Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IPE > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Pathophysiology of T1DM

A

autoimmune destruction of β-cells → absolute

insulin deficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pathophysiology of T2DM

A

insulin resistance and β-cell dysfunction → relative insulin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Presenting symptoms of diabetes mellitus

A

polyuria, polydipsia, ↓wt, lethargy

  • T1DM - DKA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diagnosis of DM

A

Symptoms and 1 abnormal result
Fasting ≥7mM
Random ≥11.1mM
HbA1c ≥ 6.5% (T2DM)

Or 2 results at different times

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Secondary causes of DM

A

 Drugs: steroids, anti-HIV, atypical neuroletics, thiazides
 Pancreatic: CF, chronic pancreatitis, HH, pancreatic Ca
 Endo: Phaeo, Cushings, Acromegaly, T4
 Other: glycogen storage diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define Metabolic Syndrome

A

Central obesity (↑ waist circumference) and two of:  ↑ Triglycerides
 ↓ HDL
 HTN
 Hyperglycaemia: DM, IGT, IFG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lifestyle Modifications in DM

A 
Diet - healthy, reduced refined CHO, avoid alcohol 
Exercise
Lipids (T2 - >40 - statin)
ABP - <130/80
Aspirin >50y/o
Yearly/6m check up 
- control, complications, competency, coping
Smoking cessation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Examination for DM complications

A 
Macro
Pulses
 BP
 Cardiac auscultation
Micro
 Fundoscopy
 ACR + U+Es
 Sensory testing plus foot inspection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Medical management of T2DM

A

1) Metformin
2) + sulphonylura/Gliptin/ Pioglitazone
3) + another
4) + insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Metformin - action, SE and CI

A

↑ cells sensitivity to insulin
SE - diarrhoea, abdo pain, vitamin b12 deficiency, lactic acidosis
CI - GFR<30, tissue hypoxia (sepsis, MI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Sulphonylureas - example action and SE

A

Gliclazide
↑ insulin release from β-cells

SE - weight gain, GI disturbances, ↑ risk hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pioglitazone - Action and SE

A

binding PPAR- γ- upregulates genes that affect glucose and lipid metabolism
SE - weight gain, oedema, liver dysfunction, effects on bone metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gliptins - example, action and SE

A

Sitagliptin - protect native GLP-1 from inactivation by DPP-4
SE - GI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Sodium – Glucose Co-transporter 2 inhibitors - example, action and SE

A

Dapagliflozin - Inhibit SGLT2 (PT) in kidney- decrease glucose reabsorption.

SE - weight loss, Low risk of hypoglycaemia, polyuria and lower UTIs/ Thrush/Urosepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Common Insulin Regimes

A

Biphasic - Twice daily pre-mixed

  • Mixed intermediate and rapid acting insulin BD - before breakfast and dinner
  • regular lifestyle: children, older pts.

Basal-Bolus Regime

  • Bedtime long-acting + short acting before each meal
  • allowing flexible lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Insulin requirements when ill

A

Insulin requirements usually ↑ (even if food intake ↓)
 Maintain calories (e.g. milk)
 Check BMs ≥4hrly and test for ketonuria
 ↑ insulin dose if glucose rising

if in hospital and NBM - variable rate insulin infusion (check capillary blood glucose every 1-2 hours)
- stop when eating and drinking and and long acting insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

SE of Insulin

A

 Hypoglycaemia
- At risk: EtOH binge, β-B (mask symptoms), elderly
 Lipohypertrophy
- Rotate injection site: abdomen, thighs
 Wt. gain in T2DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Macrovascular DM complications and Rx

A

 MI: May be “silent” due to autonomic neuropathy
 PVD: claudication, foot ulcers
 CVA

Rx: Manage CV risk factors
 BP (aim <130/80)
 Smoking
 Lipids
 HBA1c <6%
- regular fundoscopy, foot check
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Features of diabetic feet

A 
ISCHAEMIA
 Critical toes
 Absent pulses (do ABPI)
 Ulcers: painful, punched-out, foot margins, pressure
points

NEUROPATHY
 Loss of protective sensation
 Deformity: Charcot’s joints, pes cavus, claw toes
 Injury or infection over pressure points
 Ulcers: painless, punched-out, metatarsal heads, calcaneum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Management of diabetic feet

A

Conservative
 Daily foot inspection (e.g. ̄c mirror)
 Comfortable / therapeutic shoes
 Regular chiropody (remove callus)

Medical
 Rx infection: benpen + fluclox ± metronidazole

Surgical
 Abscess or deep infection 
 Spreading cellulitis
 Gangrene
 Suppurative arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Pathophysiology of nephropathy in DM

A

Hyperglycaemia → nephron loss and glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Features of nephropathy in DM

A

 Microalbuminuria: urine albumin:Cr (ACR) ≥30mg/mM
 If present → ACEi / ARA
 Refer if UCR >70

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Pathogenesis of retinopathy in DM

A

 Microvascular disease → retinal ischaemia → ↑VEGF

 ↑ VEGF → new vessel formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Presentation of retinopathy of DM

A

 Retinopathy and maculopathy
 Cataracts
 Rubeosis iris: new vessels on iris → glaucoma
 CN palsies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Stages of Diabetic retinopathy

A

Background Retinopathy
 Dots: microaneurysms
 Blot haemorrhages
 Hard exudates: yellow lipid patches

Pre-proliferative Retinopathy
 Cotton-wool spots (retinal infarcts)
 Venous beading
 Haemorrhages

Proliferative Retinopathy
 New vessels
 Pre-retinal or vitreous haemorrhage

Maculopathy
 ↓ acuity may be only sign
 Hard exudates w/i one disc width of macula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Pathophysiology of neuropathy

A

 Metabolic: glycosylation, ROS, sorbitol accumulation

 Ischaemia: loss of vasa nervorum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Features of polyneuropathy in DM

A

 Glove and stocking: length-dependent ( feet 1st)
 Loss of all modalities
 Absent ankle jerks
 Numbness, tingling, pain (worse @ night)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Treatment of polyneuropathy of DM

A

 Paracetamol
 Amitriptyline, Gabapentin, SSRI
 Capsaicin cream
 Baclofen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Pathogenesis of DKA

A

Ketogenesis
 ↓ insulin → ↑ stress hormones and ↑ glucagon
 → ↓ glucose utilisation + ↑ fat β-oxidation
 ↑ fatty acids → ↑ ATP + generation of ketone bodies.

Dehydration
 ↓ insulin → ↓ glucose utilisation + ↑ gluconeogenesis → severe hyperglycaemia
 → osmotic diuresis → dehydration
 Also, ↑ ketones → vomiting

Acidosis
 Dehydration → renal perfusion
 Hyperkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Precipitants of DKA

A

 Infection / stress ± stopping insulin
 New T1DM
 Alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Presentation of DKA

A 
 Abdo pain + vomiting
 Gradual drowsiness/ confusion
 Sighing “Kussmaul” hyperventilation
 Dehydration
 Ketotic breath
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Diagnosis of DKA

A

 Acidosis (↑AG): pH <7.3 (± HCO3 <15mM)
 Hyperglycaemia: ≥11.1mM (or known DM)
 Ketonaemia: ≥3mM (≥2+ on dipstix)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Investigations for DKA

A 
 Urine: ketones and glucose, MCS
 Cap glucose and ketones
 VBG: acidosis + ↑K
 Bloods: U+E, FBC, glucose, cultures
 CXR: evidence of infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Treatment of DKA

A
  • Fluids
  • Potassium replacement (if <5.5)
  • Insulin Infusion (actrapid) - 1 unit/kg/hr
    +- catheter; NGT; LMWH; find and treat precipitating factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Aims with DKA treatment

A

 ↓ ketones by ≥0.5mM/h or ↑HCO3 by ≥3mM/h
 ↓ plasma glucose by ≥3mM/h
 Maintain K in normal range
 Avoid hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Resolution of DKA

A

 Ketones <0.3mM + venous pH>7.3 (HCO3 >18mM)
 Transfer to sliding scale if not eating
 Transfer to SC insulin when eating and drinking
 Pt Education and action plan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Hyperglycaemic Hyperosmolar State presentation

A 
Usually T2DM, often new presentation
 Usually older
 Long hx (e.g. 1wk)
 Marked dehydration and glucose >30mM/L
 No acidosis (no ketogenesis)
 Osmolality >320mosmol/kg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Complications of HHS

A

Occlusive events are common: DVT, stroke, leg ischaemia

- Give LMWH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Management of HHS

A 
 Rehydrate --> 0.9% NS over 48h 
- May need ~9L
 Wait 1h before starting insulin 
- It may not be needed
-  Start low to avoid rapid changes in osmolality
 --> E.g. 1-3u/hr (to avoid cerebral oedema)
 Look for precipitant 
 - MI
 - Infection
 - Bowel infarct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Symptoms of hypoglycaemia

A 
Autonomic: 2.5-3
 Sweating
 Anxiety
 Hunger
 Tremor
  Palpitations
Neuroglycopenic: <2.5
 Confusion
 Drowsiness
 Seizures
 Personality change
 Focal neurology (e.g. CN3) 
 Coma (<2.2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Causes of hypoglycaemia

A

 Usually insulin or sulfonylurea Rx in a known diabetic
 Exercise, missed meal, OD

 Exogenous drugs
 Pituitary insufficiency
 Liver failure
 Addison’s
 Islet cell tumours (insulinomas)
 Immune (insulin receptor Abs: Hodgkin’s)
 Non-pancreatic neoplasms: e.g. fibrosarcomas

42
Q

Investigations of hypoglycaemia

A

 72h fast ̄c monitoring

 Symptom: Glucose, insulin, C-peptide, ketones

43
Q

Management of hypoglycaemia

A

Conscious and able to help self –> Rapid acting: lucozade or 5-7 glucose tablets
Conscious but unable to help self –> Dextrogel

  • wait 15 min and check; can repeat up to 3x
    If corrected then give long acting snack (toast)

Unconscious (GET SENIOR HELP)and IV access –> 20% glucose 75ml in 15min (can repeat)
Unconscious and no Iv access –> IM 1g Glucagon

If responded long acting snack

After snack check CBG in 30-60 mins then refer for hypoglycaemic education. Monitor CBG for 24-48 hours.

44
Q

Thyrotoxicosis symptoms

A 
 Diarrhoea
 ↑ appetite but ↓ wt.
 Sweats, heat intolerance
 Palpitations
 Tremor
 Irritability
 Oligomenorrhoea ± infertility
45
Q

Thyrotoxicosis signs

A 
Hands
 Fast / irregular pulse
 Warm, moist skin
 Fine tremor
 Palmer erythema
Face
 Thin hair
 Lid lag
 Lid retraction
Neck
 Goitre or nodules
Graves’ Specific
 Ophthalmopathy
 Exophthalmos
 Ophthalmoplegia: esp. up-gaze palsy 
 Eye discomfort and grittiness
 Photophobia and ↓ acuity
 Chemosis
 Dermopathy: pre-tibial myxoedema
 Thyroid acropachy
46
Q

Investigations for thyrotoxicosis

A 
 ↓TSH, ↑T4/↑T3
 Abs: TSH receptor, TPO
 ↑Ca, ↑LFTs
 Isotope scan
 ↑ in Graves’
 ↓ in thyroiditis
 Ophthalmopathy: acuity, fields, movement
47
Q

Management of thyrotoxicosis

A

Medical
 Symptomatic: β-B (e.g. propranolol 40mg/6h)
 Anti-thyroid: carbimazole (inhibits TPO)
 Titrate according to TFTs or block and replace  In Graves’ Rx for 12-18mo then withdraw
 ~50% relapse → surgery or radioiodine  SE: agranulocytosis

Radiological: Radio-iodine
 Most become hypothyroid
 CI: pregnancy, lactation

Surgical: Thyroidectomy
 Recurrent laryngeal N. damage → hoarseness  Hypoparathyroidism
 Hypothyroidism

48
Q

Features of thyroid storm

A 
 ↑temp
 Agitation, confusion, coma
 Tachycardia, AF
 Acute abdomen
 Heart failure
49
Q

Precipitants of thyroid storm

A

 Recent thyroid surgery or radio-iodine
 Infection
 MI
 Trauma

50
Q

Management of thryoid storm

A
  1. Fluid resuscitation + NGT
  2. Bloods: TFTs + cultures if infection suspected
  3. Propranolol PO/IV (counteracts peripheral effects of t3/4)
  4. Carbimazole
  5. Hydrocortisone (I. thyroid hormone synthesis)
  6. Rx cause (e.g. Abx)
  7. no change in 24h > thyroidectomy
51
Q

Signs of hypothyroidism

A 
 Bradycardic 
 Reflexes relax slowly 
 Ataxia
 Dry hair and skin
 Yawning (lethargy)
 Cold hands
 Ascites and Myxoedema
 Round Puffy face
 Depression and mental slowing
 Intolerant to cold
 Appetite ↓; ↑wt
Other:
 Constipation
 Menorrhagia
 CTS
 Goitre
 Myopathy, neuropathy
52
Q

Causes of hypothyroidism

A

Primary
 Atrophic thyroiditis (commonest UK)
 Hashimoto’s thyroiditis
 Subacute thyroiditis (e.g. post-partum)
 Post De Quervain’s thyroiditis
 Iodine deficiency (commonest worldwide)
 Drugs: carbimazole, amiodarone, lithium
 Congenital: thyroid agenesis

Post-surgical
 Thyroidectomy  Radioiodine

Secondary
 Hypopituitarism (v. rare )

53
Q

Investigations for hypothyroidism

A 
 ↑TSH, ↓T3/T4
 ↑MCV ± normochromic anaemia 
 ↑ triglyceride + ↑ cholesterol
 Hyponatraemia (SIADH)
 ↑ CK if assoc. myopathy
 Abs: TPO, TSH
54
Q

Management of hypothyroidism

A

 Levothyroxine
- Titrate to normalise TSH
- Enzyme inducers ↑ thyroxine metabolism
0 Clinical improvement takes ~2wks
 Check for other AI disease: e.g. Addison’s, PA

55
Q

Features of hashimoto’s thyroiditis

A

 TPO +ve
 Atrophy + regeneration → goitre
 May go through initial thyrotoxicosis phase
 May be euthyroid or hypothyoid

56
Q

Features of myxoedema coma

A 
 Looks hypothyroid
 Hypothermia
 Hypoglycaemia
 Heart failure: bradycardia and ↓BP 
 Coma and seizures
57
Q

Precipitants of myxoedema coma

A

 Radioiodine
 Thyroidectomy
 Pituitary surgery
 Infection, trauma, MI, stroke

58
Q

Management of myxoedema coma

A

 Bloods: TFTs, FBC, U+E, glucose, cortisol
 Correct any hypoglycaemia
 T3/T4 IV slowly (may ppt. myocardial ischaemia)
 Hydrocortisone 100mg IV
 Rx hypothermia and heart failure

59
Q

Complications of thyroid surgery

A
  • haematoma
  • laryngeal oedema
  • recurrent laryneal nerve palsy
  • hypoparathyroidism
  • thyroid storm
  • hypothyroidism
60
Q

Features of cushing

A 
Cataracts
Ulcers
Striae/ thin skin
Hypertension/ Hirsutidsm
Immunosuppresion/ INfection 
Necrosis of femoral head
Glucose high
Osteoporosis, obesity
Impaired wound healing and bruising 
Depression
  • Moon face and thin limbs
  • Proximal myopathy
  • Acne
  • hypokalaemia
    Interscapular and supraclavicular fat pad
61
Q

Causes of Cushing’s

A

ACTH Independent causes

  • Iatrogenic steroids
  • Adrenal adenoma/ Ca
  • Adrenal nodular hyperplasia

ACTH - dependent causes

  • Cushing’s disease
  • Ectopic ATCH
62
Q

Ix for Cushings

A

1) 24h urinary free cortisol x 3
2) Dexamethosone suppression test
- Suppression at high dose - cushing’s disease (bilateral hyperplasia from ACTH secreting pituitary tumour)
> MRI pituitary
- No suppression - Adrenal cause/ Ectopic ACTH
> CT thorax/ adrenals

+- DEXA scan

63
Q

Treatment for Cushing’s

A
  • Iatrogenic steroids –> stop meds
  • Adrenal adenoma/ adrenal nodular hyperplasia –> adrenelectomy
  • Ectopic ACTH - - tumour excision +- metyropone
  • Cushing’s disease - transphenoidal excision
64
Q

What is Nelson’s syndrome

A

Rapid enlargement of a pituitary adenoma i fhave cushing disease following bilateral adrenelectomy

65
Q

Physical effects of Cushing’s disease

A
  • Bitemporal hemianopia (compresses optic chiasm)
  • hypopituitarism and hyperprrolactinaemia (compresses stalk and removes I)
  • Headache and double vision (invades cavernous sinus)
  • -> opthalmoplegia, Chemosis, Proptosis, Horners, CN sensory loss
66
Q

Features of Hyperaldosteronism

A

 Hypokalaemia: weakness, hypotonia, hyporeflexia, cramps
 Paraesthesia
 ↑BP

67
Q

Causes of hyperaldosteronism

A

PRIMARY
 Bilateral adrenal hyperplasia (70%)
 Adrenocortical adenoma (30%): Conn’s syndrome

SECONDARY 
 RAS
 Diuretics
 CCF
 Hepatic failure
 Nephrotic syndrome
68
Q

Treatment of hyperaldosteronism

A

 Conn’s: laparoscopic adrenelectomy
 Hyperplasia: spironolactone, eplerenone or amiloride
Ix

69
Q

Actions of Angiotensin 2

A
  • ↑ADH (thirst centre and CD in kidney)
  • ↑ sympathetic activity - ↑ NAdr
  • ↑ Aldosteone
    = ↑ Na + Cl reabsorption + H20+K excretion
  • Arteriolar vasoconstriction - ↑ BP
70
Q

Pathophysiology of Addison’s Disease

A

Destruction of adrenal cortex → glucocorticoid and mineralocorticoid deficiency

71
Q

Causes of Addison’s

A 
 Autoimmune destruction: 80% in the UK
 TB: commonest worldwide
 Metastasis: lung, breast, kidneys
 Haemorrhage: Waterhouse-Friedrichson
 Congenital: CAH
72
Q

Clinical features of Addison’s

A 
 Wt. loss + anorexia
 n/v, abdo pain, diarrhoea/constipation
 Lethargy, depression
 Hyperpigmentation: buccal mucosa, palmer creases
 Postural hypotension → dizziness, faints
 Dry mouth and reduced skin turgor
 Hypoglycaemia
 Vitiligo
 Addisonian crisis
 Sparse axillary and pubic hair
73
Q

Symptoms of Addison’s

A

Tired - fatigue and weakness
Tanned - hyperpigmentation
Tearful - apathy and depression
Thin - weight loss/ n+v+d/ anorexia +/- abdo pain

74
Q

Investigations for Addison’

A

Bloods - ↓Na/↑K (as ↓ mineralocorticoid) ↓glucose (↓ cortisol); ↓Ca, (+- uraemia - dehydration)
 Anaemia

Differential
 Short synACTHen test
- Cortisol before and after tetracosactide (should stimulate adrenals to produce cortisol)
- Exclude Addison’s if ↑ cortisol; ↑ 9am ACTH (usually low)

Other
 21-hydroxylase Abs: +ve 80%  AI  
 Plasma renin and aldosterone
 CXR: evidence of TB
 AXR: adrenal calcification
 CT/MRI of adrenals
75
Q

Treatment of Addison’s

A

Replace
 Hydrocortisone
 Fludrocortisone
- emergency hydrocortisone injectino kit

Advice
 Don’t stop steroids suddenly
 ↑ steroids during intercurrent illness, injury
 Wear a medic-alert bracelet and steroid card

F/up
 Watch for AI disease e.g. pernicious anaemia
 yearly BP/ UE

76
Q

Causes of secondary adrenal insufficiency

A

hypothalamo or pituitary failure

 Chronic steroid use → suppression of HPA axis
 Pituitary apoplexy / Sheehan’s
 Pituitary microadenoma

  • No pigmentation as low ACTH
77
Q

Presentation of an Addisonian Crisis

A

 Shocked: ↑HR, postural drop, oliguria, confused
 Hypoglycaemia

Usually known Addisonian or chronic steroid user

78
Q

Precipitants of an Addisonian Crisis

A

 Infection
 Trauma
 Surgery
 Stopping long-term steroids

79
Q

Management of an Addisonian Crisis

A 
 Bloods: cortisol, ACTH, U+E, cultures
  ECG - ↑ K+
 Check CBG: glucose may be needed
 Hydrocortisone 100mg IV/IM 6hrly
- oral after 72h and ween off dose
 IV fluid bolus
 Septic screen
 Treat underlying cause
80
Q

What is a pheochromocytoma

A

Catecholamine-producing tumours arising from sympathetic paraganglia

Usually found in adrenal medulla

Extra-adrenal phaeo’s found by aortic bifurcation

81
Q

Presentation of a pheochromocytoma

A

Triad: episodic headache, sweating and tachycardia

 ↑BP, palpitations
 Headache, tremor, dizziness 
 Anxiety
 d/v, abdo pain
 Heat intolerance, flushes

May have precipitant
 Straining, abdo palpation
 Exercise, stress
 β-B, IV contrast, TCAs, GA

82
Q

Investigations for pheochromocytoma

A

 Plasma + 24h urine metadrenaline and normetadrenaline
 Also vanillylmandelic acid
 Abdo CT/MRI
 MIBG (mete-iodobenzylguanidine) scan

83
Q

Management of pheo

A

Medical: Chemo or radiolabelled MIGB

Surgery: adrenelectomy
 α-blocker first, then β-blockade pre-op
 Avoids unopposed α-adrenergic stimulation
 Phenoxybenzamine = α-blocker

Monitor BP post-op for ↓↓BP and 24hr urine 2 weeks post up
follow up is lifelong

84
Q

Hypertensive crisis features

A 
Pallor
Pulsating headache 
Feeling of impending doom 
↑↑BP
↑ ST and cardiogenic shock
85
Q

Management of a hypertensive crisis

A

Phentolamine 2-5mg IV (α-blocker) or labetalol 50mg IV
- Repeat to safe BP (e.g. 110 diastolic)
Then α-blocker PO with elective surgery 4-6 weeks latere

86
Q

Causes of raised prolactin

A 
Pregnancy 
Prolactinoma
Physiological
PCOS
Primary hypothyroidism
Pheothiazine/ metochlopramide
87
Q

Symptoms of hyperprolactinaemia

A 
High PRL --> ↓ LH/FSH
 Amenorrhoea
 Infertility
 Galactorrhoea
 ↓ libido
 ED
 Mass effects from prolactinoma - headache; bitemporal hemianopia; CN 3,4,5,6 palsy; DI; CSF rhinorrhoea
88
Q

Treatment of hyperprolactinaemia

A

prolactinoma (Prolactin 100,000 iU/L) –> treated medically (dopamine agonist e.g. bromocryptine)

Non-functioning adenoma (Prolactin 1,500 iU/L) –> treated surgically transphenotelectomy (or if visual/ pressure symptoms)

89
Q

Causes of Acromegaly

A

 Pituitary acidophil adenoma in 99%

 Hyperplasia from GHRH secreting carcinoid tumour

90
Q

Symptoms of Acromegaly

A 
 Acroparaesthesia
 Amenorrhoea, ↓libido
 Headache
 Snoring
 Sweating
 Arthralgia, back ache
 Carpal tunnel (50%)
 Change in shoe size
91
Q

Signs of Acromegaly

A 
Hands
 Spade-like
 Thenar wasting
 Boggy sweaty palms (if active)
 ↑ skin fold thickness
 Carpal tunnel: ↓ sensation + thenar wasting
Face
 Prominent supraorbital ridges
 Scalp folds: cutis verticis gyrata
 Coarse face, wide nose and big ears
 Prognathism/ Macrognathia
 Macroglossia
 Widely-spaced teeth
 Goitre
 Hirsutism 
Other
 Puffy, oily, darkened skin skin
 Acanthosis Nigricans 
 Tolling gait with bowed legs
 Proximal weakness + arthropathy
 Pituitary mass effects: bitemporal hemianopia
92
Q

Investigations for Acromegaly

A
  • GH response to OGTT (failure to suppress GH)
  • MRI pituitary
  • Plasma IGF1
    Blood - TSH+T4, prolactin, FSH + LH, GH
  • Visual fields and acuity
93
Q

Treatment of acromegaly

A

1st line: trans-sphenoidal excision

2nd line: re – octreotide

3rd line: GH antagonist – pegvisomant

4th line: radiotherapy

94
Q

Effects of GH on the body

A

Direct

  • carbohydrate metabolism - ↑ blood glucose
  • Fat metabolism - ↑ breakdown and release

Indirect

  • -> LIVER –> IGF1
  • ↑ cartilage formation & skeletal growth
  • ↑ protein synthesis, cell growth + proliferation
95
Q

Complications of Acromegaly

A

 Impaired glucose tolerance (40%)
 DM (15%)

 ↑BP
 LVH/ HF
Cardiomyopathy
 ↑ IHD and ↑ stroke

 ↑ risk of CRC

96
Q

Symptoms of Diabetes Insipidus

A

 Polyuria
 Polydipsia
 Dehydration
 Hypernatraemia: lethargy, thirst, confusion, coma

97
Q

Causes of DI

A 
Cranial - inadequate ADH secretion
 Idiopathic: 50%
 Congenital: DIDMOAD / Wolfram Syndrome
 Tumours
 Trauma
 Vascular: haemorrhage (Sheehan’s syn.)
 Infection: meningoencephalitis
 Infiltration: sarcoidosis
Nephrogenic - failure of kidneys to respond to ADH
 Congenital
 Metabolic: ↓K, ↑Ca
 Drugs: Li, demecleocycline, vaptans
 Post-obstructive uropathy
98
Q

Investigations for DI

A

Bloods: U+E, Ca, glucose
 Urine and plasma osmolality - Exclude DI if U:P osmolality >2
- Water deprivation test +/- desmopressin trial

99
Q

Management for DI

A

If mild (3-4L) - no treatment

Cranial- Find cause: MRI brain and Desmopressin PO (SE - hyponatraemia and worsen myocardial ischaemia)

Nephrogenic - Treat cause +- bendroflumethiazide

100
Q

Causes of Hirsutism

A
  • familial
  • idiopathic
  • increased androgens (PCOS; Cushings; Adrenal Ca; Steroids)
101
Q

Causes of gynaecomastia

A
  • Cirrhosis
  • Hypogonadism
  • Hyperthyroidism
  • Hypopituitary
  • oestrogen/ HCG - producing tumour
  • Drugs - spiro/ oestrogen
102
Q

Causes of erectile dysfunction

A
  • smoking
  • alcohol
  • DM
  • Endo - hypogonadism, hyperthyroidism
  • Neuro - MS; autonomic neuropathy; cord lesion
  • Pelvic surgery - bladder; prostate
  • Peyronie’s disease

IPE (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions