eastern ancestry
  • history of gestational diabetes
  • impaired fasting glucose
  • PCOS
  • Family history
  • Dislipidaemia
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12
Q

Presentation of Type 2 Diabetes Mellitus (T2DM)

A

onset typically gradual & majority of pts are asymptomatic

elderly pts present in HHS

symptoms of complications may be first presentation

polyuria, polydipsia
candidal/skin/urinary tract infections
acanthosis nigricans

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13
Q

Investigations for Type 2 Diabetes Mellitus (T2DM)

A

Fasting glucose
-≥7.0 mmol/L

Random glucose / post OGTT
-≥11.1 mmol/L

HbA1c
-≥48 mmol/L

NB needs to by on 2 occasions if asymptomatic

Lipid profile, U&Es (GFR), LFTs

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14
Q

Pre-diabetes

A

HbA1c:
-42-47 mmol/mol

Impaired fasting glucose:
-≥6.1 but <7.0 mmol/L (i.e. 6.1-6.9)

Glucose tolerance impaired:

  • fasting glucose <7.0
  • 2h post OGTT glucose = 7.8-11.1
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15
Q

Management of Type 2 Diabetes Mellitus (T2DM)

A

Patient education
Dietary advice
weight loss
exercise

Pharmacological

  • 1st line: Metformin
    • give if HbA1c >48 on lifestyle intervention
    • give max dose before adding a further drug
  • if HbA1c >58 on metformin = add 2nd drug
    • e.g. sulfonylurea / gliptin / pioglitazone / SGLT-2 inhibitors
  • if HbA1c >58 on metformin + other drug = add 3rd drug
    • metformin + gliptin + sulfonylurea
    • metformin + pioglitazone + sulfonylurea
    • metformin + sulfonylurea + SGLT-2 inhibitor
    • metformin + pioglitazone + SGLT-2 inhibitor
    • Or consider Insulin therapy
  • if triple therapy not tolerated / effective & BMI >35
    • metformin + sulfonylurea + GLP-1 mimetic
  • If metformin contraindicated / not tolerated
    • 1st line = sulfonylurea / gliptin / pioglitazone
    • add 2nd drug if HbA1c >58
      - gliptin + pioglitazone
      - gliptin + sulfonylurea
      - pioglitazone + sulfonylurea
    • if HbA1c >58 on 2 drugs
      - consider insulin therapy

NB see the NICE T2DM treatment diagram for a clearer picture

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16
Q

HbA1c targets for Type 2 Diabetes Mellitus (T2DM)

A

Lifestyle = 48mmol/mol
-if >48 on lifestyle then offer drug

Lifestyle + metformin = 48mmol/mol

Lifestyle + other drug e.g. sulfoylurea =53mmol/mol

NB if HbA1c ≥ 58mmol/mol on drug therapy then add another agent

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17
Q

Pharmacological management of Type 2 Diabetes Mellitus (T2DM)

A

1st line: Metformin

  • give if HbA1c >48 on lifestyle intervention
  • give max dose before adding a further drug

If HbA1c >58 on metformin = add 2nd drug
-e.g. sulfonylurea / gliptin / pioglitazone / SGLT-2 inhibitors

If HbA1c >58 on metformin + other drug = add 3rd drug

  • metformin + gliptin + sulfonylurea
  • metformin + pioglitazone + sulfonylurea
  • metformin + sulfonylurea + SGLT-2 inhibitor
  • metformin + pioglitazone + SGLT-2 inhibitor
  • Or consider Insulin therapy

If triple therapy not tolerated / effective & BMI >35
-metformin + sulfonylurea + GLP-1 mimetic

If metformin contraindicated / not tolerated

  • 1st line = sulfonylurea / gliptin / pioglitazone
  • add 2nd drug if HbA1c >58
    - gliptin + pioglitazone
    - gliptin + sulfonylurea
    - pioglitazone + sulfonylurea
  • if HbA1c >58 on 2 drugs
    - consider insulin therapy
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18
Q

Metformin

A

A biguanide that helps ↑insulin sensitivity & ↓insulin resistance

Contra-indications:

  • eGFR <30 (causes
  • NB ↓ dose if eGFR <45

Side effects:

  • GI upset (nausea, anorexia, diarrhoea)
    • try modified release to combat these

Does not cause hypoglycaemia

NB stop 48h before procedure using iodine enhanced contrast media due to ↑ risk of nephropathy

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19
Q

Sulfonylureas

A

Examples:
-gliclazide, glimipramide, glipizide

MOA:
-↑ pancreatic insulin secretion by enhancing pancreatic islet cell function

Side effects:

  • hypoglycaemia**
  • weight gain

NB beta blockers can ↓ hypoglycaemic awareness and should therefore be used with caution

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20
Q

Thiazolidinediones (Glitazones)

A

Examples:
-Pioglitazone

MOA:
-↓ peripheral insulin resistance

Side effects:

  • weight gain
  • ↑ risk of fractures
  • liver impairments
  • fluid retention

Contraindicated in HF due to fluid retention

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21
Q

Gliptins (DPP-4 inhibitors)

A

Examples:
-linagliptin, sitagliptin

MOA:
-inhibit DPP-4 = ↑GLP-1 = ↑ insulin secretion & ↓glucagon secretion

Side effects:

  • ↑risk of pancreatitis
  • GI sumptoms
  • ↑ feeling satiety

NB no weight gain

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22
Q

SGLT-2 inhibitors (glifozins)

A

Examples:
-dapagliflozin, canagliflozin

MOA:
-↓glucose absorption in proximal convoluted tubule = ↑glucose excretion in urine

Side effects:

  • urinary & genital infections (due to glycosuria)
  • dehydration
  • often ↓ weight
  • ↑ risk of limb amputation

Contraindicated in ↓ renal function

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23
Q

SGLT-2 inhibitors (glifozins)

A

Examples:
-dapagliflozin, canagliflozin

MOA:
-↓glucose absorption in proximal convoluted tubule = ↑glucose excretion in urine

Side effects:

  • urinary & genital infections (due to glycosuria)
  • dehydration
  • often ↓ weight
  • ↑ risk of limb amputation

Contraindicated in ↓ renal function

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24
Q

GLP-1 agonists

A

Examples:
-exenatide, liraglutide (both S/c)

MOA:
-↓ glucagon secretion, ↑insulin secretion

Side effects:

  • nausea & vomiting
  • ↑ risk pf pancreatitis

NB consider in pts with BMI ≥35 or pts who hold LGV/PCV drivers license who may lose these if taking insulin

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25
Q

Diabetic ketoacidosis (DKA)

A

a metabolic complication of diabetes characterised by absolute/relative insulin deficiency leading to hyperglycaemia, ketoanaemia and acidosis

its a medical emergency

Most common acute hyperglycaemic complications of T1Dm

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26
Q

Precipitating factors for Diabetic ketoacidosis (DKA)

A 
Infection
discontinuation of insulin 
inadequate insulin
stress (e.g. MI/trauma/surgery)
Medications (e.g. corticosteroids, diuretics, alpha/beta blockers)
alcohol abuse
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27
Q

Presentation of Diabetic ketoacidosis (DKA)

A

polyuria, polydipsia
vomiting, dehydration
abdo pain, weakness, lethargy
altered mental state / coma
Kussmaul respiration (deep hyperventilation)
acetone smelling breath (‘pear drop’ smell)

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28
Q

Investigations for Diabetic ketoacidosis (DKA)

A

ABG/VBG

  • metabolic acidosis
  • ↑ anion gap (>16 indicates severe DKA)

Blood ketones
->3.0mmol/L

Blood glucose
->11.0mmol/L

U&Es

  • ↑ K+
  • ↓ Na+
  • NB ↓ K+ indicates severe DKA as indicated intracellular K+ depletion

FBC
-↑ WCC

Urinalysis

  • ketones ++
  • glucose ++

ECG, CXR

NB despite ↑ K+ total body K+ is depleted and K+ should be replaced

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29
Q

Diagnostic criteria for Diabetic ketoacidosis (DKA)

A

Key points

  • glucose > 11 mmol/l or known diabetes mellitus
  • pH < 7.30
  • bicarbonate < 15 mmol/l or anion gap > 10
  • ketones > 3 mmol/l or urine ketones ++ on dipstick
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30
Q

Management of Diabetic ketoacidosis (DKA)

A

Fluid replacement

  • usually NaCl 0.9%
  • deficit ~100ml/kg
  • K+ supplementation should be given early (due to cellular depletion of K+)
    • rate shouldn’t exceed 10mmol/h

Insulin

  • fixed rate IV insulin at 0.1 units/kg/h
  • once blood glucose < 15mmol/L starts 5% dextrose infusion
  • long-acting insulin should be continued
  • short-acting insulin should be stopped
  • restart normal insulin if pt eating & drinking normally
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31
Q

Hyperosmolar hyperglycaemic state (HHS)

A

an acute hyperglycaemic state characterised by profound hyperglycaemia (often >30mmol/L), hyperosmolarity and volume depletion in the absence of significant ketoacidosis

typically presents in pts with T2DM especially elderly pts (may be the initial prevention)

NB ketosis does not occur due to the presence of basal levels of insulin secretion in T2Dm

precipitants include stress e.g. MI, infection, stroke, trauma, PE, surgery

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32
Q

Presentation of Hyperosmolar hyperglycaemic state (HHS)

A

fatigue, lethargy, nausea & vomiting
weakness,, polyuria, polydipsia
altered level of consciousness, headache, papilloedema
dehydration (hypotension, tachycardia, ↓ skin turgor)
focal neurological deficits, seizures

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33
Q

Investigations for Hyperosmolar hyperglycaemic state (HHS)

A

Blood glucose
-often >30mmol/L

Blood ketones
-<3mmol/L

ABG/VBG

  • mild acidosis
  • usually lactic acidosis

Serum osmolarity
->320mOsm/kg

U&Es

  • dehydration (↑ urea)
  • pre-renal AKI
  • Na+ / K+ deranged

FBC
-↑ WCC

Urinalysis
-ketones -ve

ECG, CXR, cardiac enzymes, CRP

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34
Q

Management of Hyperosmolar hyperglycaemic state (HHS)

A

Fluid replacement

  • IV NaCl 0.9% is 1st line
  • NB if osmolarity not ↓ with 0.9% NaCl consider 0.45%
  • aim to replace ~50% by 12h & 100% by 24h
  • deficit ~100-220ml/kg
  • add K+ as required

Insulin

  • only give if ketoanaemia as it indicates hypoinsulinaemia
  • recommendation is 0.05units/kg/h

NB using insulin in HHS can cause adverse outcomes due to ↑ insulin sensitivity

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35
Q

Diagnostic criteria for Hyperosmolar hyperglycaemic state (HHS)

A

Diagnosis

  1. Hypovolaemia
  2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  3. Significantly raised serum osmolarity (> 320 mosmol/kg)

NB: A precise definition of HHS does not exist, however the above 3 criteria are helpful in distinguishing between HHS and DKA. It is also important to remember that a mixed HHS / DKA picture can occur.

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36
Q

Hypoglycaemia

A

a syndrome present when blood glucose concentrations falls below the normal fasting glucose range (glucose <3.3mmol/L)

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37
Q

Whipples Triad

A

Used for diagnosis of Hypoglycaemia

  • plasma hypoglycaemia (glucose <3.3mmol/L)
  • symptoms attributable to hypoglycaemia
  • resolution of symptoms with correction of hypoglycaemia
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38
Q

Aetiology of Hypoglycaemia

A 
insulinoma
self administration of insulin / sulfonylureas
liver failure
Addisons disease 
chronic alcohol use
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39
Q

Presentation of Hypoglycaemia

A

Neurogenic/autonomic symptoms (<3.3 mmol/L )

  • sweating, shaking, trembling, hunger
  • anxiety, nausear, palpitations
  • tingling, paraesthesia, pins & needles

Neurglycopenic symptoms (<2.8 mmol/L)

  • agitation, confusion, behavioural change
  • seizures, focal neurological signs
  • ↓ GCS
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40
Q

Investigations for Hypoglycaemia

A

Blood glucose
-<3.3 mmol/L

HbA1c, LFTs, TFTs, U&Es

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41
Q

Management of Hypoglycaemia

A

If pt alert / able to swallow

  • glucose 10-20g PO e.g. as liquid form like lucozade or granulated sugar
  • glucogel (buccal)

If pt unconscious / unable to swallow

  • at home / no IV access
    • IM glucagon 1mg
    • if ineffective after 10min give IV glucose
  • If IV access
    • IV glucose 10% / 20% (15-20g) over 15min

NB once pt recovered somewhat ensure they are given long acting glucose source e.g. bread

NB generally treatment is repeated every 15min if no response

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42
Q

Management of Hypoglycaemia in a conscious pt

A
  • glucose 10-20g PO e.g. as liquid form like lucozade or granulated sugar
  • glucogel (buccal)
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43
Q

Management of Hypoglycaemia in an unconscious pt

A

at home / no IV access

  • IM glucagon 1mg
  • if ineffective after 10min give IV glucose

If IV access
-IV glucose 10% / 20% (15-20g) over 15min

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44
Q

Diabetic nephropathy

A

one of the most common causes of CKD (NB one of the causes where kidneys do not shrink in CKD)

characterised by albuminuria & progressive ↓eGFR in the context of long standing diabetes (>10yrs especially T1DM, but may be present early in T2DM)

generally asymptomatic

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45
Q

Screening & Investigations for Diabetic nephropathy

A

Screening

  • annual screening using urine ACR (albumin:creatinine ratio) using first morning urine sample
  • also annual U&Es with eGFR

Investigations

  • urinalysis (proteinuria)
  • ACR (microalbuminuria >2.5 / albuminuria ≥30)
  • U&Es (↓eGFR)
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46
Q

Management of Diabetic nephropathy

A

Tight glycaemic control
BP control (aim for <130/80)
Control dyslipadaemia with statin

ACE-Is/ARBs
-start if ACR ≥3

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47
Q

Diabetic retinopathy

A

most common caused of blindness in adults aged 35-65yrs

essentially the retinal consequence of chronic progressive diabetic microvascular leakage & occlusion

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48
Q

Diabetic retinopathy presentation

A

often minimal symptoms until late stages
↓ visual acuity
retinal haemorrhages
-sudden onset of dark, painless floaters that resolve over several days

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49
Q

Investigations & Screening for Diabetic retinopathy

A

Screening:

  • annual eye screening
  • refer to ophthalmology when diagnosed with T2DM or if sudden unexplained ↓ visual acuity

Investigations:

  • Fundoscopy
  • dilated retinal photography (gold standard)
  • optical coherence tomography screening
  • fluorescein angiography
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50
Q

Non proliferative diabetic retinopathy (NPDR)

A

Mild:
-≥ 1 microaneurysm

Moderate:
-microaneurysms, blot haemorrhages, hard exudates, cotton wool spots (soft exudates i.e. areas of retinal infarction), venous bleed

Severe:
-blot haemorrhages & microaneurysms in all 4 quadrants, venous bleeding, intraretinal microvascular abnormalities

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51
Q

Proliferative diabetic retinopathy

A

retinal neovascularisation, may lead to vitreous haemorrhages, fibrovascular proliferation, traction retinal haemorrhages, and features of NPDR

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52
Q

Diabetic Maculopathy

A
  • any macular involvement, including macular oedema, macular ischaemia etc
  • more based on location than other features
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53
Q

Classification of Diabetic retinopathy

A

Non proliferative diabetic retinopathy (NPDR):

  • Mild = ≥ 1 microaneurysm
  • Moderate = microaneurysms, blot haemorrhages, hard exudates, cotton wool spots (soft exudates i.e. areas of retinal infarction), venous bleed
  • Severe = blot haemorrhages & microaneurysms in all 4 quadrants, venous bleeding, intraretinal microvascular abnormalities

Proliferative diabetic retinopathy:
-retinal neovascularisation, may lead to vitreous haemorrhages, fibrovascular proliferation, traction retinal haemorrhages, and features of NPDR

Maculopathy

  • any macular involvement, including macular oedema, macular ischaemia etc
  • more based on location than above features
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54
Q

Management of Diabetic retinopathy

A

Optimise BP / glycemic / lipid control

Non proliferative diabetic retinopathy (NPDR)

  • generally observed
  • may be teated with laser photocoagulation if severe

Proliferative diabetic retinopathy

  • intravitreal anti-VEGF injections
  • laser photocoagulation

Maculopathy
–intravitreal anti-VEGF injections

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55
Q

Diabetic neuropathy

A

hyperglycaemia leads to glycation of axons leading to progressive sensorimotor neuropathy

  • sensori-neuropathy is most common
  • affects up to 70% of diabetics

Presentation

  • peripheral neuropathy with glove & stocking distribution & proximal progression
  • dyesthesia (burning feet) worse at night
  • NB autonomic neuropathy with erectile dysfunction, bladder dysfunction etc can also occur

Usually a clinical diagnosis

Management includes amitriptyline / duloxetine / gabapentin / pregabalin as 1st line (if one drug doesn’t work then try other 1st line drugs, always as mono therpay)

NB tramadol may be used as rescue therapy for acute exacerbations of neuropathic pain

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56
Q

Diabetic foot disease

A

Diabetes is the most common cause on non traumatic limb amputation

Contributing factors:

  • neuropathy (loss of protective sensation)
  • PAD can be diabetes induced

Presents with recurrent foot infections e.g. cellulitis or athletes foot, Malum performs (painless neuropathic ulcers on plantar pressure points) & charcot arthropathy

screening for foot tease is done annually

Management includes BP & glycemic control as well as pt education & foot care

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57
Q

Diabetes and hypertension

A

For T2DM pts BP goal is <140/90
For T1DM pts BP goal is <135/85
-if albuminuria BP goal <130/80

First line antihypertensive for diabetics = ACE-Is/ARBs

NB avoid routine use of beta blockers due to altered autonomic response to hypoglycaemia (↓ hypoglycaemic awareness)

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58
Q

Diabetes and the DVLA

A

drivers should contact the DVLA especially if taking insulin

usually no issues unless ↓ hypoglycaemic awareness or >1 episode of hypoglycaemia requiring assistance from another person in preceding 12 months

NB if well controlled diabetes then don’t need to contact DVLA

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59
Q

Maturity onset diabetes of the young (MoDY)

A

characterised by onset of T2DM at age <25yrs

typically inherited in autosomal dominant fashion

often misdiagnosed

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60
Q

Diabetes and sick day rules

A

↑ frequency of glucose monitoring while unwell
encourage oral fluid intake (take sugary drinks if unable to eat)

if on oral hypoglycaemic

  • continue as normal even if not eating much
  • stop metformin if dehydrated

if on insulin

  • must not stop it due to risk of DKA
  • if ↑ ketones/↑ glucose = give corrective dose (total daily dose divided by 6, max 15 units)

go to hospital if unable to keep down fluids or significant ketosis in insulin dependent diabetic despite additional insulin or if glucose >20 despite additional insulin

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61
Q

Adrenal insufficiency

A

adrenal insufficiency is a condition in which there is a ↓ adrenal hormone output i.e. glucocorticoids e.g. cortisol and/or mineral corticoids e.g. aldosterone

Autoimmune destruction of the adrenal glands is the commonest cause of primary hypoadrenalism in the UK, accounting for 80% of cases.

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62
Q

Addisons disease

A

Primary adrenal insufficiency

usually due to autoimmune destruction of the adrenal glands, often associated with other autoimmune conditions (accounts for ~90% of cases)

other causes include Waterhouse-Friedrichsen syndrome, TB (~10%)

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63
Q

Adrenal insufficiency & Addisons disease aetiology

A

Primary (Addisons)

  • autoimmune destruction of the adrenal
  • TB
  • Waterhouse-Friedrichsen syndrome

Secondary

  • impaired HPA axis e.g. exogenous steroid use, radiation
  • pituitary / hypothalamic tumours

NB secondary adrenal insufficiency is more common

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64
Q

Presentation of Adrenal insufficiency

A

General adrenal insufficiency:

  • lethargy, weakness, anorexia, nausea & vomiting
  • weight loss
  • diarrhoea/constipation
  • loss of axillary & pubic hair
  • hypotension
  • hypoglycaemia
  • irritability
  • ↓ libido

Specific to Addisons:

  • hyperpigmentation (due to ↑ACTH)
  • salt cravings

NB symptoms are generally subclinical until ↑ stress e.g.in infection

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65
Q

Investigations for Adrenal insufficiency

A

Morning Cortisol
-↓ in primary & secondary

Morning ACTH

  • ↑ in primary (Addisons)
  • ↓ in secondary

ACTH stimulation / synacthen test

  • no change in primary (Addison’s)
  • ↑ cortisol after test in secondary

U&Es
-Na+ ↓, K+↑ in Primary (Addisons)

Ca2+
-↑ in Primary (Addisons)

FBC
-anaemia

Glucose
-↓ in primary & secondary

Renin & aldosterone
-Renin ↑, Aldosterone ↓ in primary in Primary (Addisons)

Anti-21-hydroxylase antibodies
-+ve in Primary (Addisons)

CT/MRI adrenals

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66
Q

Management of Adrenal insufficiency

A

Glucocorticoid replacement

  • for both primary & secondary causes
  • hydrocortisone (1st line)
  • usually 3 divided doses, with ~1/2 of total daily dose given in the morning (when natural levels are highest)

Mineralocorticoid replacement

  • only for Primary (Addisons)
  • fludrocortisone (1st line)

In Illness

  • 2x hydrocortisone dose
  • no change to fludrocortisone dose
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67
Q

Differentiating primary (addisons) & secondary Adrenal insufficiency

A

Morning Cortisol
-↓ in primary & secondary

Morning ACTH

  • ↑ in primary (Addisons)
  • ↓ in secondary

ACTH stimulation / synacthen test

  • no change in primary (Addison’s)
  • ↑ cortisol after test in secondary

U&Es
-Na+ ↓, K+↑ in Primary (Addisons)

Ca2+
-↑ in Primary (Addisons)

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68
Q

Differentiating primary (Addisons) & secondary Adrenal insufficiency

A

Morning Cortisol
-↓ in primary & secondary

Morning ACTH*

  • ↑ in primary (Addisons)
  • ↓ in secondary

ACTH stimulation / synacthen test*

  • no change in primary (Addison’s)
  • ↑ cortisol after test in secondary

U&Es
-Na+ ↓, K+↑ in Primary (Addisons)

Ca2+
-↑ in Primary (Addisons)

Renin & aldosterone
-Renin ↑, Aldosterone ↓ in primary in Primary (Addisons)

Anti-21-hydroxylase antibodies
-+ve in Primary (Addisons)

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69
Q

Addisonian crisis (Adrenal crisis)

A

an acute severe glucocorticoid deficiency & to a lesser a mineralocorticoid deficiency

a medical emergency commonly occurring in pts with longstanding adrenal insufficiency

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70
Q

Precipitating factors for Addisonian crisis (Adrenal crisis)

A

stress in pts with underlying adrenal insufficiency

  • GI illness (Most common)
  • infection
  • injury
  • surgery
  • pregnancy
  • psychological stress
  • dehydration

abrupt withdrawal of steroid treatment

bilateral adrenal haemorrhage (Waterhouse-Friedrichsen syndrome)

  • usually seen as complication of septicaemia
  • leads to adrenal necrosis

pituitary apoplexy

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71
Q

Presentation of Addisonian crisis (Adrenal crisis)

A 
hypotension & hypovolaemic shock due to dehydration
impaired consciousness
coma
malaise
low grade fever
nausea & vomiting 
severe abdo pain (may resemble peritonitis)
confusion
LOC
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72
Q

Investigations for Addisonian crisis (Adrenal crisis)

A

Clinical diagnosis generally i.e. investigations should not delay treatment

U&Es
-Na+ ↓, K+ ↑, Ca2+ ↑

ABG

  • Glucose ↓
  • normal anion gap metabolic acidosis

Cortisol
ACTh

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73
Q

Management of Addisonian crisis (Adrenal crisis)

A

IM / IV Hydrocortisone

  • 100mg in adults
  • can be repeated 6 hourly till stabilised

1L NaCl 0.9% ± dextrose over 30-60min

NB no fludrocortisone is required as high dose glucocorticoids have mineralocorticoid action

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74
Q

Cushing’s syndrome (hypercortisolism)

A

the clinical manifestation of pathological hypercortisolism from any cause

peak incidence is age 25-40yrs

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75
Q

Aetiology of Cushing’s syndrome (hypercortisolism)

A

ACTH dependent

  • Cushings disease
    • most common cause
    • pituaitray adenoma secreting ACTH
  • ectopic ACTH production e.g. from SCLC

ACTh independent

  • iatrogenic e.g. long term steroid use
  • adrenal adenoma / carcinoma

NB prolonged alcohol misuse may cause pseudo-cuhsings

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76
Q

Presentation of Cushing’s syndrome (hypercortisolism)

A 
truncal obesity, supraclavicular fat pads, buffalo hump, weight gain
moon facies & facial plethora
facial fullness 
hyperglycaemia (insulin resistance)
skin atrophy, purple striae
easy bruising
hirsutism, acne
proximal muscle weakness
depression, cognitive dysfunction, emotional liability
recurrent infections
irregular menses
slow wound healing
hypertension
osteoporosis 
unexplained fractures

NB if ACTH dependent e.g. Cushings disease

  • hyperpigmentation (due to ↑ ACTH)
  • headaches
  • galactorrhea
  • visual disturbances
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77
Q

Management of Cushing’s syndrome (hypercortisolism)

A

surgical resection of tumour where possible

cortisol suppression

  • metyrapone, ketoconazole
  • if tumour inoperable mitotane

NB cortisol suppression is generally used temporarily pre surgery / radiation to control cortisol levels

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78
Q

Investigations for Cushing’s syndrome (hypercortisolism)

A

24h urine free cortisol

  • ↑ levels
  • usually >3x upper limit of normal

overnight dexamethasone suppression test

  • no suppression of morning cortisol
  • levels >50

Morning / midnight ACTH

  • ↑ in ACTH dependent disease e.g. Cushings disease
  • ↓ in ACTH independent disease

High dose dexamethasone suppression test
-if cortisol suppressed = pituitary cause

Late night salivary / serum cortisol (↑)
Glucose (↑)
MRI/CT pituitary

NB insulin stress test can be used to differentiate pseudo-bushings

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79
Q

Differentiating ACTH dependent & ACTH independent Cushing’s syndrome (hypercortisolism)

A

Morning / midnight ACTH

  • ↑ in ACTH dependent disease e.g. Cushings disease
  • ↓ in ACTH independent disease

High dose dexamethasone suppression test
-if cortisol suppressed = pituitary cause

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80
Q

Hyperaldosteronism

A

defined as excessive levels of aldosterone which can be independent of the renin-angiotensin axis (primary) or due to high renin levels (secondary)

Most common causes are adrenal adenomas (Conn’s syndrome)

NB this is the most common curable cause of secondary HTN

81
Q

Aetiology of Hyperaldosteronism

A

Primary

  • Adrenal adenoma (Conns syndrome)*
    - ~80% of all cases of hyperaldosteronism
  • Bilateral adrenal hyperplasia (BAH)
  • adrenal carcinoma
  • familial hyperaldosteronism

Secondary

  • diuretics
  • congestive HF
  • hepatic failure
  • renal artery stenosis
82
Q

Presentation of Hyperaldosteronism

A

Hypertension

  • often >150/100
  • may be >140/90 and resistant to 3 drug therapy

Features of hypokalaemia

  • fatigue
  • muscle weakness
  • cramps
  • headaches
  • polyuria
  • polydipsia
  • constipation
  • palpatations
  • paraesthesia
83
Q

Presentation of Hyperaldosteronism

A

Hypertension

  • often >150/100
  • may be >140/90 and resistant to 3 drug therapy

Features of hypokalaemia

  • fatigue
  • muscle weakness
  • cramps
  • headaches
  • polyuria
  • polydipsia
  • constipation
  • palpitations
  • paraesthesia
84
Q

Investigations for Hyperaldosteronism

A

U&Es

  • K+ ↓
  • Na+ ↑/normal

Aldosterone / renin ratio

  • Renin ↓
  • Aldosterone↑

Adrenal venous smapling

  • to localise aldosterone production
  • if bilateral = bilateral adrenal hyperplasia

High resolution abdominal CT

NB if unclear results consider oral sodium loading test / saline infusion test

85
Q

Management of Hyperaldosteronism

A

Dietary Na+ restriction

Conn’s syndrome

  • srugical adrenalectomy
  • life long aldosterone antagonists e.g. spironolactone if unfit for surgery

Bilateral adrenal hyperplasia (BAH)
-spironolactone / epleronone

86
Q

Phaeochromocytoma

A

a rare catecholamine secreting tumour typically developing in the adrian medulla
-if outside of adrenal medulla then its called a paraganglioma

~10% are familial associated with MEN-III (bilateral), neurofibromatosis, von Hippel-Lindau

usually presents 3rd-5th decade of life

87
Q

Phaeochromocytoma presentation

A 
episodic / persistent hypertension
headache
profuse sweating 
palpitations & tachycardia
nausea, weakness, anxiety
pallor
weight loss
tremor 
abdo pain

NB hypertensive crisis can be triggered by palpation of tumour on abdo examination

88
Q

Investigations for Phaeochromocytoma

A

24h urine metanephrines (↑)

  • 1st line investigation
  • collect immediately after crisis
Plasma catecholamines (↑)
Plasma metanephrines (↑)

adrenal CT/MRI

24h urine catecholamines (↑)
-no longer first line

89
Q

Precipitants of Phaeochromocytoma hypertensive crisis

A 
anaesthetics 
opiates
decongestants 
TCAs
cocaine
X-ray contrast media
childbirth
90
Q

Hyperthyroidism (thyrotoxicosis)

A

The overactivity of the thyroid gland

most commonly due to Graves disease, an autoimmune disease leading to overstimulation of thyroid due to TSH-receptor autoantibodies

91
Q

Hyperthyroidism (thyrotoxicosis) aetiology

A

Graves disease (most common)

  • autoimmune disease
  • TSH-receptor autoantibodies

Toxic multi-nodular goitre
-autonomously functioning thyroid nodules

Thyroid adenoma

Thyroiditis
-e.g. DeQuervains causes transient Hyperthyroidism

Drugs

  • amiodarone
  • lithium
92
Q

Graves disease

A

autoimmune disease causing thyroid overstimulation due to TSH receptor stimulating antibodies

most common cause of thyrotoxicosis, typically seen in women aged 30-50yrs

presents with features of hyperthyroidism + classic triad of pretibial myxoedema, exophthalmos/opthalmoplegia and thyroid acropachy (digital clubbing, soft tissue swelling of the hands and feet, periosteal new bone formation)

93
Q

Graves disease

A

autoimmune disease causing thyroid overstimulation due to TSH receptor stimulating antibodies

most common cause of thyrotoxicosis, typically seen in women aged 30-50yrs

presents with features of hyperthyroidism + classic triad of pretibial myxoedema, exophthalmos/opthalmoplegia and thyroid acropachy (digital clubbing, soft tissue swelling of the hands and feet, periosteal new bone formation)

94
Q

Toxic multi nodular goitre

A

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

Nuclear scintigraphy reveals patchy uptake.

The treatment of choice is radioiodine therapy.

95
Q

Presentation of Hyperthyroidism (thyrotoxicosis)

A 
Heat intolerance
weight loss
↑ appetite
manic restlessness
weakness/fatigue
↑ sweating
tachycardia
fine tremor
lid lag
brisk reflexes
goitre
oligomenorrhoea 
diarrhoea / frequent bowel movements 
proximal myopathy
hynaecomastia
hair thinning
96
Q

Investigations for Hyperthyroidism (thyrotoxicosis)

A

TFTs

  • TSH ↓
  • free T3/T4 ↑

Autoantibodies

  • TSH receptor antibodies (+ve in Graves)
  • anti-thyroid peroxidase antibodies (may be seen in Graves)

Thyroid isotope scan

  • single hot nodule in thyroid adenoma
  • diffuse uptake in Graves
  • several hot nodules in multi nodular goitre
97
Q

Management of Hyperthyroidism (thyrotoxicosis)

A

Anti-thyroid drugs

  • Carbimazole (1st line)
  • propylthiouracil (reserved for pregnancy & thyroid storm)
  • may be given as block & replace along with thyroxine
  • or as dose titration to achieve euthyroid

Radio-iodine

  • treatment of choice for multi nodular goitre & relapsed Graves
  • contraindicated if breast feeding
  • can get pregnant for minimum 6months after treatment
  • avoid close contact with children & pregnant women for 3 weeks

NB TFTs should be monitored at least annually

98
Q

Hyperthyroid crisis / Thyrotoxic storm

A

an extreme manifestation of thyrotoxicosis, may rarely be the first presentation of hyperthyroidism

generally rare, but usually seen in pts with established thyrotoxicosis

NB iatrogenic thyroxine excess does not usually result in thyroid storm

99
Q

Precipitating events for Hyperthyroid crisis / Thyrotoxic storm

A 
withdrawal / non compliance with anti-thyroid medication
recent trauma / surgery 
infection
acute iodine load e.g. CT contrast media
thyroid surgery
100
Q

Investigations for Hyperthyroid crisis / Thyrotoxic storm

A

Clinical diagnosis

investigate underlying cause
FBC, U&Es, TFTs, LFTs, ABG, ECG

NB the degree of thyroid hormone elevation does not determine the presence / absence of thyrotoxic storm

101
Q

Presentation of Hyperthyroid crisis / Thyrotoxic storm

A 
Hyperpyrexia (temp >38.5°C but often >41°C)
profuse sweating 
tachycardia (>140bpm)
confusion & agitation
Delirium
Nausea & vomiting
Hypertension 
Heart failure
arrhythmia e.g. AF
seizures
jaundice
102
Q

Investigations for Hyperthyroid crisis / Thyrotoxic storm

A

Clinical diagnosis

investigate underlying cause
FBC, U&Es, TFTs, LFTs, ABG, ECG

NB the degree of thyroid hormone elevation does not determine the presence / absence of thyrotoxic storm

103
Q

Hypothyroidism

A

a clinical state resulting from the under production of thyroid hormone

most commonly caused by Hashimotos thyroiditis

generally more common in women

104
Q

Hypothyroidism

A

a clinical state resulting from the under production of thyroid hormone

most commonly caused by Hashimotos thyroiditis

generally more common in women

105
Q

Aetiology of Hypothyroidism

A

Hashimotos thyroiditis

  • most common cause
  • autoimmune condition
  • due to anti-thyroid peroxidase (TPO) and also anti-thyroglobulin (Tg) antibodies

de Quervains thyroiditis

  • subacute granulomatous thyroiditis
  • usually self limiting

Iodine deficiency
-most common cause in developing world

Medication

  • lithium
  • amiodarone

Postpartum thyroiditis

106
Q

Hashimotos thyroiditis

A

Most common cause of hypothyroidism
an autoimmune thyroiditis due to anti-thyroid peroxidase (TPO) and also anti-thyroglobulin (Tg) antibodies

10x more common in women, usually aged 30-50yrs

associated with other autoimmune conditions & MALT lymphoma

107
Q

de Quervains thyroiditis

A

Subacute thyroiditis, usually presenting after viral infection with hypothyroidism

NB the characteristic feature is the painful goitre

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

generally self limiting, thyroid pain may be treated with NSAIDs & aspirin

108
Q

Presentation of Hypothyroidism

A 
weight gain
↓ appetite
cold intolerance
lethargy 
constipation 
hoarse voice
menorrhagia
hyporeflexia
bradycardia
myalgia / stiffness / cramps
hair loss
brittle nails
cold / dry skin
poor memory & difficulty concentrating 
puffy hands / face / feet (myxoedema)
carpal tunnel syndrome
goitre
109
Q

Investigations for Hypothyroidism

A

TFTs

  • TSH ↑
  • free T3/T4 ↓

Anti thyroid peroxidase (TPO) antibodies
-+ve in Hashimotos

Anti-thyroglobulin antibodies
-+ve in Hashimotos

FBC
-anaemia

Creatine kinase (↑)
Cholesterol (↑)

Thyroid USS

110
Q

Management of Hypothyroidism

A

Levothyroxine

  • start with lower dose in IHD & elderly its
  • side effects: AF, worsening angina, ↓ bone mineral density
  • ↑ dose in women who become pregnant

NB TFTs should be monitored annually, and more frequently until correct dose established

111
Q

Myxoedema coma

A

A rare decompensation of established thyroid hormone deficiency generally seen in elderly pts

mortality rate is up to 50%

main precipitants include infection & discontinuation of thyroxine

presents with ↓ level of consciousness, seizures, hypothermia, concurrent myxoedema, hypoventilation & hypercapnia, hypotension, bradycardia and hypoglycaemia

management

  • IV thyroxine
  • IV corticosteroids
  • IV fluids
112
Q

Sick euthyroid syndrome

A

occurs in severe illness or physical stress (usually in ITU pts)

pts have normal thyroid function i.e. no symptoms of hypo/hyperthyroidism

TFTs show ↓T3, ↓T4, ↓/low normal TSH

if underlying illness is treated then TFTs normalise without further treatment

113
Q

Subclinical hypothyroidism

A

defined by ↑TSH but normal T3/T4 levels

usually seen in pts on the way to developing hypothyroidism

NB this is as TSH is a more sensitive & early marker of thyroid problems

114
Q

Poor compliance with thyroxine

A

TSH ↑ but normal T3/T4

usually as pt takes thyroxine the days before their blood test normalising T3/T4 levels but the TSH lags behind so remains ↑

115
Q

Thyroid cancer

A

A carcinoma of the thyroid gland, usually presenting age 30-50yrs

generally uncommon cancer but most common cancer of the endocrine system

Most common type is papillary thyroid cancer

116
Q

Types of thyroid cancer

A

Papillary (~70%)

  • most common type
  • more common in women

Follicular (~20%)
-usually presents as solitary thyroid nodule

medullary (~5%)

  • arises from parafollicular cells (C-Cells)
  • Part of MEN-2
  • secretes calcitonin (i.e. ↑ calcitonin levels)

Anaplastic (~1%)

  • most common in elderly females
  • rapid progression & growth
  • often presents with symptoms of compression
  • very poor prognosis

NB papillary & follicular are well differentiated & carry good prognosis

117
Q

Presentation of thyroid cancer

A

Thyroid nodule

  • hard, fixed nodules more suggestive of cancer
  • usually painless

Features of local infiltration / compression

  • hoarseness
  • dysphagia
  • dyspnoea
  • Horners syndrome (miosis (small pupil), ptosis, enophthalmos, unilateral anhidrosis)

Painless cervical lymphadenopathy

118
Q

Investigations for thyroid cancer

A 
TFTs
thyroid USS
fine needle aspiration cytology
radionucleotide scan
CT/MRI scan
serum calcitonin (↑ in medullary cancer)
thyroglobulin antibodies (used to follow up thyroid cancers)
119
Q

Management of thyroid cancer

A

Total thyroidectomy if cancer >4cm / bilateral disease

radioiodine remnant ablation after surgery

consider radiotherapy

NB there is no effective treatment for anaplastic thyroid cancer

120
Q

Hypoparathyroidism

A

a disorder caused by reactive / absolute deficiency of parathyroid hormone (PTH) leading to ↑phosphate, ↓Ca2+, ↓PTH

generally a rare disorder but most commonly a post-op complication of thyroid surgery causing damage to parathyroid glands

NB in pseudo-hypoparathyroidism ↑phosphate, ↓Ca2+, ↑PTH* due to PTH resistance

121
Q

Aetiology of Hypoparathyroidism

A

Post-op complication of thyroid surgery

  • damage to parathyroids
  • most common cause

Wilsons disease
Haemochromatosis
Radiation damage
DiGeorge syndrome (parathyroid aplasia)

122
Q

Presentation of Hypoparathyroidism

A

Mainly symptoms due to hypocalcaemia

tetany (muscle twitching/cramping/spasm)
perioral paraesthesia
Bone pain
convulsions
brittle nails / nail dystrophy 
memory impairment
facial twitching

Chvostek sign
-tapping over parotid = facial muscle twitch

Troussea sign
-carpal spasm if occluding brachial artery using BP cuff

123
Q

Investigations for Hypoparathyroidism

A 
Phosphate (↑)
Ca2+(↓)
PTH (↓)
Vit D levels (normal)
ECG (prolonged QT interval)
U&Es
124
Q

Management of Hypoparathyroidism

A

Calcium & Vit D supplements

PTH replacement
-helps ↓ dose of Ca2+ replacement

125
Q

Pseudo-hypoparathyroidism

A

results from resistance to actions of PTH produced by a loss of G-protein mediated signalling

characterised by ↑ phosphate, ↓ Ca2+ but ↑ PTH*

associated with ↓ IQ, short stature and shortened 4th & 5th digits

treated with Vit D & Calcium supplements

126
Q

Hyperparathyroidism

A

abnormally high PTH levels due to overactivity the parathyroid glands

May be

  • Primary (usually due to thyroid gland adenoma)
  • Secondary (usually due to CKD or Vit D defiency)
  • Tertiary (occurs after long standing Secondary Hyperparathyroidism)
127
Q

Primary Hyperparathyroidism

A

Usually due to parathyroid gland adenoma causing ↑ PTH secretion
most frequently seen in postmenopausal woman

presents with features of hypercalcaemia e.g. bone bone, pathological fractures, polydipsia, polyuria, depression, constipation, muscle weakness

characterised by PTH (↑), Ca2+ (↑), Phosphate (↓), ALP (↑), urine cAMP (↑)

managed with total parathyroidectomy
NB if unstable for surgery use calcimimetic e.g. cinacalcet

128
Q

Secondary Hyperparathyroidism

A

usually due to CKD or Vit D deficiency causing parathyroid gland to become hyper plastic due to chronic hypocalcaemia

presents with symptoms of CKD, bone pain & pathological fractures
NB there is no features of hypercalcaemia

characterised by PTH (↑), Ca2+ (↓), Phosphate (↑), Vit D (↓), ALP (↑)

Managed with Calcium & Vit D supplements and phosphate restriction ± phosphate binders

129
Q

Tertiary Hyperparathyroidism

A

Occurs after long standing secondary Hyperparathyroidism as parathyroid glands become autonomous and secrete PTH despite Ca2+ being corrected

presents with features of hypercalcaemia (i.e. similar to primary hyperparathyroidism)

characterised by PTH (↑↑), Ca2+ (↑), Phosphate (↑), ALP (↑)

treated with total / subtotal parathyroidectomy or with cinacalcet

130
Q

Differentiating Primary, Secondary and Tertiary Hyperparathyroidism

A

Primary

  • PTH ↑
  • Ca2+ ↑
  • Phosphate ↓
  • presents with features of Hyercalcaemia

Secondary

  • PTH ↑
  • Ca2+ ↓
  • Phosphate ↑
  • No features of hypercalcaemia

Tertiary

  • PTH ↑↑
  • Ca2+ ↑
  • Phosphate ↑
  • presents similar to primary hyperparathyroidism
131
Q

Acromegaly

A

a condition where benign pituitary adenomas lead to excess secretion of growth hormone (GH) & insulin like growth factor 1 (IGF-1)

insidious onset with slow progression, associated with MEN-1 & McCune-Albright syndrome

usually diagnosed in middle age adults ~40y/o
-NB if condition occurs in children before closure of growth plates it is known as gigantism

132
Q

Management of Acromegaly

A

Trans-sphenoidal pituitary adenoma resection (1st line)

if inoperable / unsuccessful surgery

  • 1st line = somatostatin analogues e.g. ocreotide (directly inhibit GH secretion)
  • pegvisomant (GH receptor antagonist)
133
Q

Presentation of Acromegaly

A

Tumour symptoms

  • headaches
  • visual field defects (bitemporal hemianopia)

Gradual change in appearance

  • coarse facial features
  • spade like hands
  • ↑ ring & shoe size
  • large tongue, frontal bossing
  • hyperhidrosis, doughy & oily skin
  • deepening of voice
  • painful arthropathy (ankles, knees, hips, spine)

Hyperprolactinaemia (seen in 1/3 pts)

  • galactorrhoea
  • amenorrhoea
  • erectile dysfunction
  • ↓ libido
134
Q

Investigations for Acromegaly

A

Serum IGF-1

  • levels ↑
  • gold standard investigation

Serum Growth hormone (GH)

  • Levels ↑
  • bit as grid as IGF-1 due to short T1/2

Oral glucose tolerance test (OGTT)

  • no suppression of GH in acromegaly
  • normally pts GH is suppressed <2
pituitary CT/MRI
prolactin (often ↑)
visual field testing 
ECG
Echo (for cardiomyopathy)
135
Q

Diabetes insipidus (DI)

A

A metabolic disorder characterised by an absolute or relative inability to concentrate urine either due to ↓ secretion or insensitivity to anti-diuretic hormone (ADH)

May be Cranial or Nephrogenic

136
Q

Presentation of Diabetes insipidus (DI)

A 
Polyuria 
 -urine volume >3L/24h
Polydipsia
Nocturia
chronic thirst 
dehydration if water not available
137
Q

Diabetes insipidus (DI)

A

A metabolic disorder characterised by an absolute or relative inability to concentrate urine either due to ↓ secretion or insensitivity to anti-diuretic hormone (ADH)

May be Cranial or Nephrogenic

NB Cranial DI is most common kind

138
Q

Water deprivation test results

A

Normal

Psychogenic polydipsia

Cranial Diabetes insipidus

Nephrogenic diabetes insipidus

139
Q

Investigations for Diabetes insipidus (DI)

A 
Urine osmolality (↓)
-NB urine osmolality >700mOsm/kg excludes DI
Serum osmolality (↑)
24h urine volume (>3L)

Water deprivation test

  • deprive to 5% loss of body weight / for 8h then give Desmopressin (DDVAP)
  • Cranial DI = low urine osmolality post deprivation, but normalised urine osmolality post DDVAP
  • Nephrogenic DI = low urine osmolality post deprivation & DDAVP
140
Q

Cranial Diabetes insipidus (DI)

A

Most common form of DI

due to insufficent / absent ADH synthesis / secretion

may be idiopathic, post head injury or due to craniopharyngioma, intracranial surgery or inherited (Wolframs syndrome)

Still sensitive to ADH

Water deprivation test:

  • Starting plasma osmolality: ↑
  • Urine osmolality post deprivation: <300
  • Urine osmolality post DDVAP: >600
141
Q

Nephrogenic Diabetes insipidus (DI)

A

due to insensitivity / resistance of kidney to ADH

may be inherited (often ADH receptor mutation) or medication induced e.g. Lithium (common side effect)

Water deprivation test

  • Starting plasma osmolality: ↑
  • Urine osmolality post deprivation: <300
  • Urine osmolality post DDVAP: <300
142
Q

Water deprivation test results

A

Deprive pt to 5% loss of body weight / for 8h then give Desmopressin (DDVAP)

Normal

  • Starting plasma osmolality:
  • Urine osmolality psot deprivation:
  • Urine osmolality post DDVAP:

Psychogenic polydipsia

  • Starting plasma osmolality:
  • Urine osmolality psot deprivation:
  • Urine osmolality post DDVAP:

Cranial Diabetes insipidus

  • Starting plasma osmolality:
  • Urine osmolality psot deprivation:
  • Urine osmolality post DDVAP:

Nephrogenic diabetes insipidus

  • Starting plasma osmolality:
  • Urine osmolality psot deprivation:
  • Urine osmolality post DDVAP:
143
Q

Water deprivation test results

A

Deprive pt to 5% loss of body weight / for 8h then give Desmopressin (DDVAP)

Normal

  • Starting plasma osmolality: Normal
  • Urine osmolality post deprivation: >600
  • Urine osmolality post DDVAP: >600

Psychogenic polydipsia

  • Starting plasma osmolality: ↓
  • Urine osmolality post deprivation: >400
  • Urine osmolality post DDVAP: >400

Cranial Diabetes insipidus

  • Starting plasma osmolality: ↑
  • Urine osmolality post deprivation: <300
  • Urine osmolality post DDVAP: >600

Nephrogenic diabetes insipidus

  • Starting plasma osmolality: ↑
  • Urine osmolality post deprivation: <300
  • Urine osmolality post DDVAP: <300
144
Q

Primary polydipsia / Psychogenic polydipsia

A

Characterised by excessive volitional water intake often seen in pts with severe mental illness and/or developmental disability

associated with schizophrenia, OCD, autism

generally a diagnosis of exclusion that is managed with fluid restriction & behavioural therapy

145
Q

Presentation fo Primary polydipsia / Psychogenic polydipsia

A 
Polyuria
Nausea 
Headache
water seeking
excessive water intake
146
Q

Investigations for Primary polydipsia / Psychogenic polydipsia

A 
Na+ (↓)
ADH levels (normal)
Plasma osmolality (slightly ↓)
urine osmolality (↓↓)

Water deprivation test

  • Starting plasma osmolality: ↓
  • Urine osmolality post deprivation: >400
  • Urine osmolality post DDVAP: >400
147
Q

Hyperprolactinaemia

A

a condition defined by ↑ serum prolactin levels due to ↑ prolactin secretion by the anterior pituitary

can be physiological e.g. in pregnancy, lactation of in response to stress

most common pathological cause are Prolactinomas (prolactin secreting pituitary adenoma)

overall more common in women

148
Q

Aetiology of Hyperprolactinaemia

A

Physiological

  • pregnancy
  • lactation
  • stress

Pathological

  • Prolactinomas (most common cause)
  • severe hypothyroidism
  • Acromegaly
  • PCOS

Medication / Drugs (usually those agains as dopamine antagonists)

  • metoclopramide
  • domperidone
  • haloperidol
  • risperidone
149
Q

Presentation of Hyperprolactinaemia

A

Men

  • ↓ libido, erectile dysfunction
  • ↓ beard growth
  • gynaecomastia
  • osteoporosis

Females

  • galactorrhoea
  • amenorrhoea / oligomenorrhoea
  • hirsutism
  • ↓ libido
  • atrophic endometrium & vaginal atrophy

NB if prolactinoma may have bitemporal hemianopia, headaches, cranial nerve palsy

150
Q

Investigations for Hyperprolactinaemia

A

Prolactin levels

  • ↑
  • > 5000mU/L indicates prolactinoma

TFTs
pregnancy test
pituitary MRI

151
Q

Management of Hyperprolactinaemia

A

Dopamine agonists

  • e.g. bromocriptine, cabergoline, quinagolide
  • inhibit prolactin secretion via stalls effect

Consider transsphenoidal resection of tumour if medical therapy fails in prolactinoma

152
Q

Hypopituitarism

A

a partial or complete deficiency of one or more pituitary hormones due to damage to the pituitary gland and/or hypothalamus

most common cause is compression of pituitary by non secretory pituitary macroadenoma

153
Q

Aetiology of Hypopituitarism

A

Compression of pituitary by non-secretory pituitary macroadenoma (most common)

pituitary apoplexy
Sheehans syndrome
trauma
iatrogenic irradiation 
hypothalamic tumours e.g. craniopharyngioma
sarcoidosis 
infection e.g. neurosyphilis, meningitis
154
Q

Presentation of Hypopituitarism

A

Symptoms depend on deficient hormone
GH ↓ = short stature if in childhood, otherwise subtle
ACTH ↓ = tiredness, postural hypotension, weight loss
FSH/LH ↓ = amenorrhoea, loss of libido, testicular atrophy, ↓ body hair in men
TSH ↓ = cold intolerance, constipation, tiredness,, bradycardia, weight gain
ADH ↓ = polyuria, polydipsia, inability to concentrate urine

NB if due to pituitary apoplexy = sudden onset symptoms
with severe headache, sudden hypotension

NB if tumour may have mass effect = headache, bitemporal hemianopia

155
Q

Investigations for Hypopituitarism

A 
U&Es
Serum & urine osmolality 
Hormonal assay 
-TFTs
-prolactin
-gonadotrophins
-testosterone
-cortisol
-GH
156
Q

Management of Hypopituitarism

A

treat underlying cause e.g. remove pituitary macro adenoma with surgery

hormone replacement of deficient hormones

157
Q

Pituitary adenoma

A

a common benign tumour of the pituitary gland, account for ~10% of all adult brain tumours

often asymptomatic

classified as micro adenoma <1cm or macro adenoma >1cm, may be secretory or non secretory

Prolactinomas are the most common types followed by none secretory tumours and then GH secreting adenomas (Acromegaly)

158
Q

Presentation of Pituitary adenoma

A

Local effects due to mass effect

  • headache (retro-orbital / bitemporal)
  • visual field defects (bitemproal hemianopia)
  • occular nerve palsy

hypopituitarism
hyperpituitarism (if secretory e.g. acromegaly if secreting GH)

NB sudden severe headache may indicate pituitary apoplexy

159
Q

Investigations for Pituitary adenoma

A 
pituitary function tests for hormone hyper/hyposecretion 
MRI pituitary (contrast enhanced)
160
Q

Management of Pituitary adenoma

A

trans-sphenoidal surgical resection
-1st line

Radiotherapy
-usually after incomplete resection

Bromocriptine if prolactinoma

161
Q

Pituitary apoplexy

A

sudden onset hypopituitarism caused by acute infarction / haemorrhage into pituitary adenoma

presents with sudden onset severe headache, vomiting, neck stiffness, hypotension

require urgent steroid replacement & fluid balancing

162
Q

Hypernatraemia

A

An electrolyte imbalance consisting of a rise in Sodium (Na+) defined as serum Na+ concentration >145mmol/L (normal range 135-145)

Risk factors include elderly pts, infants, altered mental status, AKI, reliance on IV fluids

163
Q

Aetiology of Hypernatraemia

A

Essentially 3 types:

  • Hypovolaemic e.g. dehydration
  • Euvolaemic e.g. renal loss
  • hypervolaemic e.g. excess fluids

dehydration, fluid loss e.g. burns / excessive sweating / GI loss, diabetes insipidus, osmotic diuresis (e.g. HHS/DKA), excessive IV saline, renal loss e.g. loop diuretics

164
Q

Investigations for Hypernatraemia

A 
U&Es (Na+ ↑)
urine & serum osmolality 
Ca2+
glucose
FBC
lithium levels (↑Na+ causes ↓lithium excretion so increased chance of toxicity)
165
Q

Investigations for Hypernatraemia

A 
U&Es (Na+ ↑)
urine & serum osmolality 
Ca2+
glucose
FBC
lithium levels (↑Na+ causes ↓lithium excretion so increased chance of toxicity)
166
Q

Management of Hypernatraemia

A

Address underlying cause where possible
-may be sufficient to address ↑ Na+

Determine fluid requirements

Correct hypernatraemia carefully

  • rate no greater than 0.5mmol/h or 10-12mmol/day
  • correction to rapidly predisposes to cerebral oedema as lowering of other osmolytes other than Na+ / K+ occurs at slower rate especially water

NB acute hypernatraemia (<24h duration) may be corrected quicker

167
Q

Hyponatraemia

A

An electrolyte imbalance consisting of a fall in Sodium (Na+) defined as serum Na+ concentration <135mmol/L (normal range 135-145)

most common electorate abnormality encountered in clinical practice

infants & elderly pts are most at risk

168
Q

Aetiology of Hyponatraemia

A

Sodium depletion (pts often hypovolaemic)

  • renal loss (↑ urine Na+) e.g. loop diuretics
  • Addisons
  • diuretic stage of renal failure
  • extra renal losses (normal urine Na+) e.g. burns, diarrhoea

Euvolaemic

  • SIADH (e.g. in SCLC, storke, SSRIS, SAH, carbamazepine)
  • hypothyroidism

Hypervolaemic

  • HF / liver cirrhosis (secondary hyperaldosteronism)
  • IV dextrose
  • psychogenic polydipsia
169
Q

Presentation of Hyponatraemia

A

symptoms are dictated by absolute Na+ levels & rate of fall of Na+

If rapid ↓

  • confusion, coma, seizures, ataxia, respiratory failure, headaches, N&V, brain stem herniation
  • due to cerebral oedema

if slow ↓
-forgetfulness, gait disturbance, headache, dizziness, fatigue, lethargy

NB sudden drop even if midl can cause significant symptoms

170
Q

Investigations for Hyponatraemia

A

U&Es

  • Na+ ↓
  • NB if K+ ↑ consider addisons

Serum osmolality

  • most commonly ↓,
  • if ↓ = true hyponatraemia e.g. renal loss / SIADH

urine Na+
->20mmol/L indicates renal cause

171
Q

Management of Hyponatraemia

A

If hypovolaemic
-give NaCl 0.9%

If euvolaemic

  • fluid restriction to 500-1000ml / day
  • consider demeclocycline or vaptans

If hypervolaemic

  • fluid restriction to 500-1000ml / day
  • consider loop diuretics & vaptans

If severe i.e. Na+ <120mmol/L

  • monitor in HDU
  • giver hypertonic saline (i.e. NaCl 3%)

NB if untreated hyponatraemia can cause cerebral oedema so prompt treatment is vital

172
Q

Complications of Hyponatraemia

A

Osmotic demyelination syndrome (central pontine myelosis)

  • irreversible
  • can be due to overcorrection of hyponatraemia
  • avoid replacing by >4-6mmol/L per 24h
  • presents with dysarthria, paresis, dysphagia & Locked in syndrome
173
Q

Hypercalcaemia

A

An electrolyte imbalance consisting of a rise in Calcium (Ca2+) defined as serum Ca2+ concentration >2.6mmol/L (normal range 2.1-2.6)

uncommon issue generally but often seen in pts with malignancy

174
Q

Aetiology of Hypercalcaemia

A

Primary hyperparathyroidism & malignancy account for ~90% of cases)

Others:
sarcoidosis, TB, Pagets disease, familial hypocalciuric hypercalcaemia, Vit D intoxication, dehydration

175
Q

Presentation of Hypercalcaemia

A

Stone, Bones, Groan, Psychiatric moans

polyuria, polydipsia 
depression
muscle weakness
constipation, abdo pain
fatigue 
bone pain
kidney stone 
pancreatitis 
dehydration 
cardiac arrhythmias, palpitations
176
Q

Investigations for Hypercalcaemia

A 
Ca2+ (↑)
ECG (short QTc)
phosphate
ALP
urine Ca2+
album level 
calcitonin
PTH
X-rays
177
Q

Management of Hypercalcaemia

A

rehydration with NaCL 0.9%

after rehydration give bisphosphonates

  • IV pamidronate or zolendronic acid
  • NB consider calcitonin if quicker action needed

Use furosemide it pt cannot tolerate fluid therapy

  • use with caution
  • may worsen other electrolyte abnormalities

Steroids
-if sarcoidosis or Vit D toxicity are cause

178
Q

Common blood pictures in hypercalcaemia

A

Primary hyperparathyroidism

  • Ca2+ ↑
  • Phosphate ↓
  • ALP ↑
  • PTH ↑
  • urine calcium ↑

Malignancy

  • Ca2+ ↑
  • Phosphate ↓
  • ALP ↑
  • PTH normal/↓
179
Q

Hypocalcaemia

A

An electrolyte imbalance consisting of a fall in Calcium (Ca2+) defined as serum Ca2+ concentration <2.1mmol/L (normal range 2.1-2.6)

NB factitious hypocalcaemia = asymptomatic ↓ total Ca2+ but normal ionised Ca2+ which is usually due to ↓ serum protein levels

180
Q

Aetiology of Hypocalcaemia

A 
Hypoparathyroidism (↓PTH)
Secondary Hyperparathyroidism (↑PTH)
Pseudohypoparathyroidism 
Others
-acute pancreatitis
-acute rhabdomyolysis 
-massive blood transfusion (citrate in blood products chelates calcium)
-hyperventilation
-medication e.g. citrate, bisphosphonates

NB contamination of blood samples with EDTA may give falsely low Ca2+ readings

181
Q

Presentation of Hypocalcaemia

A 
Paraesthesia (perioral, fingers/toes)
Tetany, muscle cramps / twitching
carpopedal spasm
seizures 
papilloedema 
sub capsular cataracts

Trousseau sign
-carpal spasm if brachial artery occluded by BP cuff i.e. wrist flexion & fingers drawn together)

Chvostek sign
-tapping over parotid leads to facial muscle twitching

182
Q

Investigations for Hypocalcaemia

A 
Ca2+ (↓)
U&Es
amylase
PTH
creatine kinase 
Mg2+
phosphate 
Vit D studies
ECG (↑ QT interval)
urine Ca2+ & Mg2+
fundoscopy
183
Q

Management for Hypocalcaemia

A

Acute:

  • treat if symptomatic or Ca2+ <1.90mmol/L
  • 10ml of 10% calcium gluconate IV over 10min
  • calcium chloride is an alternative but causes local irritation
  • if Mg2+ ↓ then correct this
  • ECG monitoring recommended

Chronic
-Calcium & Vit D supplementation

184
Q

ECG findings in different electrolyte abnormalities

A

Hypocalcaemia
-↑ QT interval

Hypercalcaemia
-↓ QT interval

Hypokalaemia

  • U waves
  • small or absent T waves
  • prolonged PR interval
  • ST depression

Hyperkalaemia

  • Peaked or ‘tall-tented’ T waves (occurs first)
  • Loss of P waves
  • Broad QRS complexes
  • Sinusoidal wave pattern
  • Ventricular fibrillation

Hypomagnasaemia

  • ECG features similar to those of hypokalaemia
  • Wide QRS
  • prolonged QT
  • flat T waves
  • U waves
  • Torsades des pointes
185
Q

Hyperkalaemia

A

An electrolyte imbalance consisting of a rise in Potassium (K+) defined as serum K+ concentration >5.5mmol/L (normal range 3.5-5.0)

Mild = 5.5-5.9 mmol/L
Moderate = 6.0-6.4 mmol/L
Severe = ≥6.5 mmol/L

NB K+ & H+ are competitors, ↑K+ is associated with acidosis as fewer H+ particles can enter cells

186
Q

Aetiology of Hyperkalaemia

A 
AKI
Medication e.g. ACE-Is/ARBs, amiloride, spironolactone, NSAIDs, tacrlimus
Addisons disease
Rhabdomyolysis 
massive blood transfusion
metabolic acidosis

NB errors in blood drawing e.g. prolonged tourniquet time or haemolysed samples may lead to ↑K+

187
Q

Presentation of Hyperkalaemia

A 
Cardiac arrhythmias e.g. VF (i.e. pt may present in cardiac arrest)
muscle weakness
paralysis 
paraesthesia
↓ reflexes
nausea & vomiting
diarrhoea
flaccid paralysis
palpitations

NB cardiac conduction abnormalities are more likely if rapidly ↑ K+

188
Q

Investigations for Hyperkalaemia

A

ECG

  • peaked/tall tented T waves
  • loss of P waves
  • broad QRS complex
  • sinusoidal wave pattern

U&Es (↑ K+)
FBC
ABG
Glucose

NB cardiac conduction abnormalities are more likely if rapidly ↑ K+

189
Q

Management of Hyperkalaemia

A

K+ ≥6.5 or ECG changes require emergency treatment

  • 10ml of 10% calcium gluconate IV
    - helps stabilise cardiac membranes
  • Insulin + dextrose infusion
    - shifts K+ into cells
    - short term ↓ in K+
  • Nebulised salbutamol
    - shifts K+ into cells

Stop exacerbation drugs & treat underlying cause

↑ K+ excretion

  • calcium resonium (PO or enemas*)
  • loop diuretics
  • dialysis (for AKI & persistently ↑K+)
190
Q

ECG features of Hypokalaemia

A 
Peaked or 'tall-tented' T waves (occurs first)
Loss of P waves
Broad QRS complexes
Sinusoidal wave pattern
Ventricular fibrillation
191
Q

Hypokalaemia

A

An electrolyte imbalance consisting of a fall in Potassium (K+) defined as serum K+ concentration <3.5mmol/L (normal range 3.5-5.0)

probably the most common electrolyte disturbance seen in hospitalised pt

192
Q

Aetiology of Hypokalaemia

A 
Vomiting  
thiazide & loop diuretics
Cushing's
Conns syndrome 
diarrhoea
renal tubular necrosis 
acetazolamide
laxatives (especially laxative abuse)
hypomagnesaemia 
RAS
DKA
excessive liquorice ingestion
chronic alcoholism

NB if ↓Mg2+ it can be hard to correct K+ if Mg2+ isn’t normalised

193
Q

Investigations for Hypokalaemia

A

ECG

  • U waves
  • small/absent T waves
  • prolonged PR interval
  • ST depression
  • pseudo QT prolongation
U&Es (↓K+)
Glucose
Mg2+
ABG 
serum digoxin

Nb if K+ ↓ it predisposes to digoxin toxicity so if pt on digoxin then should check digoxin levels

194
Q

Management of Hypokalaemia

A

If mild / low risk pts

  • oral K+ supplementation(40-120mmol/day)
  • regular monitoring

If severe / high risk pts

  • IV KCl in NaCl 0.9%
  • rate of K+ not to exceed 10mmol/h
  • NB ITU may be able to supplement at higher rate

NB if ↓Mg2+ it can be hard to correct K+ if Mg2+ isn’t normalised

NB if hypokalaemia along with hypertension should consider Conn’s syndrome, Cushings syndrome or Liddles syndrome

195
Q

Presentation of Hypokalaemia

A

Mild forms are generally asymptomatic, symptoms generally arise if rapid fall or levels <3.0 mmol/L

muscle weakness, hypotonia, tetany
hypotension
cardiac arrhythmias, palpitations
irregular pulse
constipation
respiratory failure
ileus
196
Q

Hypermagnesaemia

A

Mg2+ levels >1.05 mmol/L (normal range 0.70-1.05), much less common than ↓Mg2+

commonly seen in renal failure, rhabdomyolysis or trauma

presents with facial flushing, N&V, paralytic ileus, hypotension, flaccid muscle paralysis, absent reflexes, bradycardia, respiratory depression, complete heart block or cardiac arrest

investigations show ↑Mg2+, ↓Ca2+

Management includes IV calcium gluconate, IV fluids, Loop diuretics and dialysis (especially if severe i.e. >4mmol/L, renal insufficiency or CVS / neuromuscular symptoms)

197
Q

Hypomagnesaemia

A

Mg2+ levels <0.7mmol/L (normal range 0.70-1.05)

aetiology includes PPIs (especially long running), diuretics, digoxin, theophylline, total parenteral nutrition, malabsorption, acute pancreatitis, refeeding syndrome

presents with paraesthesia, tetany, seizures, arrhythmias, fasciculations, tremor & confusion

198
Q

Management & Investigations for Hypomagnesaemia

A

Investigations

  • Mg2+
  • U&Es
  • Ca2+
  • ECG (Wide QRS, prolonged QT, flat T waves, U waves, Torsades des pointes)

Management

  • Mg2+ <0.4mmol/L or tetany/arrhythmias/seizures
    - IV Magnesium e.g. Magnesium sulphate
  • Mg2+ >0.4mmol/L
    - PO Magnesium salts (NB may cause diarrhoea)

offending medications e.g. PPIs should be stopped

Year 3 (6 decks)

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