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Endocrine 1 Flashcards

1
Q

Adrenal cortex structure and function

A

Go Fetch Rex, Makes Good Sex

Zona Glomerulosa - Mineralocorticoids - ALDOSTERONE
Zona Fasciculata - Glucocorticoids - CORTISOL
Zona Reticularis - Sex hormones - Androgens - TESTOSTERONE

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2
Q

Renin

A

Secreted by juxtaglomerular cells
In response to low BP - SNS activation
Converts ANGIOTENSINOGEN to AT1

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3
Q

Angiotensin

A

AT1 converted to AT2 by ACE (from lungs)

Causes systemic vasoconstriction
Stimulates thirst centres in brain
Causes CV hypertrophy
Stimulates ZG to produce ALDOSTERONE

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4
Q

Aldosterone

A

Secreted by zona Glomerulosa
Acts on DCT and collecting ducts
Increases SODIUM reabsorption
Increases POTASSIUM excretion

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5
Q

ADH - Vasopressin

A

Secreted by PP - In response to low BP
Acts on collecting ducts
Increases water reabsorption

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6
Q

Hypervolaemic state

Hypertension

A

Cardiac distension
Raised AT2

Atrial myocytes secrete ANP

  • Vasodilation
  • Inhibits RENIN production
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7
Q

Addison’s aetiology

A

Primary adrenal insufficiency

Primary HYPOaldosteronism - AI

TB
Metastatic disease
HIV

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8
Q

Addison’s presentation

A

TTTT
Thin, Tanned, Tired, Tearful

N/V
Dizziness
Fatigue

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9
Q

Addison’s investigations

A

Bloods - U+E, FBC, serum CORTISOL

Short synACTHen test

  • Give ACTH
  • Should stimulate an increase in CORTISOL
  • Will not happen in Addison’s

CT adrenals

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10
Q

Addison’s clinical findings

A

Low CORTISOL

  • HYPOglycaemia
  • HYPERpigmentation - Palmar creases, joints, buccal mucosa

Low ANDROGENS

Low BP
Low SODIUM
High POTASSIUM

Metabolic acidosis

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11
Q

Addison’s management

A

Replace Mineralocorticoids - FLUDROCORTISONE
Replace Glucocorticoids - HYDROCORTISONE

Vaccinations

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12
Q

Addison’s - Adrenal crisis precipitants

A

Infection
Missed medication
Stress
Surgery

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13
Q

Addison’s - Adrenal crisis presentation

A

Abdo pain
Cramps
Fatigue

Very low BP - Circulatory collapse

Metabolic acidosis

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14
Q

Addison’s - Adrenal crisis management

A

IV FLUDROCORTISONE

IV HYDROCORTISONE

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15
Q

Cushing’s aetiology

A

Gushing CORTISOL

ACTH dependent

  • Pituitary tumour - Increased ACTH
  • Ectopic - SCLC

ACTH independent

  • Adrenal tumour
  • Exogenous CORTISOL - Steroids
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16
Q

Cushing’s signs and symptoms

A

BBIIGGGG

Bone - Osteoporosis and fractures
Blood pressure ^^^

Infections
Irritability

GLUCOSE ^^^
Gynaecomastia
GnRH inhibition - Amenorrhoea
Gluconeogenesis

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17
Q

Cushing’s - Gluconeogenesis signs

A

Buffalo hump
Moon face

Diabetes
Central obesity
Muscle wasting
Abdominal striae

Thick skin
Bruising

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18
Q

Cushing’s investigations

A

24hr urinary free CORTISOL
ACTH levels - Low in ACTH independent

DEX suppression test - Low dose
- DEX will not suppress CORTISOL in Cushing’s

DEX - High dose

  • Differentiate between pituitary and ectopic
  • Suppression of Cortisol = Pituitary problem
  • NO suppression of cortisol = Ectopic problem

MRI adrenals
CT pituitary and thorax (SCLC)

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19
Q

Cushing’s management

A

Treat cause

  • Tumour excision
  • Steroid reduction

KETOCONAZOLE and METYRAPONE
- Decrease CORTISOL production

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20
Q

Conn’s aetiology

A

Primary HYPERaldosteronism

Primary - Low RENIN

  • Idiopathic
  • Adenoma

Secondary - High RENIN

  • Chronically low BP
  • Cardiac failure
  • Liver cirrhosis
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21
Q

Conn’s presentation

A

High ALDOSTERONE
High BP
High SODIUM

Low POTASSIUM

  • Cramps
  • Weakness
  • Paraesthesia

Metabolic alkalosis

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22
Q

Conn’s investigations

A

ALDOSTERONE:RENIN ratio

Primary - High ALDOSTERONE and low RENIN

Secondary - High ALDOSTERONE and high RENIN

CT adrenals

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23
Q

Conn’s management

A

ALDOSTERONE antagonist - SPIRONOLACTONE

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24
Q

HYPERcalcaemia aetiology

A

METASTASES
MYELOMA

Granulomatous disease
TB/Sarcoidosis

HYPERthyroidism
HYPERparathyroidism

Dehydration
Addison’s

Drugs

  • THIAZIDES
  • LITHIUM
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25
HYPERcalcaemia presentation
``` Bones - Bone pain Stones - Renal stones Groans - Abdominal pain Moans - Depression Thrones - Polydipsia, polyuria, constipation ``` Short QT
26
HYPERcalcaemia investigations and management
ECG - Short QT! Calcium profile - Including vitamin D HyperPTH screen - PTH ^ - Should be LOW if Calcium ^ - Low phosphate - Tech-99 scan - PTH gland Skeletal survey CXR - TB/sarcoid Myeloma screen - Protein electrophoresis / ESR Management - IV fluids - IV bisphosphonates
27
HYPOcalcaemia aetiology
Diet - Vitamin D deficiency Malabsorption HYPOparathyroidism - Secondary HYPERparathyroidism Renal disease Acute pancreatitis
28
HYPOcalcaemia presentation
``` Tetany - Chvostek sign Weakness Paraesthesia - Peri-oral Trosseau's sign- Abnormal hand posturing with BP cuff Long QT ```
29
HYPOcalcaemia investigations
``` Serum CALCIUM PTH U+E CRP Faecal calprotectin Anti-TTG ```
30
HYPOcalcaemia management
Calcium supplementation - ADCAL IV CALCIUM GLUCONATE - Risk of tissue necrosis Treat cause
31
Acromegaly aetiology
Abnormal GH secretion | Pituitary adenoma
32
Acromegaly presentation
Bitemporal hemianopia - Tunnel vision Headaches Dizziness Greasy skin Sweating Large facial features Large square hands Large feet Carpal tunnel Diabetes HTN
33
Acromegaly investigations
IGF-1 | MRI pituitary
34
Acromegaly management
Somatostatin analogue - OCTREOTIDE | Transspenoidal tumour resection
35
HYPERkalaemia aetiology
Addison's Rhabdomyolysis AKI Metabolic acidosis Drugs - SPIRONOLACTONE - ACE-I - ARB - HEPARIN
36
HYPERkalaemia presentation
Weakness Fatigue Flaccid paralysis Decreased reflexes
37
HYPERkalaemia investigations
ECG - TTT ``` Tall Tented T waves Absent P waves Broad QRS Long PR Sinusoidal wave VT ```
38
HYPERkalaemia management
C BBIG, K DRop CALCIUM GLUCONATE - Cardiac membrane protection - Only give if K > 6.5 or ECG signs - Can cause tissue necrosis ``` Beta agonist - SALBUTAMOL Bicarbonates - SODIUM BICARBONATE INSULIN - Moves POTASSIUM back into cells GLUCOSE - DEXTROSE Diuretics - Eliminate POTASSIUM Renal dialysis ```
39
HYPOkalaemia aetiology
FUROSEMIDE THIAZIDES Conn's N/V DKA management - INSULIN
40
HYPOkaelaemia presentation
Weakness Hypotonia Cramps Paraesthesia
41
HYPOkalaemia investigations
ECG Inverted T waves Prolonged PR U waves ST depression
42
HYPOkalaemia management
Oral POTASSIUM - SANDOK
43
SIADH aetiology
Ectopic secretion - SCLC Lung - TB, pneumonia Brain - Meningitis, stroke, abscess Drugs - Carbamazepine
44
SIADH pathophysiology
``` ADH made in hypothalamus Secreted by PP Binds to V2 receptors Increases number of aquaporin-2 channels in collecting tubule Leads to increased reabsorption of water ```
45
SIADH presentation
Irritability Muscle cramps Tremor
46
SIADH investigations
Low serum osmolality High urine osmolality Identify cause - CT head - CXR
47
SIADH management
SLOW TO AVOID CENTRAL PONTINE MYELINOLYSIS Treat cause Restrict fluids HYPERTONIC SALINE DEMECLOCYCLINE
48
Diabetes insipidus aetiology
Cranial - Pituitary tumour - Trauma - Surgery Nephrogenic - CKD - LITHIUM - Low POTASSIUM - High CALCIUM
49
Diabetes insipidus presentation
Low ADH Polydipsia Polyuria Postural HYPOtension
50
Diabetes insipidus investigations
High serum osmolality Low urine osmolality DESMOPRESSIN stimulation test - Cranial - Change in osmolality - Nephrogenic - Unable to respond - No change in osmolality Find cause - Imagine
51
Diabetes insipidus management
Cranial - DESMOPRESSIN Nephrogenic - THIAZIDES + low salt diet Treat cause
52
Pheochromocytoma aetiology
MEN-2 Malignant proliferation of chromaffin cells Production of catecholamines
53
Pheochromocytoma presentation
TRIAD! 1. Headaches 2. Sweating 3. Palpitations HTN Cafe au lait spots
54
Pheochromocytoma investigations
24hr Metanephrines 24hr catecholamines MRI adrenal medulla
55
Pheochromocytoma management
ALPHA-BLOCKER BETA-BLOCKER Tumour resection
56
Thyroid structure and function
Hypothalamus secretes TRH AP secretes TSH Thyroid produces T3 and T4 T3 and T4... - Regulate use of energy sources - Protein synthesis - Control body's sensitivity to other hormones
57
Classification of thyroid disorders
HYPOthyroidism - Primary - Problem affecting thyroid galnd - Secondary - Problem with pituitary - Congenital HYPERthyroidism - Primary - Secondary < 1%
58
HYPOthyroidism aetiology
Hashimoto's thyroiditis - AI disease associated with DM1, Addison's or pernicious anaemia - Transient thyrotoxicosis in acute phase Drugs - LITHIUM - AMOIDARONE Subacute thyroiditis - de Quervain's - Associated with painful goitre and raised ESR Iodine deficiency - Most common cause in developing world
59
HYPERthyroidism aetiology
Graves' disease - Most common cause of thyrotoxicosis - May be associated with thyroid eye disease Toxic multinodular goitre - Autonomously functioning thyroid nodules that secrete excess thyroid hormones Drugs - AMOIDARONE
60
HYPOthyroidism presentation
Weight gain Lethargy Cold intolerance Dry cold yellow skin Non-pitting oedema - Hands and face Dry coarse scalp hair Loss of lateral aspect of eyebrows Constipation Menorrhagia Decreased deep tendon reflexes Carpal tunnel syndrome
61
HYPERthyroidism s/s
Weight loss Restlessness Heat intolerance Palpitations Arrhythmias - AF? Sweating Pretibial myxoedema Thydoid acropachy - Clubbing Diarrhoea Anxiety Tremor
62
TFTs Graves' disease Primary HYPOthyroidism Secondary HYPOthyroidism
Graves' - Low TSH - High T4 Primary HYPOthyroidism - High TSH - Low T4 Secondary HYPOthyroidism - Low TSH - Low T4
63
Sick euthyroid syndrome
Low TSH Low T4 Common in hospital inpatients Changes reversible upon recovery from systemic illness No treatment required
64
Subclinical hypothyroidism
High TSH Normal T4 Patients on their way to developing HYPOthyroidism
65
Poor THYROXINE compliance
High TSH Normal T4 Patients only taking THYROXINE in the days before a routine blood test T4 normal but TSH lags - Reflects long-term low T4 levels
66
Thyroid disorders- Additional investigations
Autoantibodies - Hashimoto's - Anti-thyroid peroxidase (TPO) - Graves' - TSH receptor antibodies - Thyroglobulin antibodies Nuclear scintigraphy - Toxic multinodular goitre reveals patchy uptake
67
Thyroid disorder management
HYPOthyroidism - LEVOTHYROXINE HYPERthyroidism - Propranolol - Control symptoms - CARBIMAZOLE - Radioiodine treatment
68
HYPOnatraemia definitions
Normal SODIUM = 135-145 HYPOnatraemia < 135 Severe < 125 Acute < 48 hours Chronic > 48 hours
69
HYPOnatraemia aetiology
EXCESS WATER HYPOvolaemic EUvolaemic HYPERvolaemic
70
HYPOnatraemia presentation
Chronic - Asymptomatic Acute moderate - Headache - Irritability - N/V - Confusion/delirium - Unsteady gait Acute severe - Stupor/coma - Convulsions - Respiratory arrest
71
HYPOnatraemia - Effect on the brain
Low serum osmolality Water moves into the brain causing swelling Loss of SODIUM, POTASSIUM, CHLORINE, to compensate
72
HYPOnatraemia management
HYPER or EUvolaemic = Fluid restriction HYPOvolaemic = SALINE replacement

3B (23 decks)

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