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medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is a hormone?

A

endogenous, signalling molecule released from endocrine gland travelling in the blood and binding to target cells causing a change/response

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2
Q

What is the other term for the neurohypophysis?

A

Posterior pituitary

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3
Q

What is the other term for the adenohypophysis?

A

Anterior pituitary

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4
Q

What neurones originate in the SON and PVN of the hypothalamus and project into the posterior pituitary?

A

Magnocellular neurones

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5
Q

What hormones are stored in the posterior pituitary gland?

A

OT and AVP

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6
Q

Outline the blood supply to the anterior and posterior pituitary gland.

A

Superior hypophyseal artery supplies entering primary capillary plexus then hypophyseal portal veins of infundibulum and then to the secondary plexus of hypophyseal portal system 

Inferior hypophyseal artery supplies posterior pituitary gland by entering capillary plexus of infundibular process and leaves by posterior hypophyseal veins

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7
Q

What is the venous drainage of the pituitary gland?

A

Posterior hypophyseal vein drains posterior pituitary



Anterior hypophyseal vein drains anterior pituitary

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8
Q

Where is the pituitary gland located?

A

3/4cm directly between middle of the eyebrows in sphenoid bone fossa called sella turcica

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9
Q

Outline the MOA of ADH in dehydration.

A

Dehydration —> plasma osmolarity increases —> osmoreceptors in hypothalamus (circumventricular organs) fire —> ADH released —> retain water by absorption at the collecting duct of the nephron in kidney —> homeostatic

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10
Q

What hormones are released from the anterior pituitary gland?

A

Mnemonic: FLAT PeG

FSH
LH
ACTH
TSH

PL
GH

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11
Q

What is a tropic hormone?

Give an example of a pituitary hormone that is a tropic hormone.

A

stimulates another gland to produce its hormone

FSH
LH
ACTH
TSH

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12
Q

What two anterior pituitary cell types exist?

How may these be detected?

A

Eosin staining in histology

Acidophilic (pink cytoplasm):

  • Sommatotrophs
  • Lactotrophs

Basophilic (purple cytoplasm):

  • Corticotrophs
  • Thyrotrophs
  • Gonadotrophs

Mnemonic: PeG is Pink

Prolactin
GH

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13
Q

What is unique about somatomammotrophs?

A

degree of plasticity and under differing physiological conditions can be converted to allow production of more than one type of hormone

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14
Q

What is the MOA of Tolvaptan?

A

V2 receptor non-selective antagonist binding at V2r in kidney

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15
Q

What tubular protein allows retrograde movement of AQP2 vesicles towards the apical membrane along actin filaments?

A

Dynein

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16
Q

Which type of cells produced GH?

A

Somatotrophs in the anterior pituitary gland

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17
Q

What gene polymorphism can increase your risk of T1DM?

A

DR4-DQ8

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18
Q

Where is Insulin produced?

A

ß-cells of Islets of Langerhans in Pancreas

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19
Q

Outline the process of Ketogenesis.

A

Prolonged starvation with insufficient intracellular glucose, leading to exhaustion of glycogen stores which then results in ketogenesis involving lipolysis and conversion to ketones.

Three ketones:

  • Acetoacetate
  • ß-HB
  • Acetone
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20
Q

What is the clinical presentation of T1DM?

A
  • Polyuria (b/c osmotic diuresis > tubular reabsorption)
  • Polydipsia (fluid and electrolyte losses 2º to polyuria)
  • Weight loss (fluid depletion and muscle atrophy 2º insulin deficiency)
  • Fatigue
  • Candida infection
  • Young individual
  • Blurred vision
  • Nausea/ vomiting (DKA)
  • Abdominal pain (DKA)
  • Tachypnoea (DKA)
  • Coma/ Unresponsive (DKA)
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21
Q

What investigations would you order in a suspected case of T1DM and what would you expect to see?

A
  • Random Plasma Glucose (RPG): ≥ 11mmol/L
  • Oral Glucose Tolerance Test (OGTT): ≥11mol/L
  • Fasting Plasma Glucose (FPG): ≥7mmol/L
  • Serum/urine ketones: Present
  • HbA1c: ≥48mmol/L (≥6.5%)
  • Autoimmune markers: Positive
  • C peptide (low)
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22
Q

To be positive in T1DM, what value threshold should be exceeded in a RPG?

A

> 11mmol/L

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23
Q

To be positive in T1DM, what value threshold should be exceeded in a FPG?

A

> 7mmol/L

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24
Q

To be positive in T1DM, what value threshold should be exceeded in a OGTT?

A

> 11mmol/L

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25
Q

What is the long-term management of T1DM?

A
  • Conservative: Physical activity/ Diet (low sugar, high in low GI carbs, sweeteners, protein)/ 3 meals/ Notify DVLA
    +
  • Insulin (Basal-bolus or CSII): insulin glargine (SC OD)/ insulin isophane (SC BD)/ insulin detemir (SC BD)/ insulin degludec (SC OD) + insulin lispro/ insulin aspart
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26
Q

When calculating insulin doses, how much energy is related to units of insulin?

A

1U insulin = 10g carbs

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27
Q

What drug may be given should postprandial hyperglycaemia persist?

A

Pramlintide

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28
Q

Outline how Pramlintide works?

A

Amylin is co-secreted with insulin to reduce postpradial glucose by: increases gastric emptying time, reduces appetite (anorexia) and reduces postprandial glucagon secretion

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29
Q

Give an example of a rapid-acting insulin.

A

Insulin Lispro

Insulin Aspart

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30
Q

What type of insulin is Isophane insulin?

A

Intermediate

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31
Q

Give an example of a long-acting insulin.

A

Insulin Glargine

Insulin degludex

Insulin Detemir

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32
Q

How is Insulin Glargine made?

A

Glycine substituted for Asparagine (N-terminal) and 2 arginine AAs added to end of beta chain thus ∆ isoelectric point = less soluble thus dissolve slowly

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33
Q

How is insulin degludec made?

A

Conjugation to FA (hexadecanedioic acid) -> hexamer formation

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34
Q

How is Insulin Detemir made?

A

FA (myristic acid) conjugated to lysine -> albumin binding = slowly dissociates

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35
Q

Give some side effects of insulin.

A

Oedema;

Lipodystrophy

Hypoglycaemia

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36
Q

Give 5 RFs of T2DM.

A
  • Ageing
  • Physical inactivity
  • Overweight/Adiposity
  • Hypertension
  • Dyslipidaemia
  • FHx
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37
Q

Outline the pathophysiology involved in T2DM.

A
  • Reduced insulin sensitivity: pre-receptor (Abs/secretion defects)/receptor (volume/ affinity)/ post-receptor (IRS-1/PI3K/AKT/GLUT4) -> reduced uptake of glucose = hyperglycaemia -> increased conversion to lipid (WAT) = adiposity -> reduced HDL/ increased TGs/ increased LDL; accumulation of AGEPs/free radicals -> chronic inflammation -> macroscopic + microscopic complications of diabetes
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38
Q

What are the clinical features of T2DM?

A
  • Fatigue
  • Blurred vision
  • Recurrent candida infection: vaginal/ penile/ skin folds
  • Skin infection: cellulitis/abscesses
  • UTI: Cystitis/ Pyelonephritis
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39
Q

What are the glucose thresholds for the following investigations:

  • FPG
  • RPG
  • OGTT
  • HbA1c
A
  • HbA1c: ≥ 48mmol/L (6.5%)
  • FPG: ≥ 7mmol/L
  • RPG: ≥ 11mmol/L
  • OGTT: ≥ 11mmol/L
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40
Q

What is the long-term management of a patient with T2DM?

A
  • Conservative: diet/ physical activity/ sweeteners/ weight loss/ smoking cessation
    +
  • Biguanide: Metformin
    ±
  • Antihypertensives: Lisinopril/Enalapril/ Amlodipine/ Diltiazem
    +
  • Lipid control: Atorvastatin/ Rosuvastatin/ Simvastatin/ Pravastatin
    +
  • Antiplatelets: Aspirin/ Clopidogrel

HbA1c above goal on metformin
- Metformin
+
- Hypoglycaemic drug: SGLT2i/ GLPi/ DPP4i/ Sulfonylurea/ Basal insulin

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41
Q

What is the MOA of Metformin?

A

Enters via OCT-1 and acts on Mt to increase AMP:ATP ratio. Activation of AMPK increases glucose transport, FA oxidation, reduces lipogenesis and reduces glycogenolysis

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42
Q

What are the side effects of Metformin?

A

Appetite suppression
Weight gain
Diarrhoea

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43
Q

Give an example of a Sulfonylurea.

A

Gliclazide
Tolbutamide
Glibenclamide

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44
Q

What is the MOA of the sulfonylureas?

A

Block ATP-sensitive K+ channels in ß-cells which causes ß-cell depolarisation and increased insulin secretion

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45
Q

What are the side effects of Gliclazide?

A

Nausea

Diarrhoea

Hypoglycaemia

Abdominal pain

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46
Q

Give an example of a GLP-1 analogue.

A

Exenatide

Liraglutide

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47
Q

What is the MOA of Exenatide?

Give the class of Exenatide.

A

Mimic GLP-1 binding at A-cells and ß-cells to cause insulin release and reduce glucagon

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48
Q

What side effects would you warn a patient about regarding commencing Exenatide?

A

Reduced appetite

Nausea/Vomiting

Diarrhoea

GI disorder/discomfort

Dizziness

Skin reactions

Pancreatitis

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49
Q

Which anti-diabetic medication may cause Pancreatitis?

A

GLP-1 Analogues such as Exenatide/Liraglutide

DPP4-i such as Sitagliptin

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50
Q

Give an example of a drug that is a DPP4-inhibitor?

A

Sitagliptin

Linagliptin

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51
Q

What class of drug is Sitagliptin?

A

DPP4-i

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52
Q

What class of drug is Sitagliptin?

A

DPP4-i

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53
Q

What is the MOA of Sitagliptin?

A

Inhibit DPP4 thus enhance endogenous incretin effects to increase insulin and decrease glucagon

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54
Q

A patient is about to commence drug trial on Sitagliptin. What side effects should you warn them about?

A

Headache

Pancreatitis

Hypersensitivity

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55
Q

What class of drug is Empagliflozin?

A

SGLT2 inhibitor

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56
Q

What is the MOA of Cangliflozin?

A

Inhibit Na+-Glucose transporters in PT and LoH thus giving glycosuria

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57
Q

A patient is about to commence drug treatment on Empagliflozin. What side effects would you warn them about?

A

Hypoglycaemia

Hypovolaemia

Skin reaction

UTI

Urosepsis

Balanoposthitis

Constipation

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58
Q

What class of drug is Pioglitazone?

A

Thiazolidnediones (TZD)

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59
Q

What is the MOA of Glitzone?

What class is it?

A

Thiazolidinedione (TZD)

PPARy agonist thus increases transcription of insulin signalling

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60
Q

What side effects would you warn a patient commencing Glitazone?

They ask you what class this drug is, what do you say?

A

Risk of infection

Visual impairment

Weight gain

Bone fracture

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61
Q

What anti-diabetic medication may increase the risk of bone fracture?

A

Thiazolidinediones (TZDs) such as Pioglitazone which suppress bone formation

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62
Q

What class of drug is acarbose?

A

Alpha-glucosidase inhibitor

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63
Q

Give an example of an alpha-glucosidase inhibitor.

A

Acarbose

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64
Q

What is the MOA of acarbose?

A

Alpha-glucosidase inhibitor which results in reduced carbohydrate absorption.

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65
Q

What are the common side effects of alpha-glucosidase inhibitors such as Acarbose?

A

Flatulence

Diarrhoea

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66
Q

Outline the pathophysiology of a DKA.

A

Reduced insulin production causing hyperglycaemia which results in osmotic diuresis causing polyuria and polydipsia whilst starvation state leads to lipolysis and ketogenesis with ketoacidosis resulting in metabolic acidosis and abdominal pain due to gastroparesis

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67
Q

What are the clinical features of DKA?

A
  • Nausea/ vomiting
  • Pear smelling breath
  • Reduced consciousness: Reduced mental status
  • Abdominal pain: peritonitis (guarding)/ early bowel obstruction (tinkling bowel sounds)/ late bowel obstruction (absent bowel sounds)
  • Hyperventilation: Kussmaul breathing
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68
Q

What breathing pattern may be noted in DKA?

Why does it happen?

A

Deep, rapid breathing pattern as respiratory compensation to blow of CO2 to counteract metabolic acidosis

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69
Q

What investigations may be suggestive of a DKA?

A
  • Blood glucose: ≥ 11.0mmol/L
  • VBG: Metabolic acidosis (raised anion gap, reduced bicarbonate); pH ≤ 7.40
  • Blood ketones: Ketonaemia (≥ 3.0mmol/L)
  • U+E: Raised SCr and hyperkalaemia
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70
Q

How would you manage a patient with DKA?

A
  • Insulin: 0.1units/kg/hr
  • IV Fluids: NaCl (0.9%) at 1L in 30 minutes, 1L over 1hr, 1L over 2hr, 1L over 4hr

± (Hypokalaemia)

  • IV Fluids: KCl added (1L for 2hr, 1L for 2hr, 1L for 4hr, 1L for 4hr, 1L for 6 hr)
  • -> 10mmol/L KCl if [K+] = 3-5mmol/L; 20mmol/L KCl if [K+] = ≤3.5mmol/L

± (Glucose ≤ 14mmol/L)
- IV Glucose: Glucose (10%)

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71
Q

Describe a Hyperosmolar Hyperglyaecimic State?

A

Profound hyperglycaemia (≥ 30mmol/L) and hyperosmolality (≥ 320mOsm/kg) and volume depletion in the absence of ketoacidosis – a complication of diabetes.

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72
Q

What are the osmolality and blood glucose thresholds for HHS?

A
  • Blood glucose: ≥30mmol/L

- Serum osmolality: ≥ 320mOsm/kg

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73
Q

How do you manage a Hyperosmolar Hyperglycaemic State?

A 
-	Insulin: 0.05units/kg/hr 
\+ 
-	IV Fluids: NaCl (0.9%) at 1L in 30 minutes, 1L over 1hr, 1L over 2hr, 1L over 4hr 
\+
-	IV Fluids: KCl added (1L for 2hr, 1L for 2hr, 1L for 4hr, 1L for 4hr, 1L for 6 hr) 
\+ 
± (Glucose ≤ 14mmol/L)
-	IV Glucose: Glucose (10%)
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74
Q

A patient asks you what the complications of Diabetes Mellitus are. Outline what you may tell them.

A

Infection: Hyperglycaemia reduces function of leucocytes which increases risk of infection: cellulitis, boils, abscesses, candidiasis.

Skin disease: Diabetes produces a myriad of common dermatological manifestations

Iatrogenic hypoglycaemia: Increased usage of insulin results in hypoglycaemia.

Lactic Acidosis: Rare complication when taking Metformin presenting with severe metabolic acidosis without hyperglycaemia or ketosis. Treat by rehydrating and infusing bicarbonate (1.26%)

Retinopathy (background/proliferative): Damage to the vessels supplying the retina (central retinal artery) seen as haemorrhage, oedema, microaneurysms and exudate (HOME).

Nephropathy: Damage to vessels (ischaemic lesion) or urinary tract (infective lesion, UTI) or glomerular basement membrane (glomerulopathy) leading to compromised filtration (renal insufficiency) demonstrated by proteinuria, Hypercreatinemia and hypoalbuminemia.

Erectile Dysfunction (ED): Damage to vasculature of penis (pudendal artery)/ cavernosal artery leading to inability for corpus cavernosum to remain filled in erect state. Manage with PDEi (sildenafil) and counselling.

Diabetic Foot: Potential damage due to neuropathy which results in tissue necrosis, similar to PAD: pale, pulseless, painless, absence of hair, shiny skin. Diabetic foot ulcers may be seen

Macrovascular complications: Diabetes is a risk factor for atherosclerosis which is summative with other risk factors (hypertension/hyperlipidaemia/obesity/ low physical inactivity) resulting in damage to large vessels which is territory-dependent – PAD (peripheral), CVA (brain) and MI (heart).

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75
Q

What types of Diabetic Neuropathy exist?

A

Symmetrical sensory neuropathy: reduced sense of vibration, pain sensation and temperature

Diabetic amyotrophy: painful wasting which is asymmetrical in the quadriceps causing loss of bulk and diminished reflexes

Acute Painful neuropathy: Neuropathic pain with paraesthesia dn dysesthesia

Mononeuritis (/Multiplex): Inflammation of nerves with sudden onset and pain common at sites of external pressure (e.g. Carpal Tunnel Syndrome)

Autonomic neuropathy: affects ANS causing CVS and GI and urinary and sexual Sx and S

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76
Q

What is the most common form of pituitary disease?

A

Pituitary adenoma

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77
Q

How may a pituitary adenoma present?

A

Headache

Visual changes: Reduced visual acuity; Bitemporal hemianopia; Diplopia

Hypogonadism Sx: infertility; reduced libido; hot flushes

Prolactinoma: gynaecomastia; galactorrhoea; reduced libido; amenorrhoea/oligomenorrhoea

Acromegaly: coarsened facial features; joint pain; soft tissue hypertrophy; galactorrhea; erectile dysfunction

Cushing’s Disease: Mood change; Striae; Facial plethora; Amenorrhoea; Weight gain; OP; Acne; Reduced libido

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78
Q

What is the first-line, gold standard investigation used to diagnose a Pituitary Ademona?

A

MRI-Pituitary to delineate characteristics of tumour including invasion and compression of surrounding structures

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79
Q

How do you manage a Pituitary Adenoma?

A

Microadenoma:
- Observation

Macroadenoma: Abutting or Not Abutting Optic Chiasm
- Trans-sphenoidal surgery
+
- Hormone replacement (FLAT PeG): Testosterone; Estradiol; Progesterone; Hydrocortisone; Levothyroxine; Somatropin

± Mass Effect
- Radiotherapy: Stereotactic gamma knife

± (Residual tumour if surgery + radiotherapy fails)
- Octreotide

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80
Q

How may pituitary adenomas be classified?

A

Non-Functional: No hyper secretion of hormone
‘Clinically Non-Functioning Pituitary Adenoma’ (CNFPA)

Functional: Hyper-secretion of hormone

Microadenoma <1cm

Macroadenoma >1cm

Functional (hormone type):

  • Prolactinoma
  • Somatrotroph adenoma
  • Gonadotroph adenoma

Pituitary apoplexy: associated with neurological deficit or symptomatic (haemorrhage/infarction) with few/no symptoms

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81
Q

The rapid enlargement of a pituitary tumour due to infarction or haemorrhage causing severe headache and sudden, severe vision loss is termed?

A

Pituitary Apoplexy

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82
Q

In hypopituitarism, radiographic imaging of via MRI-Pituitary showing an empty space is termed?

A

Empty sella syndrome

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83
Q

A deficiency of GnRH in a patient with anosmia is termed?

A

Kallmann’s Syndrome

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84
Q

Pituitary infarction following severe postpartum haemorrhage is termed?

A

Sheehan’s Syndrome

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85
Q

What is the aetiology of Hypopituitarism?

A

VITAMIN-C

Vascular: Pituitary apoplexy; Sheehan’s Syndrome; Carotid artery aneurysms
Infective: Basal meningitis; Encephalitis; Syphilis
Infiltrations: Haemochromatosis; Sarcoidosis
Trauma: Skull Fx; Surgery
Acquired: Drugs
M
Immunological: Pituitary antibodies
Neoplasia: Primary tumour; Secondary tumour; Lymphoma

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86
Q

What investigations would you conduct in a suspected Hypopituitarism?

A

FBC
Hormones
MRI-Pituitary

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87
Q

How do you manage hypopituitarism?

A

HRT: Hydrocortisone; Levothyroxine; Testosterone; Estriol; Somatropin

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88
Q

What is the most common cause of Hyperprolactinaemia?

Give other causes.

A

Prolactinoma (functional pituitary adenoma)

Pituitary adenoma which compresses pituitary stalk to disinhibit DA which suppresses PL (disconnection)

Primary hypothyroidism

Drugs (D2 antagonists)

Acromegaly/PCOS (co-secretion)

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89
Q

What effect does thyroid have on prolactin?

A

High TSH levels in hypothyroidism can stimulate prolactin

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90
Q

What is the criteria for a macroadenoma?

A

> 10mm

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91
Q

How do you manage Hyperprolactinaemia?

A 
Conservative: Withdraw offending drugs
\+
Medical: Cabergoline; Bromocriptine
\+
Surgery: Transphenoidal approach

± Macroadenoma pressing optic chaise
- Radiotherapy

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92
Q

What is the difference between acromegaly and gigantism?

A

Excessive GH production in children prior to growth plate closure results in gigantism

Excessive GH production in adults once epiphyseal plates are closed results in acromegaly

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93
Q

What is the main cause of acromegaly?

A

Somatotroph adenoma (functional GH-secreting pituitary adenoma)

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94
Q

What are the clinical features of acromegaly?

A

Changes n facial appearance
Headaches
Visual deterioration
Deep voice

Galactorrhoea; Impotence; Poor libido

Tiredness; Weight gain; Diaphoresis; Musculoskeletal pain

Prognathism
Interdental separation
Large tongue

Hirsutism
Spade-like hands and feet
Tight rings
CTS

Arthropathy
Glycosuria 
Hypertension
Heart failure 
Oedema
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95
Q

What is the management of Acromegaly?

A

Medial: Octreotide; Cabergoline
+
Surgical: Trans-sphenoidal surgical resection

± Incomplete surgical excision
External radiotherapy

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96
Q

Explain the difference between Cushing’s Disease and Cushing Syndrome.

A

Cushing disease is a condition caused by ectopic cortisol production in pituitary adenoma or ectopic ACTH production from adrenal adenoma

Cushing Syndrome is the myriad of symptoms associated with elevated cortisol

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97
Q

Outline the clinical features of Cushing’s Syndrome.

A 
Mood change 
Facial plethora; Facial rounding 
Dorsocervical rounding (buffalo hump)
Supraclavicular fullness
Violaceous striae 
Weight gain and central adiposity 
Easy bruising 
Reduced libido; Impotence
98
Q

How would you manage a patient with Cushing’s Disease?

A

Surgery: Transphenoidal pituitary adenomectomy
±
Medical: Pasireotide; Octreotide
+
Medical (HRT): Hydrocortisone; Levothyroxine; Testosterone; Estradiol; Somatotropin; Desmopressin

99
Q

Outline how you would treat Cushing’s Syndrome.

A

Tx cause: Adrenalectomy (adrenaloma); Trans-sphenoidal pituitary adenomectomy
+
Medical (HRT)
–> If no output e.g. in trans-sphenoidal pituitary adenomectomy; or bilateral adrenalectomy

100
Q

What role does mifepristone have in Cushing’s syndrome?

A

Anti-progesterone thus blocks cortisol at receptor level, attenuating effect of cortisol elevation

101
Q

Which thyroid hormone is produced in greater amounts?

A

T4

102
Q

What binding protein is the majority of thyroid hormone bound to?

A

Thyroid Binding Globulin (TBG)

103
Q

How can you assess thyroid function?

A

TFTs: TSH; T4

Thyroid antibodies

104
Q

Outline the differences between Primary, Secondary and Subclinical hypothyroidism.

A

The following are classifications of Hypothyroidism based on the balance of TSH and T4.

Primary: elevated TSH; low T4

Secondary: low TSH; low T4

Subclinical: slightly elevated TSH; normal T4

105
Q

What conditions are Hashimoto’s Thyroiditis associated with?

A

Type 1 Diabetes

Addison’s Disease

Pernicious anaemia

Lupus

106
Q

How may hypothyroidism present?

A 
Lethargy
Constipation
Weight gain
Coarse skin and hair 
Bradycardia 
Bradyreflexia 
Cold sensitivity 
Eyelid oedema 
Tibial myxoedema
107
Q

What is Myxoedema?

A

Accumulation of mucopolysaccharide in subcutaneous tissues

108
Q

What is the most common cause of primary hypothyroidism?

What investigations would show this?

A

Autoimmune Thyroiditis

anti-TPO Abs; high TSH; low T4

109
Q

How do you manage Hypothyroidism?

A

Supportive: Monitoring 4-6 weeks post-initiation; Annual review
+
Medical: Levothyroxine 1.6mcg/kg/day PO

110
Q

What are some of the common side effects of Levothyroxine?

A 
Anxiety
Insomnia 
Thyrotoxic crisis 
Angina pectoris 
Arrhythmias
SOB
Muscle weakness 
Reduced weight 
Tremor 
Arthralgia
111
Q

What is Myxoedema coma?

What derangements occur in it?

A

Severe hypothyroidism in a vulnerable elderly patient resulting in reduced consciousness.

Features:

  • Cardiac failure
  • Hypoventilation
  • Hypoglycaemia
  • Hyponatraemia
  • Hypothermia
112
Q

What is Myxoedema madness?

When may this occur?

A

Severe hypothyroidism in elderly patients resulting in psychoses - delusions, demented, depression etc.

May occur after starting thyroxine.

113
Q

How do you manage a myxoedema coma?

A

Correct the derangements

Supportive: A-E; Oxygen; IV fluids; Gradual rewarming;
+
Medical: Glucose infusion; IV Thyroid hormone (T3)

114
Q

Outline the causes of Hypothyroidism?

A

Autoimmune

Drug-induced

Iatrogenic

Congenital

Post-partum

Iodine deficiency

115
Q

What drugs may commonly cause drug-induced hypothyroidism?

A

Amiodarone
Lithium
Carbimazole
Interferon

116
Q

What are the causes of Hyperthyroidism?

Give the key aspects of each.

A

Grave’s Disease: TSH-R Abs (TRAbs)

Toxic Multinodular Goitre: multiple nodules

Solitary toxic adenoma: sole nodule

Amiodarone-induced: I (Jod-Basedow phenomenon); II (release of pre-made hormones)

De Quervain’s Thyroiditis: post-viral, painful and progressive (hyperthyroid, hypothyroid, normal)

Follicular thyroid cancer

Struma ovarii: ectopic thyroid tissue from dermoid tumour and ovarian teratoma

ß-hCG related: Pregnancy; hydatidiform mole; choriocarcinoma; testicular germ cell tumour

117
Q

What are the clinical features of Hyperthyroidism?

A 
Weight loss 
Irritability; Restlessness; Diaphoresis 
Exopthalmos; Lid lag; Stare; Periorbital oedema
Goitre; Bruit
SOB
Palpitations; Arrhythmia (AF) 
Thirst; Vomiting; Diarrhoea;
Tremor; Arthralgia; Choreoathetosis 
Oligomenorrhoea; Loss of libido; Gynaecomastia
118
Q

How do you manage Hyperthyroidism?

A 
Supportive: ß-blockers
\+ 
Medical: Propylthiouracil; Carbamizole
\+ 
Surgical: Thyroidectomy; Hemithyroidectomy
119
Q

What are the complications of Thyroidectomy?

A

Recurrent laryngeal nerve damage

Hypocalcaemia

120
Q

What are the common side effects of Carbimazole?

A

Agranulocytosis thus infections

Thrombocytopaenia

Haemolytic anaemia

121
Q

How is Grave’s ophthalmopathy classified?

A

ATA - 6 grades

Mnemonic: NO SPECS

N = 0 = no Sx + S
O = I = only signs 
S = II = Soft tissue involvement
P = III = Proptosis 
E = IV = Extra-ocular involvement
C = V = Corneal involvement 
S = VI = Sight loss
122
Q

How do you manage a Thyroid storm?

A

Supportive: A-E assessment; admission; IV fluids;

Medical: Propylthiouracil
\+
Hydrocortisone
\+
Propanalol
\+
Potassium iodide
123
Q

What antithyroid drug is given as first line to pregnant women?

A

Propylthiouracil

124
Q

What is the management of Grave’s Orbitopathy?

A

Supportive: Smoking cessation; monitoring; annual review; Selenium; eye drops
+
Medical: Propylthiouracil (maintain euthyroidism); oral prednisolone (0.3-0.5mg/kg/day);
+
Surgery: Surgical decompression

125
Q

Why may administration of corticosteroids be useful in Thyroid storm?

A

Glucocorticoids reduce conversion of T4 to T3 thus reduce active form of thyroid

126
Q

What are the potential causes of a goitre?

A

Hypothyroidism:
Iodine deficiency
Autoimmune thyroiditis
Congenital hypothyroidism

Hyperthyroidism:
Grave’s
Solitary adenoma
Toxic Multinodular Goitre

Pituitary disease (pituitary adenoma)

Thyroid cancer

127
Q

What investigations may you conduct for a patient presenting with a goitre?

A

Bloods: FBC; U+Es; TFTs; CRP

Abs: TPO; TSH-R

US-Thyroid

Fine-Needle Aspiration (FNA)

128
Q

How is thyroid cancer diagnosed?

A

Fine-needle aspiration

129
Q

What are the clinical features of Thyroid Cancer?

A

Thyroid nodule/mass
Hoarseness of voice
Cervical lymphadenopathy
Stridor

130
Q

When should you admit someone urgently with a neck lump?

A

Stridor (signs of upper airway obstruction)

131
Q

What are the suspected thyroid cancer criteria for the urgent cancer referral (2-week)?

A

Unexplained thyroid lump

Lymphadenopathy and lump

Voice change

Rapidly increasing size

132
Q

What investigations would you conduct for a patient presenting initially with a thyroid lump?

A

Bloods: FBC; U+E; TFTs; LFTs; Hormones;

Abs: TPO; TSHR

US-Thyroid

Fine-Needle Aspiration and Cytology

Diagnostic hemithyroidectomy (if Thy3f cytology and cannot differentiate between follicular cancer and benign lesions)

133
Q

What classification system is given in US-Thyroid?

Which ones get referred for FNAC?

A

British Thyroid Association U1-5

U1 = Normal

U2 = benign

U3 = indeterminate

U4 = suspicious

U5 = malignant

134
Q

What cytological classification system is there for FNAC in suspected Thyroid cancer?

A

Thy1 = non-diagnostic

Thy2 = non-neoplastic

Thy3a = atypical features

Thy3f = follicular neoplasm suspected - cannot determine

Thy4 = likely malignancy (<70%)

Thy5 = malignancy (98%

135
Q

What does triple assessment in suspected Thyroid cancer consist of?

A

TFTs

USS

FNAC

136
Q

When would a diagnostic hemithyroidectomy be indicated?

A

Following FNAC with classification as Thy3f whereby cannot differentiate.

137
Q

What is the most common form of Thyroid cancer?

A

Papillary

138
Q

What Thyroid cancer has the worst prognosis?

A

Anaplastic

139
Q

Which thyroid cancer most commonly appears in the elderly?

A

Anaplastic

140
Q

What type of thyroid cancer is associated with MEN type 2?

A

Medullary

Remember Medullary is associated with MEN 2

141
Q

Which form of Thyroid cancer occurs at a higher frequency in females?

A

Follicular

Remember: Follicular is for Females

142
Q

Elevated calcitonin and hypocalcaemia are associated with what type of Thyroid Cancer?

A

Medullary Carcinoma

143
Q

Elevated Thyroglobulin is associated with what type of Thyroid cancer?

A

Follicular or Papillary Thyroid Cancer

144
Q

What is Riedel’s Thyroiditis?

A

Rare autoimmune condition resulting in fibrosis of the thyroid and surrounding soft tissues resulting in enlargement and subsequent compression of adjacent tissues

145
Q

LH binds to ___ cells to increase ___ production?

A

Leydig

Testosterone

146
Q

FSH stimulates ____ cells to produce ____?

A

Sertoli cells

Inhibins and Activins

147
Q

47, XXY is the genotype for what condition?

A

Klinefelter’s Syndrome

148
Q

What are the causes of male hypogonadism?

A 
HP axis:
Hypopituitarism
Kallann's Syndrome 
Malnutrition 
Hyperprolactinaemia 
Primary Gonadal Disease:
Anorchia/Leydig Cell Agenesis 
Cryptorchidism 
Chromosomal abnormality (Klinefelter's)
Enzyme defects (e.g. 5a-reductase deficiency)
Testicular torsion
Orchidectomy 
Chemotherapy
Orchitis
CKD
Cirrhosis
149
Q

Why may CKD cause hypogonadism?

A

CKD is related to a reduction in LH thus low T occurs

150
Q

What investigations may you conduct in a patient with suspected hypogonadism?

A

Bloods: FBC; U+Es; TFTs; LFTs

Sex hormones: FSH; LH; Testosterone

Chromosomal analysis

MRI-Pituitary

US-Abdomen

151
Q

Define erectile dysfunction.

A

Inability to attain or sustain an erection until ejaculation

152
Q

What drug is commonly used to treat Erectile Dysfunction?

A

Sildenafil

153
Q

Define Gynaecomastia.

A

Enlargement of breast tissue in males

154
Q

Outline some causes of gynaecomastia.

A

HP axis:

  • Any cause of hypogonadism
  • Hyperthyroidism

Neoplasm:

  • Oestrogen-producing tumours
  • hCG-producing tumours
  • Carcinoma of the breast

Drugs:

  • Oestrogen
  • Digoxin
  • Cannabis
  • Diamorphine
  • Spironolactone
  • Cimetidine
  • Gonadotrophins
155
Q

Define the menopause.

A

Cessation of periods for 12 months with oestrogen decline resulting in symptoms of hot flushes, vaginal dryness and breast atrophy. There may also be symptoms of mood change.

156
Q

How is the menopause managed?

A

HRT is the mainstay and Tx concomitant symptoms

HRT is either continuous (menopause) or sequential (perimenopause)

HRT should be oestrogen and progesterone (if uterus)

Vaginal Atrophy:
- Vaginal oestrogen

Mood changes:
- SSRIs

Urinary incontinence:
- Pelvic floor exercises

157
Q

What are the indications for Transdermal Oestrogen in the menopause?

A

Mnemonic: ABCDE

Allergy - lactose intolerance 
BMI - BMI >30kg/m2
CVD - CV RFs
Disabling symptoms - from oral medication and GI conditions 
Embolism risk - VTE risk is high
158
Q

When should bleeding on HRT be investigated?

A

Breakthrough bleeding bleeding after 6 months on Tx

159
Q

What are the adverse effects of HRT?

A

Oestrogen-related:

  • Bloating
  • Mastalgia
  • Breast enlargement
  • Leg cramps
  • Dyspepsia

Progesterone-related:

  • Headaches
  • Mood swings
  • Acne vulgaris
  • Lower abdomen pain/back pain
160
Q

Define Primary Amenorrhoea.

A

Absence of menses by 16 years old

161
Q

How may amenorrhoea be classified.

A

Primary: No menses by 16

Secondary: No menses for 3 months

162
Q

What are the causes of amenorrhoea.

A

Hypothalamic:

  • GnRH deficiency
  • Post-OCP therapy

Pituitary:

  • Hypopituitarism
  • Hyperprolactinaemia

Gonadal:

  • PCOS
  • Premature ovarian failure
  • Ovarian dysgenesis
  • Androgen-secreting ovarian tumours
  • Radiotherapy

Other:

  • Thyroid dysfunction
  • Cushing’s syndrome
  • Adrenal tumours

O+G:

  • Imperforate hymen
  • Absent uterus
163
Q

What is the difference between hirsutism and hypertrichosis?

A

Hirsutism is excess hair growth in a woman in the male pattern (androgen-dependent) such as: beard, abdominal wall, thigh, axilla and around nipples.

Hypertrichosis is androgen-independent with increase in general body hair

164
Q

Give 3 signs of virilisation.

A

Hirsutism

Clitoromegaly

Deepening of voice

Loss of female body shape

165
Q

What are the clinical features of Polycystic Ovarian Syndrome?

A 
Amenorrhoea/Oligomenorrhoea 
Hirsutism
Acne 
Obesity 
Virilisation
166
Q

What criteria is used to diagnose PCOS?

A

Rotterdam Criteria (2/3):

  • Menstrual irregularity
  • Clinical features of hyperandrogenism
  • Polycystic ovaries (multiple cysts) on TVUS
167
Q

What investigations would be diagnostic in a suspected case of PCOS?

A

Hormones: LH:FSH ratio >3; elevated Testosterone; elevated DHEAS

TFTs: Negative

PL: Negative

TVUS: multiple fluid-filled lesions in the ovaries

168
Q

How is PCOS managed?

A

Supportive: Weight loss

± Fertility desired
- Clomiphene

± Fertility not desired
- COCP

± Excess hair
- Minoxidil
or
- Mechanical removal

169
Q

What is the MOA of Clomiphene?

A

GnRH agonist thus release FSH and LH leading to development and release of ovum.

170
Q

Outline the structural anatomy of the adrenal glands.

A

Adrenal gland consists of a cortex and a medulla.

Cortex is derived from the intermediate mesoderm

Medulla is derived from ectoderm (neuroendocrine cells)

Adrenal cortex comprises of 3 layers (GFR; ‘Salt, sugar’ sex’)

Zona glomerulosa = salt

Zona fasciculata = sugar

Zona reticularis = sex

171
Q

Which hormones are secreted from the anterior pituitary gland?

A

FSH
LH
ACTH
TSH

PL
GH

Mnemonic: FLAT PG

172
Q

How may Addison’s disease be classified?

A

Addison’s disease is classified with respect to where the dysfunction is within the HPA Axis.

Primary: Addison’s (adrenal)
Secondary: ACTH (pituitary)
Tertiary: CRH (hypothalamic)

173
Q

What are the clinical features of Addison’s Disease?

A 
N/V
Fatigue 
Anorexia 
Weight loss 
Hyperpigmentation

Salt craving (secondary to hyponatraemia)

174
Q

What is the gold-standard investigation for Addison’s disease?

What would you expect to see if Addison’s Disease is present?

A

Short Synacthen test

Cortisol will remain <487nm/L as adrenal glands are failing

175
Q

How do you manage a patient with Addison’s Disease?

A

Replace what is lost

Medical: Hydrocortisone (15-30mg/day) + Fludrocortisone (0.1-0.2mg/day)

176
Q

What is the dosage of steroid replacement in Addison’s disease and how is this administered?

A

Hydrocortisone PO BD 15-30mg/day

2/3 am; 1/3 nocte

177
Q

What are the clinical features of an Addisonian crisis?

A 
= acute episode of severe Addisons
Altered consciousness
Hypotension
Hypoglycaemia
Hyponatraemia 
Hyperkalaemia
178
Q

What are the types of Conn’s Syndrome?

A

Determined by level of HP axis has excess Aldosterone

Primary: Adrenal adenoma
Secondary: High renin due to RAS, renal artery obstruction, HF

179
Q

What are the clinical features of Conn’s Syndrome?

A 
Nocturia 
Polyuria 
Mood ∆ -> irritable, depressed
Hypertension
Muscle weakness
Palpitations
180
Q

What is the gold-standard investigation for suspected Conn’s Syndrome?

A

Aldosterone: Renin Ratio

Aldosterone
Renin

High aldosterone, low renin = primary Conn’s

High aldosterone, high renin = secondary Conn’s

181
Q

What investigations should be conducted following elevated aldosterone in suspected Conn’s Syndrome?

A

CT/MRI-Adrenals

US-Kidneys

182
Q

How may RAS be treated?

A

Percutaneous Renal Artery Angioplasty

183
Q

What would you expect the Us+Es to come back as in a patient with Conn’s Syndrome?

A

Hypokalaemia; Hypernatraemia

184
Q

What would you expect the Us+Es to come back as in a patient with Addison’s Disease?

A

Hyponatraemia

Hyperkalaemia

185
Q

How do you manage a patient with Conn’s Syndrome?

A

Medical: Spironolactone (12.5-50mg PO OD) or Eplerenone (25-100mg PO OD)±
Surgery: Lap adrenalectomy  >2.5cm

186
Q

A patient is to be started on Hydrocortisone 30mg PO BD as part of their treatment for Addison’s disease.

They are worried about the potential side effects, what are they?

A

Hypertension

Weight gain
Glycosuria
Hyperglycaemia

Peptic ulcers
Acute pancreatitis

Osteoporosis
Myopathy
Aseptic necrosis of hip/Jaw

Polyuria
Nocturia

Depression
Euphoria
Psychosis
Insomnia

Cataracts

Skin thinning; Bruising

Increased risk of infection (immunosuppression)

187
Q

What are the potential causes of Cushing’s Syndrome?

A

Pituitary adenoma
Ectopic ACTH tumour - carcinoid tumour; SCLC

Adrenal adenomas
Adrenal carcinomas

Drugs
Alcohol-induced pseudo-Cushing’s Syndrome

188
Q

What is the gold-standard investigation of Cushing’s Syndrome?

How is this conducted?

A

Dexamethasone-suppression test

Dexamethasone 0.5mg QDS for 48 hours which if positive, cortisol >50nmol/L 2 hours after last dose of dexamethasone

189
Q

Where is Angiotensinogen produced?

A

Liver

190
Q

Where is renin produced?

A

Juxtaglomerular cells of Kidney

191
Q

Where is ACE produced?

A

Pulmonary endothelium

192
Q

What enzyme converts Angiotensin I to Angiotensin II?

A

ACE

193
Q

What are the functions of Angiotensin II?

A

Powerful vasoconstriction

Stimulates adrenal zona glomerulosa to increase aldosterone production

194
Q

What type of cells are undergoing proliferation in Phaeochromocytoma?

A

Chromaffin Cells of the adrenal medulla

195
Q

What are the clinical features of Phaeochromocytoma?

A

Headache
Palpitations
Diaphoresis
Hypertension

196
Q

What is the gold-standard investigation in a patient with suspected Phaeochromocytoma?

A

Urinary metanephrines

Appropriate if clinical suspicion is high

197
Q

How is Phaeochromocytoma managed?

A

Supportive: IV Fluids; High salt diet (>5g/day)
+
Medical: Prazosin; Atenolol

± Surgical candidate
- Lap total/partial adrenalectomy

± Non-surgical candidate
- Continue medical treatment
+
Iobenguane

198
Q

Why are alpha-blockers given before beta-blockers in Phaeochromocytoma?

A

Chronically vasoconstrictor due to high circulating levels of catecholamines thus secondary decrease in blood volume.

Full alpha blockage allows restoration of blood volume with ß-blockers following after.

199
Q

What gene is responsible for MEN I?

A

Menin gene on chromosome 11

200
Q

What gene is responsible for MEN II?

A

Ret gene on chromosome 10

201
Q

What are the functioning adenomas in MEN I?

A

3Ps

Pituitary adenoma

Parathyroid

Pancreatic tumours (gastrinoma; insulinoma; glucagonoma; VIPoma)

202
Q

What are the functioning adenomas in MEN 2A?

A

2Ps and 1M

Parathyroid
Phaeochromocytoma

MTC

203
Q

What are the functioning adenomas in MEN 2B?

A

2Ms, 1P

MTC
Mucosal neuroma

Phaeochromocytoma

204
Q

What is the management for Multiple Endocrine Neoplasia?

A

Treat abnormalities; Family screening

Surgical excision of tumours

205
Q

Where is ADH released from?

A

Posterior pituitary

206
Q

What are the functions of ADH?

A

Reabsorption of water in the collecting duct via AQP4 transporters

Vasoconstriction

207
Q

What are the two types of Diabetes Insipidus?

A

Cranial DI

Nephrogenic DI

208
Q

What are the causes of Diabetes Insipidus?

A 
Iatrogenic: Neurosurgery 
Trauma 
Idiopathic 
Infiltrative: Sarcoidosis; Histiocytosis
Congenital: Wolfram Syndrome (DIDMOAD)
Vascular: RAS
Idiopathic
Trauma 
Metabolic: hypercalcaemia; hypokalaemia
Iatrogenic: Surgery; Lithium
Neoplasm: Pituitary stalk lesions; Craniopharyngioma

Congenital: Wolfram syndrome

209
Q

What is histiocytosis?

A

Group of syndromes resulting in increased numbers of histiocytes: macrophages; monocytes and dendritic cells

210
Q

What are the clinical features of Diabetes Insipidus?

A

Polyuria

Polydipsia

Dilute urine

211
Q

What are the clinical features of Wolfram Syndrome?

A

Mnemonic: DIDMOAD

Diabetes Insipidus

Diabetes Mellitus

Optic atrophy

Deafness

212
Q

What is the gold-standard investigation in suspected Diabetes Insipidus?

A

Water deprivation test: urine osmolality <300mOsm/kg

Urine osmolality < 300mOsm/kg

213
Q

How is Diabetes Insipidus managed?

A 
Supportive: Oral/IV Fluids 
\+
Medical: Desmopressin
\+
Tx underlying cause
214
Q

What are the causes of SIADH?

A

Vascular

Iatrogenic: Opiates; Carbamazepine; Vincristine

Trauma: Head injury

Metabolic: Porphyria; Alcohol withdrawal

Infection: Meningitis; Cerebral abscess; Pneumonia

Neoplasm: SCLC; Brain tumour

215
Q

What are the clinical features of SIADH?

A

Nausea

Irritability

Headache

If severe hyponatraemia (<115mmol/L)
Fits and comas

216
Q

What is the gold-standard investigation to diagnose SIADH?

A

Urine sodium and osmolality: Elevated

Absence of:

  • Diuretic use
  • No D/V/burns/fistula/diaphoresis
  • Negative Synacthen test
  • No excessive polydipsia
217
Q

Why is it important to correct sodium slowly in SIADH?

A

Avoid central pontine myelinolysis - no greater change than 10mmol/L per 24 hours

218
Q

Outline what may happen if you correct hyponatraemia too quickly in SIADH?

Outline the pathophysiology behind this.

What are the clinical features of the potential condition?

A

Chronic hyponatraemia leads to the brain adapting to reduce the solutes of brain cells to ensure water balance across BBB to counteract potential cerebral oedema.

Rapid rise in blood sodium causes water to shift out of brain cells at BBB causing demyelination of neurones at the Pons presenting with spastic quadriparesis, pseudo bulbar palsy and cognitive behavioural changes.

219
Q

What is the management of SIADH?

A 
Tx cause
\+
Supportive: Fluid restriction; Furosemide 
\+ 
Medical: Tolvaptan
220
Q

Explain how PTH increases calcium concentration.

A

Calcium reabsorption

Activation of Vitamin D

221
Q

How does corrected Calcium differ from total plasma calcium? Explain.

A

40% of Calcium is free, the remainder is bound to albumin.

Normal range is 2.2-2.6mmol/L however corrected Calcium accounts for albumin concentration.

You add or subtract 0.02mmol/L for every 1g/L by which the albumin differs from 40g/L

222
Q

What are the causes of hypercalcaemia?

A

Infection: TB; Sarcoid
Metabolic: Primary hyperparathyroidism; Tertiary hyperparathyroidism; Addison’s Disease
Iatrogenic: Vitamin D toxicity; Vitamin A; Lithium; Thiazides
Neoplasia: Multiple myeloma; Metastasis; PTH-related protein secretion

223
Q

What are the clinical features of hypercalcaemia?

A

Bones, groans, stones and moans

224
Q

Outline some key causes of Hypocalcaemia.

A

Vascular:

Inflammation/Infection: Acute Pancreatitis;

Metabolic: CKD; Phosphate therapy; Malabsorption; Reduced exposure to UV light; Severe hypomagnesaemia

Iatrogenic: Thyroidectomy; Parathyroidectomy; Antiepileptic drugs; Calcitonin; Bisphosphonates

Congenital: DiGeorge Syndrome;

225
Q

What are the causes of hypophosphataemia?

A

DKA Tx
Refeeding syndrome

Poor oral intake
Diarrhoea

Hyperparathyroidism
Vitamin D Deficiency
Primary renal abnormality

226
Q

What are the 3 pathophysiological mechanisms by which hypophosphataemia may occur?

A
  • Reduced intake
  • Reduced absorption of phosphate
  • Increased excretion
227
Q

What are the clinical features of hypophosphataemia?

A

Muscle weakness
Encephalopathy
Haemolysis

Mnemonic: MEH

228
Q

How is hypophosphataemia managed?

A

Oral phosphate supplements
or
IV phosphate

229
Q

What is the threshold for hypothermia?

A

<35C

230
Q

What are the clinical features of hypothermia?

A

Depends on severity

Shivering

Altered consciousness
Coma

Reduced HR
Reduced BP

Muscle stiffness
Bradyreflexia

Ventricular arrhythmias

231
Q

How is Hypothermia managed?

A

Supportive: Admission; A-E assessment; Oxygen; ECG monitoring; passive external warming (core T >32) or active external rewarming (core T 28-32) or active internal rewarming (core T <28)

Active rewarming involves humidification and warmed oxygen and warmed fluids

232
Q

What is the threshold for hyperthermia?

A

> 41C

233
Q

What is the management for Hyperthermia?

A

Tx cause
+
Medical: Dantrolene sodium

234
Q

What two signs may be pathognomonic for Hypocalcaemia?

A

Chvostek Sign (Cheek)

Trousseau Sign (Tense)

235
Q

Other than pituitary adenoma, what other conditions may yield a bitemporal hemianopia?

A

Suprasellar meningioma

Craniopharyngioma

236
Q

Should a patient on Carbimazole for Grave’s disease develop a chest infection, what must you do?

A

Immediately stop

Request urgent same day bloods - could be neutropenic due to agranulocytosis from medication

237
Q

What are the biochemical criteria for DKA?

A

raised blood glucose(>11.1 mmol/L), or known diabetes
ketonuria ++ or more
serum bicarbonate <15 mmol/L
pH<7.3 (if measured)

238
Q

What is the difference between MEN 4 and MEN 1?

A

Clinically indistinguishable. With MEN IV, patients can have reproductive organ tumours and/or adrenal/renal tumours

239
Q

What are the features of Wermer’s Syndrome?

A

Pituitary tumour

Parathyroid hyperplasia

Pancreatic islet tumour (ZES/Insulinoma)

240
Q

What are the clinical features of Sipple’s Syndrome?

A

MEN 2A

Parathyroid hyperplasia
Phaeochromocytoma

Medullar thyroid carcinoma

241
Q

Which antibody in type 1 diabetes mellitus is strongly correlated with age?

A

Insulin autoantibody (IAA) - 90% of young people with T1DM

medicine (18 decks)

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