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Final > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

T1 and T2 diabetes pathophys

A

T1 = Autoimmune destruction of pancreatic islet cells cause reduced insulin

T2 = Insulin resistance and hyper secretion of insulin which fails to keep up with inc demand leading to failure of beta cells

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2
Q

C-peptide in diabetes

A

low in T1

high in T2

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3
Q

Assoc features of diabetes

A

Retinopathy (cotton wool spots, haemorrhage)
Neuropathy (glove stocking)
Nephropathy
Skin infection/UTI

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4
Q

Pancreatic Islet cell and function

A

Alpha cells = Glucagon

Beta cells = Insulin

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5
Q

Mechanism of insulin release

A

Glucose enters beta cells via GLUT2, increased ATP, this closes K+ channels to depolarise cell, opens Ca channels and cellular release of Insulin

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6
Q

Role of insulin

A

Increase live and muscle uptake of glucose

Suppress: Gluconeogenesis, Lipolysis, Proteolysis, Ketogenesis

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7
Q

T1DM

  • Aetiology,
  • Presentation,
  • Complications
A
  • Genetic predisposition, autoimmune process (env trigger??)
  • FH of autoimmune disease (HLA DR3/4)
    Polyuria, polydipsia, weight loss, lethargy, DKA (dehydration, ketones, abdominal pain)
  • DKA
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8
Q

T2DM

  • RF
  • Presentation
A
  • BMI over 30, low activity, PCOS, metabolic syndrome, FH, South Asian, Gestational diabetes
  • Polyuria, polydipsia, lethargy, prolonged/frequent infections (e.g. thrush)
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9
Q

Investigating DM

A

Urine dip, Oral Glucose tolerance test, Fasting glucose (over 7 is diagnostic)

HbA1c (over 48mmol.mol or 6.5%)

Ix for complications - urine dip (protein), fundoscopy, BP for HTN, fasting lipids (hyperlipidaemia)

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10
Q

when might HbA1c not be accurate?

A

In anaemic patients, esp haemolytic anaemia

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11
Q

HbA1c treatment goal

A

below 58mmol/mol of 7.5%

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12
Q

Diabetic Neuropathy

A

Hyperglycaemia causes oxidative stress and destruction of myelin sheath. Glove and stocking distribution

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13
Q

Diabetic Nephropathy

A

Hyperglycaemia thickens glomerular BM (sclerosis)

Narrowing efferent artery inc pressure in glomerulus.

The above cause inc gaps between podocytes (more permeable)

Proteinuria and decreased GFR occur due to kidney damage

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14
Q

Diabetic Retinopathy

A

microvascular occlusion - retinal ischaemia, can see neovascularisation

Pericyte loss - diffuse haemorrhage and oedema

Microaneurysms and haemorrhages

Cotton wool spots from axonal debris build up

number of microaneurysms and quadrants involved determine severity

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15
Q

CVS risks in DM

A

MI/Stroke

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16
Q

Autonomic dysfunction in DM

A

Erectile dysfunction, Bladder retention, postural hypotension, tachycardia, diarrhoea

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17
Q

infection in diabetes

A

due to hyperglycaemia causing reduced phagocytosis

Give pneumococcal vaccine and annual influenza

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18
Q

Diabetic foot

  • Incidence
  • importance
  • Presentation
  • Mech
  • Chronic features
A
  • 10% diabetics
  • most common cause of amputation
  • Hot, swollen foot, painless punched out (neuropathic) ulcers
  • loss of sensation during damage, ulcer development, bone degeneration, poor healing
  • Rockerbottom sole, Charcot foot
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19
Q

Diabetic eye probs presentation and treatment

A
  • Painless reduction in central vision, Haemorrhage (sudden onset dark painless floater)
  • optimise BP/glycaemic control/lipid control, Anti-VEGF, Intravitreal steroids (laser photocoagulation)
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20
Q

Emergency referral of diabetic eye

A

Sudden loss of vision
Red eye
Retinal detachment

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21
Q

Diabetes Tx

A

lifestyle and diet (6weeks) inform DVLA
- low glucose, dairy, control fats, limit sugar and lose weight.

HbA1c 3-6monthly and then 6 monthly aim for 48mmol/mol or 6.5%

single drug therapy - Metformin (unless not tolerated) - 6.5% target

dual therapy - metformin + gliptin/sulfonylurea/pioglitazone - target 7% (53mmol/mol

Triple therapy - if still not 58mmolmol/7.5% add third drug or consider insulin

if can’t give metformin then on of the above, add another if not control and then third line is insulin

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22
Q

Diabetes annual review checks

A

BMI

Complications: Hypos, Hyperosmolar hypoglycaemic state, DKA

CVS assess: BP, pulses, bruits

inspect injection sites (lipodystrophy)

Foot check (neuropathy and pulses)

Urine: protein, nitrites, ketones

Eyes: acuity and ophthalmoscopy

Erectile dysfunction

Bloods: HbA1c

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23
Q

Metformin

  • mech
  • CI
  • SE
A

Increases sensitivity to insulin

CKD

GI upset: nausea and diarrhoea (20% don’t tolerate)

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24
Q

Gliptin

  • mech
  • SE
A

Raised incretin produce more insulin when needed

GI upset, flu-like symptoms

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25
Q

Sulfonylurea

  • mech
  • CI
  • SE
A

increase pancreatic insulin secretion (S for secretion and Sulfonylurea)

Pregnancy CI

Can cause Hypo (affecting insulin release), weight gain

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26
Q

Pioglitazone

  • mech
  • CI
  • SE
A

increases insulin sensitivity

osteoporosis, heart failure (due to fluid retention SE)

weight gain, fluid retention, osteoporosis

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27
Q

Insulin Regimes

A

Once daily

  • Long/intermediate acting at bedtime
  • only for T2DM

Twice daily
- Pre-breakfast/evening meal

Basal-bolus
- Long/intermediate acting at bedtime with short acting to cover meals

Continuous subcut or insulin pump
- in those with v poor control

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28
Q

NICE Tx T1DM

A

Basal Bolus regimen

  • twice daily insulin deter (long acting)
  • Rapid acting insulin analogue (humalog, novorapid) before meals
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29
Q

Nice Tx T2DM

A

Intermediate acting insulin twice per day: Humulin N or Novolin N

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30
Q

SE of insulin Tx

A

Hypoglycaemia
- Sweating, confused, aggression, blurred vision
Lipodystrophy

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31
Q

Tx for a Hypo

A

Conscious:
- 10-20g short acting carb (glass of lucozade, glucogel)

Unconscious:
- IM Glucagon

Inform DVLA

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32
Q

What to do if Diabetic is unwell

A

4 hourly BG monitoring, monitor ketones
3L fluid every 24 hours

continue oral med, continue insulin with inc monitoring

Stress response = inc cortisol this increases blood sugars and decreases insulin so may need more control

seek help: glucose more than 13mmol/L, DKA signs, BG over 25 and giving more insulin.

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33
Q

DKA precipitants

A
  • Missed insulin
  • Infection (corticosteroid risk hyperglycaemia)
  • Intoxication (live impairment)
  • Ischaemia
  • Infarction
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34
Q

Presentation of DKA

A

Abdominal Pain + Vomiting

Polyuria, polydipsia, dehydration

Kussmaul breathing (deep hyperventilation to correct acidosis)

Acetone breath

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35
Q

Pathophysiology DKA

A
  • Decreased insulin
  • Inc protein and fat metabolism
  • Ketogenesis from lipolysis
  • Acidosis(ketones), hyperglycaemia, Osmotic diuresis, Hypokalaemia (Due to acidosis)
  • Dehydration, Acidosis, Coma, Death
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36
Q

ECG Hypokalaemia

A

PRSTTU

PR prolonged
ST depression
T flat/inverted
Prominent U wave after T

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37
Q

DKA investigation findings

A

Plasma glucose: over 11
Plasma Ketones: over 3mmol/l
ABG: pH over 7.3
Urine dip: Ketones and glucose high

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38
Q

DKA management

  • Fluids
  • Hyperglycaemia
  • What to watch out for
  • Acidaemia
A
  • IV NaCl: 1L in 1st hour, 1L in 2nd hour, 1L in following 2hrs and 1L every 4 hours. When BG below 180mg/mol use 5-10% dextrose
  • IV Insulin
  • Hypokalaemia (insulin causes K+ to enter cells)
  • IV Bicarbonate
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39
Q

Hyperosmolar hyperglycaemic state

  • Who gets
  • What can be seen on blood tests
A

T2DM (no DKA as enough insulin to suppress ketogenesis)

Very high blood glucose (over 40) V. high serum osmolality.
over 320mosmol/kg- normal is 285-290
Hypovolaemia

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40
Q

What is osmolality

Osmolarity

A

concentration expressed as number of solute particles per Kg fluid

Osmolarity is per L fluid

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41
Q

Precipitants to Hyperosmolar hyperglycaemic state

A

Infection, MI, Dehydration, Thiazides and loop diuretics, poor glucose control.

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42
Q

Hyperosmolar hyperglycaemic state Pathogenesis

A

Hyperglycaemia, osmotic diuresis, hyperosmolarity gives fluid shift into intravascular compartment = severe dehydration

No ketogenesis as some residual pancreatic function surpasses ketogenesis

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43
Q

Hyperosmolar hyperglycaemic state Presentation

A

Extreme dehydration and altered mental state
± seizures
± delirium

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44
Q

Investigation findings Hyperosmolar hyperglycaemic state

A

Urinalysis - glycosuria and sometimes ketonuria (mild)
Blood glucose - over 30
Serum osmolality - over 320mmol/L
U&E - shows AKI (high creatinine+urea)
ABG - normal

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45
Q

Hyperosmolar hyperglycaemic state Tx

A

Treat cause (e.g. infection, dehydration)

replace fluid and electrolytes to normalise osmolality (NaCl, positive balance of 3-6 L by 12 hours)

Insulin if glucose not falling with other medications.

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46
Q

Hyperosmolar hyperglycaemic state complications

A

Seizures
Cerebral oedema (if glucose drop too quick)
Pontine myelinosis

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47
Q

Pathogenesis of Cerebral Oedema in DKA and Hyperosmolar hyperglycaemic state

A

Sudden drop in blood glucose and decrease in osmolality

Brain traps osmotially active particles

Conc gradient means fluid moves from intravasc to brain parenchyma

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48
Q

Metabolic syndrome criteria for Dx

A 
Truncal obesity or BMI over 30
BP systolic over 130 or prev HTN
High triglycerides
Reduced HDL
fasting glucose over 6.1mmol/l (prediabetes)
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49
Q

Metabolic Syndrome complications

A

Atherosclerosis (CVD), Diabetes, PCOS, NAFLD

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50
Q

Cause of metabolic syndrome

A

Obesity epidemic - Overnutrition, atherogenic diet, sedentary lifestyle

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51
Q

BMI Levels

A 
under 18.5 = under
18.5 - 24.9 = Optimal
25-29.9 = Over
30-34.9 = Obese I
35-39.9 = Obese II
Over 40 = Obese III
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52
Q

Medication causes of Obesity

A 
Glitazone, Sulfonylurea
Anticonvulsants
Antidepressants: tricyclics, mirtazapine
Lithium
Progesterone only contraception
BB
Corticosteroids
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53
Q

Conditions that cause obesity

A 
PCOS
Hypothyroidism
Cushing's
Hypogonadism
Prader-Willi
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54
Q

When to consider surgery in Obesity

A 
Obese II (BMI 35-39.9)
Always try lifestyle (diet & exercise) and drug (e.g. Orlistat)
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55
Q

How does Orlistat work

A

Inhibits lipase

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56
Q

Gynaecomastia pathophysiology

A

balance between oestrogen (stimulate) and androgens (inhibit).

Conditions raising oestrogen, dropping testosterone or increase in conversation androgen to oestrogen (aromatisation by inc fats)

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57
Q

Physiological causes of gynaecomastia

A

in early teenage assoc with delayed testosterone.

Unilateral and tender

Also seen with ageing (dec in testosterone)

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58
Q

Pathological causes gynaecomastia

A

Low testosterone:
- Androgen resistance, Klinefeltners, Viral Orchitis (mumps), renal disease

High Oestrogen
- HCG secreting neoplasms (seminoma), ectopic BCG (lung, renal, adrenal tumours), CAH, Liver disease, Obesity, Hyperthyroid, Prolactinoma

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59
Q

Medications causing Gynaecomastia

A

DISCO:

  • Digoxin
  • Isoniazid
  • Spironalactone
  • Cimetide
  • Oestrogen
Anabolic steroids
(inc androgens = inc conversion to oestrogen)

Prolactin - antipsychotics, TCA, Metoclopramide

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60
Q

LH and testosterone in gynaecomastia

A

LH high Testosterone low = testicular failure

LH low Testosterone low = inc oestrogen

LH high Testo high = Androgen resistance or neoplasm

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61
Q

Investigations in Gynaecomastia

A

Hormones: Estradiol, testosterone, Prolactin, bHCG, AFP, LH,

LFT, TFT

Imaging - USS/mammography or needle core biopsy if suspicious.

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62
Q

Thyroid-Hypothalamic-Pituitary axis

A

TRH from Hypothalamus to Pituitary

TSH from pituitary to Thyroid follicular cella

Thyroid secrets Active T3 and also T4
(peripheral conversion to T3 also occurs). T3 both free (active) and also bound to TBG/Albumin.

Negative feedback of T3/4 to Pituitary and Hypothalamus

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63
Q

How is Thyroid hormone excreted

A

Liver conjugation/Excretion

Renal excretion

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64
Q

Which is active form of thyroxine.

Function of Thyroid hormones

A

T3 (Tri-iodothyronine)
Must be unbound (free

Control metabolic rate of tissues

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65
Q

Target for Thyroxine

A

THRa and THRb

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66
Q

What is

TRH
TSH

A

Thyrotropin releasing hormone

Thyroid stimulating hormone

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67
Q

Where does T4 get converted to T3

A

80% Liver

20% Thyroid

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68
Q

Cause of goitre:

  • Diffuse goitre
  • Nodular goitre
  • Painful goitre
A
  • Physiological, Graves, Hashimoto’s (autoimmune)
  • Mulitnodular goitre, Adenoma, adenocarcinoma
  • De Quervain’s (sub-acute hypothyroiditis)
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69
Q

Hypothyroidism

- Most common cause and what other assoc diseases

A

Hashimoto’s Thyroiditis

Other autoimmune conditions: T1DM, Addisons, pernicious anaemia

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70
Q

Causes of Hypothyroidism

A 
Atrophic hypothyroidism 
Subacute hypothyroidism (De Quervain's - painful and raised ESR)
Riedels
Post partum
Iatrogenic - surgery and radio iodine Tx
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71
Q

Secondary causes of hypothyroidism

A 
TSH deficiency, Hypopituitary disorders (Neoplasm, Radiotherapy, infection)
Hypothalamic disorders (Neoplasm, Trauma)
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72
Q

Hypothyroidism Signs

A 
Bradycardia
Delayed tendon reflex 
Ataxia (cerebellar)
Dry thin skin/hair
Puffy face/hands/feet (myxoedema)
Obesity
Carpal tunnel
Megacolon
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73
Q

Hypothyroidism symptoms

A 
Tired & Lethargic
Cold intolerance
Slow intellectually (poor memory, difficult concentrate)
Constipation
Weight gain + low appetite
Deep/Hoarse voice
Monorrhagia
Reduced libido
Depression
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74
Q

Acute presentation of severe Hypothyroid & Tx

A

Features of hypothyroidism + seizures + decreased consciousness + hypoventilation

Tx- IV levothyroxine + IV hydrocortisones + Resp support

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75
Q

Hashimotos:

  • Goitre
  • Autoimmune Ab’s
A

Painless, diffuse, varying size, rubbery, irregular surface

Anti-thyroid peroxidase
Antithyroglobulin (90-95%)

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76
Q

De Quervains

  • pathophysiology
  • Tx
A

viral infection then local symptoms of pain and nodularity

Initially thyrotoxic and then hypothyroid

Aspirin and prednisolone can be given although most cases self resolving

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77
Q

Investigation of hypothyroidism

A
  • TFTs (TSH, T3 and T4) shows primary or secondary
  • Antibodies: antiTPO, anti Tg

if worry neoplasm - USS

is secondary cause - MRI pituitary and check visual fields

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78
Q

Diagnosis of primary or secondary thyroid disease

A

high TSH and low T3/4 = primary

low TSH, low T3/4 = secondary

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79
Q

Clinical management of hypothyroidism

  • What
  • Follow up
  • Risks of medication
A

T4 - Levothyroxine for life

check TFT every 3-4 weeks. Annual TFT once stable

Osteoporosis, Arrhythmia

for subacute treat if TSH below 10

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80
Q

Hyperthyroidism Causes

A

Grave’s disease (75%)

Toxic mutinodular goitre (high iodine diet or amiodarone)

Toxic nodule/ adenoma

Subacute/De Quervain’s (transient toxicosis, pain, raised ESR)

Drugs: amiodarone, exogenous thyroids hormone treatment excess

Ectopic thyroid tissue: metastatic follicular carcinoma, ovarian teratoma

Secondary - pituitary adenoma

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81
Q

Hyperthyroidism symptoms

A 
weight loss, inc appetite
irritable and weak
sweating
tremor
Diarrhoea
Anxiety and psychosis
Heat intolerance
loss of libido
Oligomenorrhea
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82
Q

Hyperthyroidism signs

A 
Sweaty/Warm palms
Fine tremor
Tachycardia ± AF
Hair thinning
Goitre
Proximal myopathy (wasting and weakness)
Gynaecomastia
Brisk reflexes
Pruritus
Pretibial myxoedema
Eye disease (lid lag, ophthalmoplegia, exophthalmos)
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83
Q

Graves disease

  • Pathology
  • AAb
A

Anti-TSH receptor Abs

(may also react with orbital antigens to give thyroid eye disease)

Hyperplasia of follicular cells = diffuse goitre

anti TSHR (99%), anti-thyroglobulin, anti-TPO

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84
Q

Thyroid eye disease

A

lid lag, lid retraction, ophthalmoplegia, exophthalmos, gritty eyes, diplopia, loss of colour vision, conjunctival oedema, papilloedema.

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85
Q

Investigations hyperthyroidism

A

TFT: TSH low, T3/4 high in primary

Imaging: USS to look for cancer/adenoma

Radioisotope uptake scale hot = overactivity. (if not hot then could be De Quervain’s)

ESR raised in De Quervain’s

Of suspect secondary (pituitary adenoma) then MRI head + check visual fields

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86
Q

Hyperthyroidism management

A

Betablockers (propranolol)
Lubricating eye drops
Antithyroid drugs
- Carbimazole start 10-20mg daily, monthly titration based on TFTs (enzyme inhibitor of T3/4 production)
- Propylthiouracil - causes liver failure (reserve for pregnancy or thyroid storm)

Warning - anti-thyroid drugs can cause myelosuppression and agranulocytosis/neutropaenic sepsis.

In those who relapse after 18mnths Carbimazole, Radioactive iodine (note - worsens eye disease)

Surgery = Subtotal thyroidectomy (risk or hypothyroidism and damage recurrent laryngeal nerve.

87
Q

Thyroid storm:

  • Who gets it
  • Presentation
  • Precipitation
  • Investigations
  • Tx
A
  • Graves or getting levothyroxine
  • Hyperpyrexia (over 41), HR over 140, hypotension, GI (nausea, jaundice, vomiting, diarrhoea, abdominal pain), Neuro (confusion, delirium)
  • Infection
  • Sepsis screen, TFTm ECG, CXR, ABG

Treatment:

  • Resus: O2 fluids
  • Antithyroid: oral carbimazole/propylthiouracil
  • IV propanolol
  • Lugols solution (aqueous iodine) after 4 hours.
  • Keep cool with tepid sponging.
88
Q

Thyroid cancer:

  • Types
  • Presentation
  • Management
A
  • 70% papillary carcinoma (good prognosis)
  • 20% follicular carcinoma
  • 5% medullary (parafollicular C cells which secrete calcitonin
  • Nodules and effects of secretions
  • Total thyroidectomy, radioiodine to kill residual cells
89
Q

When is PTH secreted

A

Response to low Calcium

90
Q

PTH actions

A

Bone: inc osteoclast activity (release Ca and PO4)
Kidney: 25-OH-D to 1,25 OH2-D increases calcium absorption in the gut and from urine, Inc potassium excretion

91
Q

Effect of hyperparathyroid

A

increased Ca and decreased PO4

92
Q

Calcitonin

  • From what cells
  • Effect
A
  • Parafollicular C cells in the thyroid

- Reduce osteoclasts activity

93
Q

Reasons for PTH secretion

A
  • primary: solitary adenoma (85%) - assoc with MEN1/2 and postmenopausal women
  • secondary: result of low calcium. gives PT gland hyperplasia
    almost always assoc with kidney/liver or bowel disease
94
Q

Presentation and signs of high PTH

A

80% asymptomatic and diagnosis with hyper Ca found

Excess Ca absorption from bone = Osteopenia, osteoporosis and in extreme osteitis fibrous cystica (pepper pot skull, subperiosteal resorption phalanges

Excess renal Ca excretion: calculi

95
Q

Symptoms of hypercalcaemia

A

Bones, stones, abdominal moans, psychic groans

96
Q

Parathyroid investigations

A

Most freq cause of hypercalcaemia

U&E

measure PTH, Ca, PO4, hydroxyvitamin D (25-OH-D)

X-ray: skill and hands

Annual DEXA for those with hyperparathyroid

97
Q

Complications of hyperparathyroidism

A

Osteoporosis and peptic ulcers

98
Q

Management of hyperparathyroidism

A

Correct Vitamin D deficiency - suppresses PTH, inc calcium from GI and urine

Avoid drug precipitants (thiazides)

Curative - Surgery (if developed kidney stone or if symptomatic) either of single adenoma or subtotal
- complications of common laryngeal damage, hypocalcaemia

Medical - Bisphosphonates (alendronate)

99
Q

Drug causes of hypercalcaemia

A

Thiazide, Lithium

100
Q

What disease is assoc with hypoparathyroid

A

DiGeorge - disease with abnormal tissue formation during development

  • immunodeficient
  • congenital heart disease
  • hypocalcaemia (Hypo PTH)
101
Q

Hypercalcaemia

  • Normal range
  • how does it circulate
  • most common cause of hypercalcaemia
  • important causes
A
  • 2.25-2.5mmol/L
  • bound (albumin) and unbound ( this is physiologically important form)
  • hyper PTH in post-menopausal women
  • malignancy (ectopic PTH in Squamous lung cancer, breast Ca, osteolytic activity of emts)
  • Granulomatous: TB, Sarcoid
  • Endocrine: thyrotoxicosis, Phaeo, Addison’s
  • Drugs Thiazide, Lithium
102
Q

Hypercalcemia symptoms

A

Abdo groans L pain, nausea and vomiting, acute pancreatitis

Thrones: polyuria, polydipsia

Stones: renal colic

Psychic Moans: depression, dementia, confusion

Muscle and CVS: weakness, proximal myopathy, fatigue, short QT

103
Q

Treating hypercalcemia

A

0.9% saline to inc urinary excretion

Loop diuretic for fluid overload (furosemide)

IV bisphosphonates

104
Q

Hypocalcaemia symptoms

A

CATS - emergency hypocalcaemia symptoms

Convulsions, Arrhythmias (long QT), Tetany, Stridor/Spasms

Parasthesia: fingers, toes, mouth

105
Q

Hypocalcaemia Tx

A

Give calcium , vit D

If acute presentation: CATS

give calcium gluconate IV infusion

correct hypomagnesia

106
Q

What other electrolyte abnormality may be a reason for hypocalcaemia

A

Hypomagnesia

must be corrected as part of Tx otherwise calcium levels will not respond

107
Q

What is produced by anterior pituitary (Adenohypophysis)

A

GH - stim liver to prod IGF-1, also counteracts insulin

Prolactin - mammary gland growth. inhibited by dopamine

FSH - stimulates Sex steroid release
LH - stimulates Sex steroid release
ACTH - Adenocorticotropic hormone stimulates adrenal cortex to release glucocorticoids and androgens
TSH - Thyroid stim

108
Q

What is produced by posterior pituitary (Neurohypophysis)

A

Vasopressin: ADH

Oxytocin: uterine contractions

109
Q

Pituitary Tumours: effects

A
  • Excessice hormone
  • Local effects: compress surrounding
  • inadequate production by rest of gland
110
Q

Most common pituitary tumour

A

Benign non-functioning adenoma.

111
Q

Pituitary tumours:

  • Eosinophilic
  • Basophilic
A
  • GH/Prolactin

- ACTH: Presents as Cushings

112
Q

Mass effect of pituitary tumours

A

Optic chasm - bitemporal hemianopia (more affecting upper quadrants)
Occular nerve palsy - squint
Headache - retroorbital

113
Q

Hypopituitarism
Order of functional loss

Presentation

A

order: LH, GH, TSH, ACTH, FSH
Presentation: infertility/oligomenorrhea, erectile dysfunction, loss of libido

114
Q

Differential for pituitary tumour

A

Caniopharyhgioma

  • benign and cystic growth from Rathke’s pouch
  • Headache, visual field defect (bottom half vision as it grows from above) hypopituitarism
115
Q

Surgical route to pituitary

A

Transsphenoidal

116
Q

Drug therapy for pituitary lesions

A

Prolactinoma: Bromocriptine

GH: somatostatin analogue (somatostatin = GH limiting hormone)

117
Q

Complication of pituitary lesions

A

Pituitary apoplexy: this is worrying

Rapid enlargement due to bleed int tumour/infarction

Mass effect, CV collapse, acute hypopituitarism

118
Q

Prolactinaemia Cause

A

Commonly hormone secreting adenoma, physiological in pregnancy, can be caused by drugs such as antipsychotics which block dopamine receptors, seen following head injury
MEN1 - Proactinoma

Hypothyroidism
- raises TSH, raises Prolactin

119
Q

Prolactinaemia presentation

Women
Men
Children

A
  • Oligomenorrhoea, amenorrhoea, galactorrhea (milky nipple discharge), infertility, hirtuism
  • reduced libido, erectile dysfunction, may get milky discharge
  • Growth failure, delayed puberty

If due to prolactinoma then mass effects of lesion (headache/upper temporal quadrantanopia) may be seen

120
Q

Prolactinaemia Investigations

A

Prolactin levees, TFTs, exclude pregnancy, MRI pituitary

121
Q

Symptoms of Pituitary apoplexy

A

Sudden onset headache

Sudden onset visual disturbance

122
Q

Treating prolactinaemia

A

Mass effect if prolactinoma = transsphenoidal surgery

Effects: Dopamine agonist e.g. Bromocriptine

123
Q

Long term effects of hyperprolactinaemia

A 
Hypogonadism
Osteoporosis
Reduced fertility 
Erectile dysfunction
Apoplexy
124
Q

Acromegaly hormone

A

Growth Hormone (GHRH from hypothalamus)

125
Q

Negative feedback for GH

A

GH to hypothalamus des GHRH
Dietary Carbs
Adrenal output

126
Q

End product of GH

A

Liver: IGF-1 (insulin like GF)

Adipose tissue: FFA (free fatty acids)

127
Q

Acromegaly pathophys

A

Micro/Macrodenoma (depends on if causes visual disturb etc)

excess GH and IGF1 before closure of epiphyseal plates = gigantism. inc brow/hands after plate closure

128
Q

Acromegaly associated diseases

A

Prolactinoma
MEN1
McCune-Albright

Complications of acromegaly:
T2DM
Colon cancer

129
Q

Presentation of acromegaly

A

enlargement of hands/feet, frontal bossing, thick nose, large jaw, macroglossia

skin: thick, oily, sweating

nerve compression: bilateral carpal tunnel

Cardio/hepatomegaly

130
Q

Investigating acromegaly

A

serum IGF-1 raised with high GH, OGTT glucose inhibition of GH lost in acromeg

MRI pituitary, visual field testing

131
Q

Normal GH secretion

A

Pulsatile in peaks, inhibited by glucose this inhibition is lost in acromegaly –> OGTT therefore used to test

132
Q

Acromegaly management

A

1st line - Transsphenoidal surgery

2nd line - somatostatin analogies

133
Q

Acromegaly complications

A

Carpal tunnel
impaired glucose tolerance and diabetes (insulin resistance due to GH excess)

HTN
LVH - ECG to monitor for arrhythmias

Risk colon cancer

134
Q

Adrenal axis

A

ACTH stimulates adrenal cortex

135
Q

Layers of adrenal cortex and secretions

A

GFR - deeper you go, sweeter it gets

Zona Glomerulosa - Mineralocorticoids (aldosterone)
Zona Fasciculata - Glucocorticoids (cortisol)
Zona Reticularis - Androgens (DHEA)

136
Q

Effects of cortisol

A

RIDGE suppression

  • Reproduction
  • Immunity
  • Digestion
  • Growth
  • Mobilises Energy: increases sugar
137
Q

Cortisol cycle

A

Diurnal variation (highest in morning)

138
Q

Cushing’s syndrome

- Pathophysiology

A

loss of negative feedback for cortisol (prolonged exposure to exogenous or endogenous glucocorticoids)

ACTH dependant disease - inc ACTH secretion from pituitary

139
Q

Causes of high ACTH

A
  • ACTH dependant: disease due to inc ACTH secretion/ectopic ACTH secreting tumours (e.g. lung Ca)
  • ACTH independant: due to adrenal adenoma/carcinoma/excessive glucocorticoids
140
Q

Cushings presentation

A 
Truncal obesity
Buffalo hump 
Moon face
Proximal muscle wasting
Diabetes
Hypertension
Osteoporosis
Infection prone/poor healing
mood change (depression, lethargy, irritable, psychosis)

skin: atrophy, hirtuism, acne

if adenoma: headache, visual disturbance

141
Q

Cushings investigations

A

1st line = over night dexamethasone suppression test. If cortisol not suppressed on morning testing then +ve

serum glucose: elevated (blocked effect of insulin)

Plasma ACTH (if high distinguish pituitary, from ectopic e.g. SCLC, carcinoid) IV contrast CT

142
Q

Cushings Tx

A

Transphenoidal pituitary adenomectomy, if this fails the radiation of pituitary

143
Q

Complications of Cushings

A

Metabolic syndrome: HTN, T2DM
Impaired immunity
Osteoporosis

144
Q

Pathophysiology of Addison’s

A

Autoimmune destruction of adrenal cortex and reduction of adrenal steroid hormone output (cortisol, aldosterone)

145
Q

Types of Adrenal insufficiency

A

Primary - inability of adrenal glands to produce steroid (Addison’s)

Secondary - inadequate pituitary stimulation

146
Q

Causes of Adrenal insufficiency

A

Addisons
Surgical
CAH - 21-hydroxylase deficiency
Exogenous steroids (chronic steroids suppress axis)

147
Q

Antibodies seen in Addison’s

A

Anti-21 hydroxylase in 85% of cases (enzyme involved in converting Cholesterol to Aldosterone and Cortisol)

148
Q

Why is Cortisol and Aldosterone more affected than DHEA in Addisons

A

As Anti-21 hydroxylase AAb affects conversion of cholesterol to Cortisol and Aldosterone not DHEA

149
Q

Addisons Presentation

A

Chronic: Thin, Tired, Tearful and Tumbling

  • fatigue, weakness
  • GI: anorexia, WL, vomiting
  • Craving salty food
  • Muscle cramps
  • Faintness due to hypotension
  • confusion, personality change
150
Q

Signs of Addisons

A

Pigmented palmar crease/buccal mucosa,

hypotension, low sodium/high potassium (low aldosterone)

151
Q

Investigations Addisons

A

Blood levels of:

  • sodium: low
  • potassium: high
  • glucose: low (low cortisol)
  • cortisol low
  • ACTH (high in primary/Addisons, low in secondary/hypopituitary)

Short synacthen test

  • take cortisol, give synacthen IM
  • retake cortisol in 30 min, a rise will exclude Addisons

CT adrenals

152
Q

Difference in Addisons and CAH 21-hydroxylase levels

A

in Addison’s there is autoimmune destruction ( anti-21-hyroxylase) in CAH there is deficiency

153
Q

Typical electrolytes in Addisons

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Metabolic acidosis (due to hyperkalaemia)

154
Q

Management of Addison’s

A

Glucocorticoid: hydrocortisone (3Xday) - increase if ill

Mineralocorticoid: fludrocortisone: 50-300mcg/day to correct postural hypotension and electrolyte imbalance.

Educate: importance of not missing steroids

155
Q

SE of too many corticosteroids

A
  • skin thinning
  • osteoporosis
  • weight gain/obesity
  • raised BP
156
Q

Addisonian crisis

  • Def
  • Precipitation
  • Pres + complication
A

Acute deficiency of glucocorticoids and mineralocorticoids

major/minor infection, commonly due to com/diarrhoea. Injury, surgery, pregame’s also

malaise, fatigue, vomiting, muscle cramps, confusion

can progress to dehydration hypotension and hypovolaemic shock

157
Q

Addisonian crisis

  • Investigation
  • Management
A

Bloods:

  • low sodium, high K+, raised creatinine, hypoglycaemia
  • low cortisol, high ACTH

Management:

  • IV/IM hydrocortisone(not at high dose ALSO has a mineralocorticoid effect)
  • Rehydration w fluids
  • Glucose
  • Tx underlying infection/cause
  • ECG and reg U&E
158
Q

Whats is Conn’s

A

Primary hyperaldosteronism (independant of RAAS due to adrenal adenoma)

  • Water retention
  • Hypokalaemia
  • Hypernatraemia
159
Q

Action of Aldosterone

A

Insertion of ENaC (Sodium ion channel) in the luminal side (i.e. side of collecting duct) causing inc in sodium

160
Q

Causes for high Aldosterone

A

Conn’s (Adrenal adenoma 80%, bilateral hyperplasia 20%)

Secondary due to high RAAS (e.g. due to decreased renal perfusion following renal artery stenosis –> atherosclerosis)

161
Q

Conn’s Presentation

A

Oedema (salt and water retention)
Hypertension
Hypokalaemia (weak, cramps, parasthesia)
Metabolic alkalosis (due to low K+, K+ swapped for H+ in serum&kidney)

162
Q

Conns Investigations

A

U&E high
BP high
Aldosterone:Renin ratio high (if Renin also high then consider diuretics, renal artery stenosis)

CT/MRI for adrenal adenoma

163
Q

Conns management

A

Medical management prior to surgery
- Spironolactone (aldosterone antagonist)

Surgical - laparoscopic adrenalectomy (for unilateral disease)

Bilateral adrenal hyperplasia - Spironolactone

164
Q

Spironolactone SE

A

Block Testosterone

  • Gynaecomastia
  • Erectile dysfunction
  • Mestrual problems
165
Q

Conn’s complications

A

HTN may persist

166
Q

Hyperkalaemia Causes

A

Renal: AKI, CKD, Mineralocorticoid deficiency (Addison’s)

Medicines: interfere with excretion (Spironolactone, Amiloride), interfere with RAAS (ACEi, ARB, NSAID, heparin –> block of RAAS blocks Aldosterone)

Inc circulation: Tissue damage (burns, rhabdo, trauma), shift intracell to extra cell (acidosis e.g. DKA, medications: Digoxin tox, beta blockers - remember salbutamol used to push into cell)

167
Q

Hyperkalaemia presentation

A

Weakness, fatigue, flaccid paralysis, depressed tendon reflexes

Palpitations, chest pain

168
Q

Investigating hyperkalaemia

A 
U&E
ABG - check acidosis
Check medications (e.g. Dogixin toxicity)

ECG: P loss, PR prolong, QRS wide, Peak T

PPRQRST

169
Q

Treatment for hyperkalaemia

A

ABCDE + 12 lead ECG

If ECG changes:

Reduce Potassium: stop supplemental K+ and any drugs causing

Protect cardiac membrane - IV calcium gluconate (repeat every 10 min if no improv)

Shift K+ into cells - insulin infusion with glucose with nebuliser salbutamol
- Recheck U&E at 2 hours

Remove K+ from body - Calcium resonium + Lactulose (GI removal)
- Haemodialysis

170
Q

Hypokalaemia Causes

A

Mostly due to diuretic consumption or GI fluid loss (laxative abuse, chronic diarrhoea, persistent vomiting)
Hyperaldosteronism/high RAAS

Transcellular shift - alkalosis, insulin & glucose

171
Q

Hypokalaemia presentation

A

Weakness, muscle pain, constipation

Serious: neuromuscular problems, ascending paralysis and weakness, tetany

172
Q

Hypokalaemia ECG

A

Long PR, ST depression, flat T, U

173
Q

Investigations for hypokalaemia

A

U&E, bicarb, glucose,

Serum Mg - this is important accompaniment with low K+ and must be corrected to allow K+ correction

ECG

174
Q

Tx Hypokalaemia

A

K+ replacement (always slow IV, too fast can cause fatal arrhythmia)

Cardiac monitoring & 1-3 hourly bloods

175
Q

Phaeochromocytoma definition

A

Catecholamine producing adrenal tumour in adrenal medulla

adrenaline secreted autonomously from SNS

176
Q

Phaeochromocytoma 10% rule

A

10% are bilateral / malignant / extra-adrenal / familial (MEN2)

177
Q

Phaeo familial syndromes

A

MEN (bilateral)
Neurofibromatosis
Von-Hippel Lindau

178
Q

Phaeochromocytoma Classic Quartet of symptoms

A

1) Headache
2) Sweating
3) Palpitations
4) Tremor

Other: sense of doom, anxiety

179
Q

Phaeochromocytoma examination findings

A

Hypertension
Tremor
Flushing
Tachycardia

180
Q

Phaeochromocytoma Investigations

A

24 hour urine catecholamines

VMA / Metanephrine (metabolites of epinephrine raised in serum with phase)

Abdominal CT/MRI to visual adrenal mass

Genetic testing: VHL. MEN2

181
Q

Phaeochromocytoma Tx

A

Surgery is definitive

Pre surgery alpha blocker

Monitor 24 hour catecholamines and VMA 2 weeks post op

182
Q

Pheao complications and tx

A

Hypertensive crisis = hypertension with multiple organ failure

Phentolamine - alpha blocker
IV Nitroprusside - powerful vasodilator

183
Q

Adrenergic A1 blockade

A

action on smooth muscle in blood vessels = reduce BP

relaxes smooth muscle of bladder neck to inc peeing

184
Q

Adrenergic A2 blockade

A

Stimulates insulin release

185
Q

Adrenergic B1 blockade

A

Decrease HR + CO

Decreased Renin

186
Q

Adrenergic B2 blockade

A

Bronchoconstriction

187
Q

Carcinoid syndrome cause

A

Tumour of enterochromaffin cell

188
Q

Carcinoid syndrome presentation

A

Flushing and diarrhoea

Wheeze, palpitations, telangiectasia, abdo pain

189
Q

Carcinoid syndrome what released?

What is detectable in urine

A

Serotonin and other vasoactive peptides

5HIAA detected in urine

190
Q

Location of carcinoid tumours

A

30% gut

5% Bronchail

191
Q

Genetic association carcinoid

A

MEN 1

192
Q

Carcinoid syndrome investigations and findings

A

Urinary 5-HR/5-HIAA raised
Serum Chromogranin A/B raised

CT chest abdo pelvis (find tumour and check for liver mets)

193
Q

Carcinoid syndrome Tx

A

Surgical resection and preoperative ocreotide infusion (prevent carcinoid crisis)

194
Q

Carcinoid crisis, precipitating and Tx

A

Flushing, Tachy, hypertension, diarrhoea
Can lead to altered mental state, coma and death

Precip by stress, anaesthetic, chemo

Ocreotide (somatostatin analogue inhibits release of serotonin and gastric vasoactive mediators)

195
Q

MEN:

  • Inheritance
  • Cancers
A

Autosomal dominant

Parathyroid, pituitary, Phaeo, pancreas, Thyroid etc

196
Q

Types of Diabetes insipidus

A

Nephrogenic and cranial

197
Q

What is Diabetes insipidus

A

Excretion of large amounts of dilute urine

due to hyposecretio/resistance to ADH (Vasopressin)

198
Q

ADH synthesis and excretion

A

Synthesised in the hypothalamus and transported to posterior pituitary

excreted in response to dehydration

199
Q

Mechanism of ADH

A

Inserts Aquaporin 2 to luminary’s membrane of Distal convoluted tubule and collecting duct

200
Q

Diabetes insipidus causes (Cranial)

A

Acquired: tumours (e.g. craaniopharygioma), surgery, head injury, Granulomatous tissue (Sarcoid, TB, GPA), infection (meningitis, encephalitis)

Inherited: autosomal dominant vasopressin gene

201
Q

Diabetes insipidus causes (nephrogenic)

A

Hypokalaemia, CKD, Lithium, hypercalcaemia

202
Q

Diabetes insipidus presentation

A

Polyuria (over 3L 24hr) polydipsia and chronic thirst
Nocturia
Symptoms of hyponatraemia - lethargy, weakness, confusion
Distended bladder

203
Q

Diabetes insipidus Investigations

A

Urine Osmolality less than 300
Serum osmolality normal
MRI pituitary/hypothalamus

204
Q

Treatment:

Cranial

Nephrogenic

A
  • Desmopressin replacement (overdose = hyponatraemia)
  • stop causative drug/underlying cause, drink in response to thirst
  • inc sodium with thiazide + NSAID
205
Q

SIADH

A

Hypotonic hyponatraemia with concentrated urine

206
Q

SIADH pathology

A

impaired water excretion due to high ADH secretion

207
Q

Aetiology of SIADH

A

Pulmonary: pneumonia, lung cancer (small cell)

CNS: infection, trauma, MS, haemorrhage, malignancy

Malignancy: lung, GI, GU, Lymphoma

Drugs: SSRIs, NSAIDs, chemo

208
Q

Normal AVP ADH response

A

ADH is released following decrease in osmolality by 1%

209
Q

SIADH presentation

A

Euvolaemic, nausea, confusion, irritability vomiting.

210
Q

SIADH investigations

A

Serum osmolality - low (below 280)

Hyponatraemia (dilutional)

Urine osmolality higher than plasma and high urine Na

Normal renal and adrenal function

211
Q

SIADH management

A

IV hypertonic saline

Treat cause

Furosemide if risk fluid overload

in chronic/severe: tolvaptan (vasopressin receptor antagonist)

212
Q

Sodium and Cerebral oedema

A

Acute/chronic hyponatraemia: Low serum osmolality means water moves into brain where higher Na/K/Cl

Rapid correction of dehydration:rapid movement of water our of brain = osmotic demyelination.

213
Q

Serotonin syndrome Features and Tx

A 
Altered mental state
Hypertension
Hyperthermia
Muscle rigidity
Tachycardia

Give Benzodiazepines 1st line

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