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Endocrine Flashcards

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USMLE® Step 1 flashcards
1
Q

Type 1 diabetes

A

Autoimmune disorder where insulin producing beta cells of islets of Langerhans in pancreas are destroyed by immune system leading to absolute insulin deficiency

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2
Q

classic triad of type 1 diabetes

A

weight loss, polydipsia (excessive thirst), polyuria

fatigue, blurred vision, candidal infection and sometimes DKA

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3
Q

type I diabetes Ix

A 
•	Fasting Glucose: 7.0 mmol/L
•	OGTT: 11.1 mmol/L
•	HbA1c: 48 mmol/L
•	Presence of islets autoantibodies 
o	GAD, IA-2 and ZnT8 
•	C peptide – decrease after 3-5 year after diagnosis
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4
Q

type I diabetes Mx

A

carb counting, exercise, reduce drinking and stop smoking

Inuslin: basal/bolus

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5
Q

Insulin types

A

Rapid acting: Novorapid or Humalog – 5 hours: inject at start of meal or just after

Short acting: Humulin S, Actrapid – 6 hours

Intermediate acting: Humulin I (isophane), Insulatard – 12 hours

Long acting: Lantus, Levemir – 18 hours

Rapid acting analogue-intermediate mixture – Humalog Mix 25/50, Novomix30

Short acting-intermediate mixture – Humulin M3

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6
Q

plasma glucose levels

A

5-7 on waking
4-7 before meals
5-9 after meals at least 90 minutes after

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7
Q

Type II diabetes

A

Type 2 diabetes (due to a progressive loss of β-cell insulin secretion frequently on the background of insulin resistance)

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8
Q

Type II diabetes signs/symptoms

A
  • Blurred vision
  • Recurrent UTIs
  • Tiredness
  • Polyuria
  • T2DM- Signs of complications- neuropathy, retinopathy and nephropathy
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9
Q

Pre-diabetes

A

Fasting: 6.1-6.9
OGTT: 7.8-11.0
HbA1c: 42-47

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10
Q

Diabetes management

A

lifestyle: exercise+diet: lose 5-10kg in a year
Monotherapy:
- Metformin + SU (intolerant of modified and standard release metformin)

combination: Met + SU or SLG2-inhibitor, DDP4 and pioglitazone

further combination: Met + SU + SLGT2, DDP4 or pioglitazone or injectable (GLP-1 agonist)

Further; Met + SU + SLGT2, DDP4 or pioglitazone or injectable (GLP-1 agonist + basal insulin )
o Once daily NPH (isophane – intermediate acting) Insulin is added to Metformin (+/- SU).
o If this is ineffective or becomes so then change to bd NPH insulin or mixed insulin (Humulin M3) or basal/bolus (e.g. Lantus and Novorapid)

BP 130/80: ACEi
Simvastatin 40mg or atrovastatin 10mg

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11
Q

Diabetic neuropathy

A
  1. Peripheral (stocking, absent ankle jerks, charcot joint, pes cavus, claw toes: 10g monofilament)
  2. autonomic
  3. proximal
  4. focal

Treated as neuropathic pain: amitriptyline, duloxetine, gabapentin or pregabalin

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12
Q

Diabetic nephropathy + Mx

A

damage to capillaries in glomeruli

  • proteinuria
  • diffuse scarring
  1. ACEi/ARB (dilation of renal efferent arterioles, decrease filtration pressure, GFR and proteinuria)
  2. SGL2 inhibitor
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13
Q

Microalbuminuria

A

ACR > 2.5 and >3.5 (female), PCR > 15 and negative dipstick

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14
Q

Proteinuria

A

ACR: >30 AND PCR >50 with positive dipstick

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15
Q

Diabetic retinopathy types

A

o Mild non-proliferative (Background)
o Moderate non-proliferative
o Severe non-proliferative
o Proliferative

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16
Q

diabetic retinopathy and maculopathy treatment

A

Retinopathy: (proliferative or maculopathy)

  1. Laser panretinal or macular grid photocoagulation
  2. viterectomy

Maculopathy:
1. Anti-VEGF medications

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17
Q

LADA

A

late-onset type 1 diabetes is probably quite common in patients presenting with ‘typical’ type 2 diabetes

ketosis = type 1 diabetes

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18
Q

DKA

A

Diabetic ketoacidosis (DKA) is a disordered metabolic state that usually occurs in the context of an absolute or relative insulin deficiency accompanied by an increase in the counter-regulatory hormones i.e. glucagon, adrenaline, cortisol and growth hormone.

Caused by uncontrolled lipolysis -> excess free fatty acids that are converted to ketone bodies. Dehydration, hyperglycaemia and hyperosmolar state (more electrolytes in the serum)

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19
Q

DKA precipitating factors

A

infection, missed insulin doses and MI
newly diagnosed type I diabetes
illicit and alcohol use
non-adherence to insulin

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20
Q

DKA diagnsis

A 
Glucose: >11 
Ketones > 3 or 5 and urine ketones (++)
pH<7.3 metabolic acidosis 
K+ 5.5 mmol-1
Raised lactate, creatinine and amylase 
WCC: Median 25 
Na: low 
Bicarbonate: <10
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21
Q

DKA management

A
  1. Fluid: 0.9% NaCl, glucose falls to 15, switch to dextrose
  2. Insulin: commence 6 units per hour IV and continue basal insulin (once per day) e.g. levemir
  3. Potassium: standard replacement is 40mmol/L IV fluid if K+ between 3.5 and 5 due to hypokalaemia
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22
Q

DKA complications

A

Hyperkalaemia or Hypokalaemia: Predispose to cardiac arrythmias

ARDS

Cerebral oedema

Gastric stasis

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23
Q

Hyperosmolar hyperglycaemic state (HHS)

A

Hyperosmolar hyperglycemic state is a metabolic complication of diabetes mellitus (DM) characterized by severe hyperglycemia, extreme dehydration, hyperosmolar plasma, and altered consciousness.

Osmotic diuresis, severe dehydration and electrolyte deficiency

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24
Q

HHS signs/symptoms

A

Fatigue, lethargy, Nausea and Vomiting, altered level of consciousness, headaches, papilloedema, weakness, hyperviscosity of blood -> CV events. Dehydration, hypotension, tachycardia.

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25
Q

HHS diagnosis

A
  1. Glucose over 50
  2. Hypovolaemia
  3. No ketonaemia
  4. Bicarbonate > 15
  5. ph >7.3
  6. osmolaity >320 (2xNa + urea + glucose). Normal = 275-295
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26
Q

HHS management

A

Careful fluid replacement – risk of fluid overload but try and replace/correct fluid deficit during the first 24 hours
o 3L+ve at 6 hours
o 3-6L+ve at 12 hours

Reduce glucose by 5mmol/hr and no more (prevent cerebral oedema and seizures)

Decreases osmolality 3-8 per hour

K+: 40mmol/L if K+ is between 3.5-5 due to treatment

Slower insulin or may not require (often glucose improves with fluids) e.g. 3 units/hour

Ketones > 1.0 then low dose 0.05 u/kg/hour

Sodium – avoid rapid fluctuations .g. ≤0.5mmol/l/hr and consider 0.45% Saline

Co-morbidities: screen vascular event or LMWH unless contradicted

STOP any SGLT2 inhibitors

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27
Q

Euglycaemic Keto-acidosis

A

Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis.

Look for SGLT2i

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28
Q

Severe Alcohol-induced Keto-acidosis

A

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain.

History: acomprosate

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29
Q

Severe Alcohol-induced Keto-acidosis Mx

A
  1. IV fluids (dextrose)
  2. IV pabrinex
  3. IV-antiemetics
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30
Q

Lactic acidosis

A

Type A: Tissue hypoxemia e.g. ischaemic bowel, cardiogenic and hypovolemic shock

Type B: associated with diabetes

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31
Q

Lactic acidosis management

A 
Reduced bicarbonate
Raised anion gap [(Na+ + K+) – (HCO3 + Cl-)]. Normal 10-18
Glucose variable – maybe [often] raised
Absence of ketonaemia
Raised phosphate

Treat underlying condition: Fluids and antibiotics

Withdraw offending medication

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32
Q

MODY

A

AD: genetic defect in B cell function

Types
• HNF-1α
• HNF-4α
• Glucokinase

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33
Q

MODY 2 (Glucokinase)

A

rate limiting step (glucokinase). Sensing defect, blood glucose threshold for inulin secretion is increased . Homeostatic point at 7 insead of 5

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34
Q

MODY 2 management

A

diet treatment

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35
Q

MODY 1 and 3

A

defects in HNF-1a, 1b and 4a.

Also regulate β cell differentiation and function

glycolytic flux, expression of GLUT2 transporters, cell growth, insulin secretion, glucose transport and metabolism

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36
Q

MODY 1 and 3 Mx

A

glicazide work on KATP channels

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37
Q

Neonatal diabetes

A

Kir6.2 mutations: constitutively activated KATP channels or an increase in KATP numbers

Transient or permanent

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38
Q

Neonatal diabetes Mx

A

SURs such as tolbutamide

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39
Q

Graves disease

A

Autoimmune disease: Antibodies bind to and activate thyrotropin receptors diffuse thyroid enlargement, increase in hormone production (T3) & react with orbital autoantigens

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40
Q

signs/symptoms of hyperthyroidism

A

Weight loss, ‘manic’, restlessness, heat intolerance, palpitations (even provoke arrhythmias), increased sweating, diarrhoea, oligomenorrhea, anxiety and tremor.

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41
Q

Graves disease signs/symptoms

A
  1. Exophthalmos and ophthalmoplegia
  2. Pretibial myxoedema
  3. Thyroid acropachy
  4. thyroid bruit
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42
Q

Graves diagnosis

A

TSH decrease and FT4/T3 increase

hypercalcaemia and ALP increase

Leukopenia

TRAb

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43
Q

Graves management

A
  1. Propranolol
  2. Carbimazole and PTU (1st trimester of pregnancy)
  3. Radioiodine treatment
  4. Thyroidectomy
  5. Mild eye disease (topically lubricants and steroids)
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44
Q

Carbimazole risk

A

aplasia cutis and agranulocytosis (fever, oral ulcer or oropharyngeal infection - do urgent FBC)

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45
Q

PTU risk

A

Liver failure and agranulocytosis (fever, oral ulcer or oropharyngeal infection - do urgent FBC)

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46
Q

Toxic multi nodular goitre

A

autonomously functioning thyroid nodules that secrete excess thyroid hormones

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47
Q

TMG signs/symptoms

A

Thyroid nodular and asymmetrical goitre

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48
Q

diagnosis TMG

A

FT4 increases and TSH decreases
Scintigraphy: high uptake
Thyroid USS: Exclude cancer
TRAb negative

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49
Q

Toxic adenoma

A

Solitary nodule producing T3 and T4.

Hot nodule on scintigraphy

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50
Q

Other causes of hyperthyroidism

A
  1. Ectopic thyroid tissue: follicular cancer (blood spread) or struma ovarii (ovarian teratoma with thyroid tissue)

Exogenous: iodine excess, contrast media and levothyroxine excess (T4 increases, T3 and thyroglobulin)

Subacute de Quervains thyroiditis: self-limiting post viral with painful goitre: associated neck tenderness, fever, viral symptoms, low isotpe scan and NSAIDs for treatment

Drug induced: amiodarone and lithium

Post-partum: In postpartum thyroiditis

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51
Q

Hashimotos thyroiditis

A

Autoimmune destruction of thyroid gland and reduced thyroid hormone production

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52
Q

Signs/symptoms of hypothyroidism

A

Weight gain, lethargy, cold intolerance, dry (anhidrosis), cold, yellowish skin. Non-pitting oedema e.g hands and face. Dry, coarse. Constipation. Menorrhagia. Decreased deep tendon reflexes and carpal tunnel syndrome

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53
Q

diagnosis of Hashimotos

A

TSH increase, FT4 decrease
MCV, CK, LDL increase
hyponatremia: decrease renal tubular water loss
hyperprolactinaemia: TRH increase leads to PRL increase

Anti-TPO antibodies

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54
Q

Hashimotos management

A

Younger patients: start levothyroxine at 50-100 μg daily. Review 12 weeks and adjust every 6 weeks by clinical state and to normalise it to suppress TSH

Elderly or IHD: start levothyroxine at 25-50 μg daily, adjusted every 4 weeks according to response. Cautiously as levothyroxine can cause angina or MI

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55
Q

Other causes of primary hypothyroidism

A

Goitrous
- iodine deficiency, drug (amiodarone, lithium) and maternal

Non-goitrous

  • atrophic thyroiditis
  • post ablative (radioidoine, surgery)
  • Post radiotherapy
  • congenital
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56
Q

Secondary hypothyroidism/hyperthyroidism causes

A 
Diseases of the hypothalamus and pituitary gland (multiple!)
o	Infiltrative – sarcoid
o	Infectious
o	Malignant
o	Traumatic
o	Congenital
o	Cranial radiotherapy
o	Drug-induced
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57
Q

Subclinical hypothyroidism - when to treat

A

TPO positive
TSH > 10
past graves
pregnant

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58
Q

Subclinical hyperthyroidism

A

Treatment generally advised if TSH <0.1 (or if co-existing osteoporosis/fracture or AF)

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59
Q

Thyroid storm seen when?

A

hyperthyroid patients with an acute infection/illness, recent thyroid surgery, MI or radioiodine

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60
Q

signs/symptoms of thyroid storm

A

• Agitation, confusion, tachycardia, AF, D&V, goitre, thyroid bruit, acute abdomen and heart failure
Respiratory and cardiac collapse
• Hyperthermia
• Exaggerated reflexes

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61
Q

Thyroid storm management

A

Iugol’s iodine, glucocorticoids, beta blockers, PTU, fluids and monitoring

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62
Q

Myxoedema coma

A

affects elderly women with long standing but frequently unrecognized or untreated hypothyroidism

63
Q

myxoedema coma diagnosis

A

ECG: bradycardia, low voltage complexes, varying degrees of heart block, T wave inversion, prolongation of the QT interval

Type 2 respiratory failure: hypoxia, hypercarbia, respiratory acidosis

64
Q

Myxoedema coma management

A

Passively rewarm: aim for a slow rise in body temperature

Cardiac monitoring for arrhythmias

Close monitoring of urine output, fluid balance, central venous pressure, blood sugars, oxygenation

Broad spectrum antibiotics if infection suspected

Thyroxine cautiously and hydrocortisone

65
Q

Papillary thyroid

A

Most common form of thyroid cancer

Cystic solitary nodule in thyroid and derived from follicular epithelium

Lymph spread more

66
Q

Papillary thyroid FNA

A

Orphan Annie eye nuclear inclusions: clear nucleus?

Psnommona bodies

67
Q

Papillary Thyroid cancer management

A

Thyroid lobectomy with ismuscetomy – papillary microcarcinoma (<1 cm diameter)

Sub-total thyroidectomy – nodal involvement and extrathyroidal spread

Total thyroidectomy

Nodal clearance: Central compartment clearance and lateral lymph node sampling for papillary tumours

3-6 months: WBIS. If remants, thyroid remnant ablation

sorafenib and lenvatibib: refractory

68
Q

Follicular thyroid cancer

A

2nd commonest thyroid cancer

Single nodule with invasive growth pattern.

Haematogenous spread

69
Q

Follicular thyroid cancer management

A

same as papillary apart from

Thyroid lobectomy with ismuscetomy – minimally invasive follicular carcinoma with capsular invasion

Sub-total thyroidectomy – distant mets and extrathyroidal spread

70
Q

Medullary thyroid cancer

A

parafollicular C cells (neuroendocrine). Bilateral (familial) and MEN 2A and 2B

Secrete calcitonin

Total thyroidectomy

71
Q

Anaplastic carcinoma

A

Undifferentiated and aggressive tumours

72
Q

Primary parahyperthyroidism

A

Primary activity of the parathyroid gland through various causes

Solitary/multiple adenomas, hyperplasia of all glands, and carcinoma

73
Q

Primary parahyperthyroidism

A

stereotypical - elderly females with unquenchable thirst and a normal or elevated

74
Q

signs/symptoms of parahyperthyroidism

A

Bones, stones, abdominal groans and psychic moans
• Polydipsia, polyuria but dehydrated
• Peptic ulceration/constipation/pancreatitis
• Bone pain/fractures/osteopenia/osteoporosis due to bone resorption
• Renal stones
• Depression
• Hypertension
• Associations: hypertension. Multiple endocrine neoplasia: MEN I and MEN II

75
Q

Primary parahyperthyroidism diagnosis

A
  1. Raised calcium
  2. Raised PTH
  3. Increased calcium excretion (urine)
  4. decrease serum phosphate
  5. Increase in ALP
  6. DEXA
  7. Sestamibi scanning
76
Q

Primary parahyperthyroidism management

A

Mild: Increase fluid intake to prevent stones, avoid thiazides (hypercalcaemia) and high Ca2+ and Vit D intake

Rehydrate with 0.9% saline 4-6L in 24hours. Consider loop diuretics
Bisphosphonates- single dose will lower Ca over 2-3d.

surgery: adenoma or hyperplasia but needs to be end organ damage
- bone disease e.g. pepper pot skull
- gastric ulcers & renal stones
- Very high calcium (>2.85)
- Under age 50
- eGFR < 60ml/min

77
Q

Secondary PTH

A

excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia (low blood calcium levels) or Vitamin D with resultant hyperplasia of these glands or CKD

78
Q

Secondary PTH diagnosis

A

PTH increased
Ca low
Phosphate high
Vit D low

79
Q

Tertiary PTH

A

Tertiary hyperparathyroidism is a state of excessive secretion of parathyroid hormone (PTH) after a long period of secondary hyperparathyroidism and resulting in a high blood calcium level. It reflects development of autonomous (unregulated) parathyroid function following a period of persistent parathyroid stimulation.

80
Q

Tertiary PTH diagnosis

A 
PTH high 
Ca high 
Phosphate low 
Vit D normal 
ALP elevated
81
Q

Malignant PTH diagnosis

A

Ca and ALP high

PTH low as PTHrp

82
Q

Primary hypoparathyroidism

A

PTH is low due to gland failure

Autoimmune and congenital absence (DiGeorge syndrome)
Symptoms/signs

83
Q

signs/symptoms of primary Hypoparathyroidism

A

Tetany: muscle twitching, cramping and spasm

Perioral paraesthesia

Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic. Wrist and fingers flex

Chvostek’s sign: tapping over the parotid gland causing facial muscles to twitch

84
Q

Primary hypoparathyroidism diagnosis

A

Reduced PTH

Reduced Calcium

Increased phosphate

Normal ALP?

85
Q

Primary Hypoparathyroidism Mx

A

Calcium supplements >1-2g per day

Tablet: calcitriol or alfacalcidol (active metabolite of Vitamin D)

Depot injection: Cholecalciferol 300,000 units 6 monthly (vitamin D)

86
Q

Emergency acute hypocalcaemia treatment

A

IV calcium gluconate 10 ml, 10% over 10 mins (in 50ml saline or dextrose)

Infusion (10ml 10% in 100 ml infusate, at 50 ml/h)

87
Q

Pseudohypoparathyrodism

A

Pseudohypoparathyroidism (PHP) is a genetic disorder in which the body fails to respond to parathyroid hormone.

88
Q

Pseudohypoparathyrodism signs/symptoms

A

Bone abnormalities (McCune Albright syndrome): Short metacarpals (esp 4th and 5th)

Round face, short stature, calcified basal ganglia

Obesity

Learning disability

Brachdactyly (4th metacarpal)

89
Q

Pseudohypoparathyrodism dx

A

low calcium and high PTH

90
Q

Pseudopseudohypoparathyrodism

A

• The same features as Pseudohypoparathyrodism but with normal biochemistry. Both genetic

91
Q

Hypocalciuric hypercalcaemia

A

rare autosomal dominant condition.

It occurs as a result of mutations in the calcium-sensing receptor gene (CASR) causing decreased receptor activity. mild hypercalcemia, hypocalciuria, hypermagnesemia, hypophosphatemia

92
Q

Cushing’s Disease vs Cushing’s syndrome

A

Cushing’s disease refers to the specific condition where a pituitary adenoma secretes excessive ACTH and causes Cushing’s syndrome.

93
Q

ACTH dependent (problem arising with pituitary gland and excess of ACTH)

A

Pituitary adenoma (68%): Cushings Disease

Paraneoplastic Ectopic ACTH 12% (carcinoid/carcinoma)

Ectopic CRH <1%

94
Q

ACTH independent (too much cortisol)

A
  1. Adrenal adenoma 10%
    Adrenal carcinoma 8%
  2. Nodular hyperplasia 1%
  3. Exogenous steroids e.g. asthma, rheumatoid arthritis, inflammatory bowel disease, transplants
    - Chronic suppression of pituitary ACTH production and adrenal atrophy. Unable to respond to stress (illness/surgery). Need extra doses of steroid when ill/surgical procedure
95
Q

Cushings syndrome signs/symptoms

A
  • Easy bruising
  • Facial plethora: fullness
  • Abdominal Striae
  • Proximal myopathy
  • Central obesity
  • Buffalo hump
  • Hypertension, cardiac hypertrophy, hyperglycaemia, depression and insomnia
  • Osteoporosis, easy skin bruising
  • Gonadal dysfunction: oligio/amenorrhoea, hirsutism, acne
96
Q

Cushings diagnosis

A

Establish cortisol excess: low dose dexamethasone suppression test (1mg): suppress cortisol

High dose dexamethasone (6-8mg) over 48 hours and measure ACTH:

  • Pituitary adenoma: some negative feedback and cortisol is suppressed
  • Adrenal adenoma: cortisol production is independent from pituitary, therefore is not suppressed however ACTH is suppressed (negative feedback)
  • Ectopic ACTH: Neither cortisol or ACTH are suppressed because ACTH production is independent of hypothalamus and pituitary gland

MRI: brain and adrenal glands
CT lungs and adrenal glands for cancer
Hypokalaemia

97
Q

Cushings management

A

Pituitary:

  • Hypophysectomy and external radiotherapy
  • bilateral adrenalectomy (refractory)

Adrenal
- adrenalectomy and steroid replacement

Ectopic
- remove source or the above

98
Q

Addison’s Disease

A

primary adrenal insufficiency and hypocortisolism, is a long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones (autoimmune: adrenal cortex destroyed).

99
Q

signs/symptoms of addisons

A

> 90% destroyed before symptomatic.
• Anorexia, weight loss
• Fatigue/lethargy
• Dizziness and low BP
• Abdominal pain, vomiting, diarrhoea
• Skin pigmentation – darkness in the palmar creases and buccal hypopigmentation
o ACTH very high and cross react with melanin receptors to cause pigmentation disease

100
Q

Addisons biochem

A

low Na, high K+

hypoglycaemia

101
Q

Addisons test

A

SHORT SYNACTHEN TEST

  • Measure plasma cortisol before and 30 minutes after iv/im ACTH injection
  • Normal: baseline >250nmol/L
  • post ACTH >550nmol/L (needs to peak)

Plasma ACTH: increased

Renin/aldosterone:
increased renin, decreased aldosterone due to adrenal cortex destruction

102
Q

Addison’s management

A

IV fluid resus
correct hypoglycaemia
Hydrocortisone (15-30mg): split into 3 doses
Fludrocortisone: aldosterone replacement

103
Q

Secondary Adrenal insufficiency

A

Inadequate ACTH stimulating the adrenal glands resulting low cortisol release

104
Q

Secondary Adrenal insufficiency causes

A 
Pituitary/hypothalamic disease tumours e.g. Surgery/radiotherapy
•	Infection
•	Sheehan’s syndrome 
•	Loss of blood flow 
•	Exogenous steroid use
105
Q

Secondary Adrenal insufficiency Mx

A

hydrocortisone replacement (fludrocortisone unnecessary)

106
Q

Primary Aldosteronism

A

Autonomous production of aldosterone independent of its regulators (angiotensin II/potassium)

107
Q

Primary Aldosteronism causes

A

Adrenal adenoma secreting aldosterone: Conns syndrome

Bilateral adrenal hyperplasia

Familial hyperaldosteronism type 1 and type 2

Adrenal carcinoma

108
Q

Primary Aldosteronism signs/symptoms

A

Often asymptomatic

Weakness, cramps

Signs of hypokalaemia and hypernatremia

Polyuria and polydipsia

Hypertension

109
Q

Primary Aldosteronism diagnosis

A

Low serum renin and high aldosterone: express as ratio

If raised: saline suppression test
- Failure of plasma aldosterone to suppress by > 50% with 2 litres of normal saline confirms PA

Adrenal CT/MRI to demonstrate adenoma

Sometimes adrenal vein sampling to confirm adenoma is true source of aldosterone excess

110
Q

Conns management

A

Surgical: Unilateral laparoscopic adrenalectomy
cases

Medical: In bilateral adrenal hyperplasia, use MR antagonists (spironolactone or eplerenone)

111
Q

Secondary Aldosteronism causes (excess renin)

A

Several causes for high renin levels and they occur when the BP in the kidneys is disproportionately lower than BP in the rest of the body

  • Renal artery stenosis
  • Renal artery obstruction
  • Heart failure
112
Q

Secondary Aldosteronism diagnosis and management

A

Serum renin will be high and high aldosterone

US, CT and MRI angiogram

Percutaneous renal artery angioplasty via femoral artery to treat renal artery stenosis

113
Q

Congenital Adrenal Hyperplasia

A

Congenital adrenal hyperplasia (CAH) is a group of rare inherited autosomal recessive disorders characterized by a deficiency of one of the enzymes needed to make specific hormones

21-hydroxylase deficiency is one of a group of disorders known as congenital adrenal hyperplasia’s that impair hormone production and disrupt sexual development.

114
Q

Congenital Adrenal Hyperplasia diagnosis

A

Increase in androgens (ambiguous female genitilia) but deceases in aldosterone (hypotension) and cortisol

increased 17-OH progesterone

115
Q

CAH management

A 
Paediatricians
o	Timely recognition
o	Glucocorticoid replacement
o	Mineralocorticoid replacement in some
o	Surgical correction
o	Achieve maximal growth potential

Adult Physicians
o Control androgen excess
o Restore fertility
o Avoid steroid over-replacement

116
Q

Pheochromocytoma

A

Tumour of the chromaffin cells in the adrenal glands in the adrenal medulla

Extra adrenal [sympathetic chain] – paraganglioma
- MEN 2, NFL and VHL

117
Q

Pheochromocytoma classic triad

A

hypertension, headaches and sweating

118
Q

Pheochromocytoma diagnosis

A

Hyperglycaemia – adrenaline secreting tumours

low potassium level

High haematocrit – i.e. raised Hb concentration

Mild hypercalcaemia

Lactic acidosis – in absence of shock

Urine – 2x24hour catecholamines or metanephrins (more biologically stable)

MRI, MIBG and PET scan

119
Q

Pheochromocytoma management

A

Full α and β- blockade (α before β): if you block B first, all adrenaline goes to A and it vasoconstricts (significant) too much causing a stroke

  • Phenoxybenzamine (α-blocker)
  • Propranolol, atenolol or metoprolol (β-blocker)
  • Fluid and/or blood replacement

Surgical: laparoscopic: need to have symptoms controlled medically first

  • Adrenalectomy
  • Tumour de-bulking
  • Chemotherapy if malignant
  • Radio-labelled MIBG
120
Q

Prolactinoma

A

noncancerous tumour (adenoma) of the pituitary gland in your brain overproduces the hormone prolactin. The major effect is decreased levels of some sex hormones — oestrogen in women and testosterone in men.

121
Q

Prolactinoma causes

A

Physiological: breast feeding, pregnancy, stress and sleep, drugs (dopamine antagonists, antipsychotics e.g. phenothiazines, anti-depressants e.g. TCA

Pathological: Hypothyroidism, stalk lesions (iatrogenic, road accident – stalk affect), Prolactinoma (adenoma)

122
Q

Prolactinoma signs/symptoms

A

Female (early presentation)
• Galactorrhoea (normal milk production but at abnormal time: 30-80%)
• Menstrual irregularity
• Ammenorrhoea: body is fooled into thinking it is pregnant
• Infertility

Male (Late presentation)
•	Impotence
•	Visual field abnormal
•	Headache
•	Ant pit malfunction
123
Q

Prolactinoma management

A

Dopamine agonists:

  • Cabergoline
  • Bromocriptine: three times per day oral
  • Quinagolide

Surgery: Pituitary and radiotherapy alone

124
Q

Acromegaly signs/symptoms

A

Giant (before epiphyseal fusion)

Thickened soft tissues e.g. skin, large jaw, sweaty, large hands. Prominent forehead and brow, large nose, large tongue (macroglossia), protruding jaw

Snoring/Sleep apnoea (thickened nasopharynx)

Hypertension (heart), cardiac failure (hypertrophic)

Headaches (vascular) – not pressure

Diabetes mellitus – stress hormone so releases glucose and raises BG (type 2)

Local pituitary effects: visual fields (bitemporal hemianopia), hypopituitarism

Early CV Death

Colonic polyps and colon cancer (colorectal cancer)

125
Q

Acromegaly diagnosis

A

IGF1

OGTT: Glucose increases and GH should decrease

126
Q

Acromegaly management

A 
Surgery 
Medical 
- somatostatin analogues
 - dopamine agonists 
-   GH antagonist e.g. Pegvisomant
127
Q

Pan Hypopituitarism

A

inadequate or absent production of the anterior pituitary hormones.

GGAT: Gonadotrophins (women present first due to periods going quickly), GH, ACTH and TSH

128
Q

Pan Hypopituitarism management

A

Thyroxine: 100-150mcg/day

Hydrocortisone: 10-25 mg/day (am/pm).

ADH: Desmospray (nasal) or desmopressin tablets

GH: GH nightly sc

HRT/Oest/prog pill for female

Testosterone for males

129
Q

Cranial diabetes Insipidus/Nephrogenic Diabetes Insipidus

A

Cranial diabetes insipidus is a condition in which the hypothalamus does not produce enough anti-diuretic hormone.

Nephrogenic diabetes insipidus is a condition in which the kidneys fail to respond to anti-diuretic hormone

130
Q

Cranial diabetes Insipidus/Nephrogenic Diabetes Insipidus signs/symptoms

A 
Polyuria 
Polydipsia 
Dehydration 
Postural hypotension 
Hypernatremia
131
Q

DI diagnosis

A

Ur/Serum Osmol ratio >2 then it is normal, otherwise DI

Water deprivation test

ADH given - urine osmality increases (cranial) if not, nephrogenic

132
Q

Cranial DI management

A

Desmospray, desmopressin

133
Q

Nephrogenic DI management

A

Correct reversible causes such as hypokalaemia, hypercalcaemia and stop offending drugs e.g. lithium
• Massive doses of ADH can sometimes help and drink lots
• Thiazides potentially

134
Q

SIADH diagnosis

A

low plasma sodium and osmolality

High urine osmolality and sodium

135
Q

SIADH management

A

Exclude hypothyroidism (not able to excrete enough water at kidneys: low sodium and plasma osmolarity) and Addison’s

Fluid restrict them: 1-1.5 Litres per day

Demeclocycline – old fashioned antibiotic that uncouples the aquaporin 2 receptor from vasopressin (V2) receptor

Tolvaptan: V2 receptor antagonist allow the free water excretion that is required – diuretics not good as they excrete sodium along with water and therefore there is no change in osmolality and the hyponatraemia is exacerbated. Very expensive

136
Q

WHO infertility

A

Group I Hypothalamic pituitary failure – not producing GnRH, ovaries then don’t get FSH or LH (Hypogonadotrophic hypogonadism)

group II Hypothalamic pituitary dysfunction

Group III: Ovarian failure

137
Q

Anorexia management

A

Pulsatile GnRH (pump): SC or IV. SC or IV. Pump worn continuously (Pulsatile administration every 60-90 mins/Mono pregnancy)

Gonadotrophin (FSH+LH) daily injections: higher multiple pregnancy rates

138
Q

PCOS diagnosis

A

Bloods: high free androgens, high LH, impaired glucose tolerance

Diagnosis: score 2 out of three:

  • chronic anovulation: Oligio/amenorrhoea
  • polycystic ovaries – ultrasound
  • hyperandrogenism (clinical or biochemical) e.g. acne, hirsutism

Insulin resistance - lowers SHBG: increased free testerstone

139
Q

PCOS management

A

lifestyle: wt loss

  1. Clomifene citrate, add in metformin
  2. Gonadotrophin therapy
  3. Laparoscopic ovarian diathermy
140
Q

Primary Hypogonadism

A

Testes primarily affected

Decreased testosterone = decreased -ve feedback

Anterior pituitary secretes higher amounts of LH/FSH to help testes to produce more testosterone “hypergonadotrophic hypogonadism”

Spermatogenesis is affected more than testosterone production

141
Q

Primary Hypogonadism (problem with testes) Ix

A

Measure Total Testosterone and SHBG (between 8-11am: 9am)

FSH and LH

Karotyping

Iron studies

142
Q

Primary Hypogonadism Mx

A

Testosterone replacement therapy

143
Q

Contradictions to testosterone therapy

A
  • Confirmed hormone responsive cancer (e.g. prostate/breast)
  • Possible prostate cancer (e.g. raised PSA, suspicious prostate on PR).
  • Haematocrit >50%. Stimulates bone marrow to produce RBC, will cause people to become polycythaemia – increased chance of stroke and thickened blood
  • Severe sleep apnoea/heart failure
144
Q

Secondary Hypogonadism (Kallmann’s syndrome)

A

• Hypothalamus/pituitary affected, testes capable of normal function

LH/FSH low (or inappropriately normal) despite low testosterone “hypogonadotrophic hypogonadism”

Not able to produce higher LH/FSH due low testosterone

Spermatogenesis and testosterone production are affected equally – whole testes are not being stimulated

145
Q

Kallmann’s syndrome

A

isolated hypogonadotrophic hypogonadism”)

Genetic disorder: isolated GnRH deficiency and hyposmia/anosmia

146
Q

MEN 1

A

AD: Mutations occur throughout MEN1 gene located chromosome 11q13

3Ps: parathyroid, pituitary and pancreatic

147
Q

Leading causes of death in MEN1

A

malignant pancreatic neuroendocrine tumour

thymic carcinoids

148
Q

MEN2

A

AD: RET mutations

149
Q

MEN2A

A

MEN2A accounts for 90‐95% of MEN2 cases

MEN2A describes combination of medullary thyroid cancer in association with phaeochromocytoma and parathyroid tumours

150
Q

MEN2B

A

MEN2B is less frequent (5¬‐10% of MEN2 cases)

MEN2B = MTC and phaeochromocytoma in association with a marfanoid habitus, mucosal neuromas, medullated corneal fibres, intestinal autonomic ganglion dysfunction

151
Q

VHL

A

Tumours of abnormal blood vessels – angioma of the eyes

Mutation in VHL gene

Autosomal dominant

Gene mutation leads to accumulation of HIF proteins and stimulation of cellular proliferation

Range of vascular tumours

152
Q

Carney Complex

A

autosomal dominant syndrome associated with spotty pigmentation of the skin, endocrinopathy, and endocrine and nonendocrine tumors, including the following: Myxomas of the skin, heart, breast, and other sites. Primary pigmented nodular adrenocortical disease.
Primary pigmented nodular adrenocortical disease = PPNAD

PPNAD causes the adrenal glands to produce an excess cortisol leading to the development of Cushing syndrome

153
Q

McCune¬‐Albright Syndrome

A

disorder that affects the bones, skin, and several hormone-producing (endocrine) tissues.

Medical Diseases (18 decks)

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